GreyMatters
Educational articles, BetterBrain resources, latest in brain health, and news about us. Written for you, with expertise (and love).

The Lp(a) drug that lowered the number but not the risk: what the pelacarsen trial means for you | BetterBrain
What the Lp(a)HORIZON trial found
The short version: On September 4, 2026, Novartis announced that pelacarsen, its lipoprotein(a)-lowering drug, did not meet the primary goal of its Phase 3 trial. The drug lowered Lp(a). People taking it had heart attacks, strokes, and cardiovascular deaths at about the same rate as people on placebo.
That result surprised a lot of cardiologists. It is also a useful moment to explain a marker that sits on the BetterBrain panel and on very few standard cholesterol tests.
The trial, called Lp(a)HORIZON, enrolled 8,323 people who already had cardiovascular disease and an Lp(a) level of 70 mg/dL or higher. Participants received either pelacarsen or placebo on top of standard treatment for cholesterol and blood pressure. The question was whether lowering Lp(a) would mean fewer heart attacks, strokes, cardiovascular deaths, and urgent hospital procedures.
For this drug, in this group, the answer was no. In earlier studies pelacarsen had lowered Lp(a) by as much as 80 percent, and Novartis confirmed that levels came down in this trial as well. The combined rate of cardiovascular events did not.
Full data have not been published. Novartis says the results will be presented at an upcoming medical congress, so some of what follows will get sharper over the coming months.
What is Lp(a), in plain language
Lipoprotein(a), usually written Lp(a) and pronounced "L-P-little-a," is an LDL-like particle with an extra protein attached, called apolipoprotein(a). Three things make it different from the cholesterol numbers on a standard panel.
First, your level is set almost entirely by your genes. Diet and exercise barely move it.
Second, it stays roughly the same across your lifetime, which is why guidelines recommend measuring it once rather than every year.
Third, it is common and rarely tested. About one in five people has a high level, and high Lp(a) is associated with roughly a 40 percent higher long-term risk of heart attack or stroke. Yet in one analysis of 71 million US adults, only 0.1 percent had ever been tested. The 2026 ACC/AHA cholesterol guideline now recommends that every adult have Lp(a) measured at least once.
Why Lp(a) is a brain health marker
The stroke risk is why Lp(a) matters at BetterBrain. The vessels that feed your heart are the same kind of vessels that feed your brain, and vascular damage is one of the major pathways to cognitive decline. High cholesterol in midlife is now formally recognized as a modifiable dementia risk factor, and Lp(a) is one piece of that vascular picture. That is why it sits in the Blueprint panel alongside ApoB and hs-CRP.
Why a drug can lower the number and miss the outcome
This is the question cardiology is now arguing about, and nobody has the full answer yet. Three hypotheses are getting the most attention.
The reduction may need to be bigger
Lp(a) is measured in much larger units than LDL. A Mendelian randomization analysis estimated that Lp(a) would need to fall by about 66 mg/dL to produce the same heart benefit as a standard 39 mg/dL drop in LDL. For people starting near the trial's entry threshold, an 80 percent reduction may land right around that line. Two competing drugs, Amgen's olpasiran and Lilly's lepodisiran, lower Lp(a) by more than 90 percent, and their outcome trials are expected to read out in 2028 and 2029, with others behind them.
Everything else was already well controlled
Everyone in this trial had established cardiovascular disease and was already on aggressive treatment for LDL, blood pressure, and diabetes. When LDL has been driven very low and antiplatelet therapy is standard, there may be little room left for one more lipid-lowering drug to show a benefit over five years. The genetic studies that made Lp(a) look so important reflect a lifetime of exposure. Treating someone late, after decades of arterial damage and a first event, is a different experiment.
The number may not be the thing
Cardiologist Eric Topol wrote a sharp piece pairing the pelacarsen result with the failure of an anti-inflammatory heart drug in the ZEUS trial. His argument: both trials lowered a blood marker without confirming the marker was driving disease in those particular patients. Lp(a) particles carry oxidized phospholipids, which are thought to be the inflammatory cargo doing the damage, and a standard Lp(a) test does not tell you how much of that cargo a given person is carrying. Two people with the same Lp(a) can have very different amounts of inflammation in their arteries.
None of these is proven. What is clear is that a marker being causally linked to disease, which Lp(a) is, does not guarantee that a drug targeting it will help everyone with a high level.
The honest caveats
The full data are not out. Everything above is based on a topline announcement. The event rates, subgroups, and safety data will be presented at a medical congress later.
This was a secondary prevention trial. Everyone had already had a cardiovascular event or had established disease. The trial does not tell us what Lp(a) lowering would do in people who have never had an event.
One drug, one mechanism. Pelacarsen is an antisense oligonucleotide. Other Lp(a) drugs use different mechanisms and reach deeper reductions. Their results could differ.
The genetic evidence has not changed. Hundreds of studies link high Lp(a) to heart attack, stroke, peripheral arterial disease, and aortic stenosis. A failed drug trial does not undo that.
Our takeaway
We have watched this pattern before. Raising HDL looked like a great idea until the drugs that did it failed to prevent heart attacks. Lowering triglycerides with fibrates cleared the biomarker and did not move outcomes. In each case the lesson was the same: a biomarker is a signal about your biology, and the useful question is what that signal tells you to do differently.
For Lp(a), the answer today is the same as it was last month. Your number tells you how much genetic vascular risk you are carrying. It does not, yet, tell you to take a specific Lp(a) drug, because there is not one. What it does is raise the stakes on everything else that protects your blood vessels: the ApoB you can lower, the blood pressure you can control, the blood sugar and inflammation you can manage, the fitness you can build. High Lp(a) is a reason to be more aggressive on the levers that work, and the evidence for those levers did not change on September 4.
That is also why Lp(a) stays on our panel. A failed drug trial does not make a risk factor less real. It makes knowing about it early more important, because the tools you have are the ones that need time.
What this means for you, right now
If you have never had Lp(a) measured, get it done once. It is on every Blueprint panel. If you are already a BetterBrain client, your result is in the BetterBrain dashboard with your other vascular markers.
If your Lp(a) is high, push harder on what is proven. ApoB is the number to lower, through diet, movement, and, where your physician recommends them, medications. Blood pressure, blood sugar, and hs-CRP round out the picture. A BetterBrain coach can help turn that into a small set of priorities rather than a long list.
If you have already had a heart attack or stroke, the trial's most useful lesson is what modern secondary prevention looks like: every established risk factor treated aggressively, with your cardiologist.
If you want the background, we covered how to read a cholesterol panel in Cholesterol and your brain, and why ApoB matters more than LDL in our VERVE-102 issue.
Common questions
What is Lp(a) and why does it matter?
Lipoprotein(a) is an LDL-like particle with an extra protein attached. Levels are mostly inherited and stable over a lifetime. High Lp(a) is associated with higher long-term risk of heart attack, stroke, and aortic valve disease. About one in five people has an elevated level, and most have never been tested.
Did the pelacarsen trial fail?
Yes. The Lp(a)HORIZON trial of 8,323 people with established cardiovascular disease did not meet its primary endpoint. Pelacarsen lowered Lp(a), but the rate of cardiovascular death, heart attack, stroke, and urgent revascularization was not significantly different from placebo. Full results are expected at a medical congress later in 2026.
Does this mean Lp(a) does not matter?
No. The genetic and population evidence linking high Lp(a) to cardiovascular disease is strong and unchanged. The trial tested one drug in one group of already well-treated patients. It raises questions about how, when, and in whom Lp(a) lowering helps, not about whether Lp(a) is a real risk factor.
Should I still get my Lp(a) tested?
Yes. The 2026 ACC/AHA guideline recommends every adult have Lp(a) measured at least once. Knowing your number does not change the number, but it changes how aggressively you and your doctor treat the risk factors you can move. Lp(a) is included in every BetterBrain Blueprint panel.
Can I lower Lp(a) with diet or exercise?
Not meaningfully. Lp(a) is largely set by genetics. Some medications shift it modestly, but there is no approved therapy designed to lower it. The practical strategy is to lower the risk around it: ApoB, blood pressure, blood sugar, inflammation, and fitness.
Are other Lp(a) drugs still being tested?
Yes. Amgen's olpasiran and Lilly's lepodisiran both lower Lp(a) by more than 90 percent, and their outcome trials are expected in 2028 and 2029. Oral Lp(a) inhibitors are also in development.
How is Lp(a) connected to brain health?
Through your blood vessels. Lp(a) is associated with ischemic stroke, and vascular damage is one of the main pathways to cognitive decline. Protecting the vessels that feed your heart protects the ones that feed your brain.
Does BetterBrain test Lp(a)?
Yes. Lp(a) is part of the 50+ brain-relevant biomarkers in Blueprint, alongside ApoB, hs-CRP, homocysteine, and metabolic markers. Results are reviewed with a brain health coach who helps you decide what to act on first.
One number you can measure once, and act on for decades
Everything at BetterBrain starts the same way: your health history, your lifestyle, your brain-relevant health data, and a coach who helps you make sense of it, narrow it to a few priorities, and build a plan that adjusts as you go. The only thing you decide is where you start.
If you want to begin with your data, that is Blueprint: 50+ brain-relevant biomarkers including Lp(a), ApoB, and hs-CRP, cognitive testing, and a 90-minute consultation with a brain health coach. It starts at $89 with insurance. If you would rather talk to someone first, the Coaching Program starts with the conversation and adds testing later.
The 5 Brain Health Recommendations We Make Most Often
Move your body, build strength, eat well, get enough sleep, and close your nutritional gaps. Most brain health advice comes down to some version of that list, and it is good advice for almost everyone.
But knowing what is generally good for brain health is different from knowing what will be best for yours. The highest-impact action depends on your biology. Your blood pressure, metabolic health, nutrient levels, cardiovascular fitness, sleep, genetics, and lifestyle can all change what deserves your attention first.
Still, when we looked across BetterBrain coaching action plans, five recommendations appeared again and again. Some are among the most evidence-supported things anyone can do for healthy aging. Others come up because they address nutritional gaps that are easy to identify and act on. Here are the five, what the evidence says about each, and how to tell which one matters most for you.
Summary
- The five recommendations that appear most often in BetterBrain coaching plans are strength training, omega-3s, aerobic exercise, B vitamins, and adequate protein.
- Aerobic exercise and strength training carry the broadest evidence for healthy aging. Randomized trials suggest modest cognitive benefits for both.
- Omega-3s and B vitamins help most when they correct a real gap. In people who already have adequate levels, routine supplementation has not consistently improved cognition.
- Protein supports the muscle maintenance that keeps you moving, training, and independent as you age.
- The most common recommendations are not automatically your top priorities. Bloodwork and a full picture of your health decide where to start.
Why the same five recommendations keep coming up
Because brain health is whole-body health. Your brain does not age independently of the rest of your body: muscle, metabolic health, cardiovascular function, balance, and the ability to stay physically active are deeply interconnected with how well you age.
That is why coaching plans built from very different bloodwork still converge on some of the same actions. Two of the five below are foundational behaviors that benefit nearly everyone. Two are nutrients where common gaps can be identified with a blood test and corrected relatively easily. One supports all the others.
1. Strength training
Strength training comes up more consistently in BetterBrain coaching plans than almost anything else.
Resistance training supports strength, muscle mass, mobility, and physical function. It may support cognition too: a 2025 network meta-analysis of 58 randomized trials covering 4,349 participants found improvements in global cognitive scores among older adults who trained. These are short-term cognitive measures, not dementia outcomes, so the honest summary is modest benefit with a consistent direction. We broke down the science in more detail in what six months of lifting weights does to your hippocampus.
The brain health case for strength training is bigger than any single cognitive effect. Maintaining muscle protects the metabolic and cardiovascular systems your brain depends on, and it preserves the physical capacity to keep doing everything else on this list.
A useful general goal is to train the major muscle groups a few times per week and gradually increase what your body can do. The right starting point depends on your current fitness, health, and experience.
You can learn more about strength training on the BetterBrain App here.
2. Omega-3s
Omega-3s are fats involved in brain, cardiovascular, and metabolic health. EPA and especially DHA are structural components of neuronal membranes and play roles in inflammation and neurotransmission.
The trial evidence is genuinely mixed, and the pattern matters. Meta-analyses of randomized trials have reported modest cognitive benefits, mostly in people with low fish intake or mild cognitive impairment. The two largest trials in generally healthy adults, VITAL-Cog and AREDS2, found no cognitive benefit from supplementation.
That pattern is exactly why we prefer personalization over blanket recommendations. Someone who regularly eats fatty fish and already has healthy omega-3 status may have little reason to add a supplement. Someone who gets very little EPA and DHA through their diet may have a much clearer opportunity. We cover food sources, forms, and dosing in unlocking the power of omega-3s.
The BetterBrain approach: understand your diet and biomarkers first, then supplement when there is a reason to.
3. Aerobic exercise
Of the five, aerobic exercise has the broadest overall evidence base for healthy aging.
Regular cardiovascular activity supports cardiorespiratory fitness, blood pressure, glucose regulation, and metabolic health. Randomized trials suggest modest benefits for cognition, and observational research consistently associates higher physical activity with lower rates of cognitive decline and dementia. Observational findings show association rather than cause, but the direction is consistent across decades of research, and the cardiovascular and metabolic benefits are established on their own.
Walking counts. Cycling counts. Swimming counts. Running counts. The best form of cardio is usually the one you can keep doing consistently.
Learn more about aerobic training
4. B vitamins
B vitamins are an area with real opportunity, and context matters more here than almost anywhere else.
Vitamin B12 and folate are essential for normal neurological function, and correcting a true deficiency is important: frank B12 deficiency can cause neurological symptoms that are reversible when treated. Research in people with mild cognitive impairment has also produced interesting results. In the VITACOG trial, a randomized trial of 168 adults with mild cognitive impairment, B-vitamin treatment slowed the rate of brain atrophy on MRI, with the largest effect in participants who started with higher homocysteine.
That does not mean everyone benefits from a B-complex. Across 11 randomized trials covering roughly 22,000 participants, routine B-vitamin supplementation did not improve cognition in people who already had adequate levels.
This is another example of the importance of blood testing to understand your baseline and get a better view of what is going to impact your brain health the most.
Get started with BetterBrain bloodwork
Schedule your BetterBrain retest
5. Adequate protein
Protein might not be the first thing you associate with brain health. But healthy aging depends in part on maintaining the physical capacity to keep moving, exercising, and functioning independently, and adequate protein supports muscle maintenance, recovery, and the adaptations that come from resistance training.
How much protein someone needs depends on age, activity level, body size, health, and goals. A commonly used target is at least 0.7 grams of protein per pound of body weight daily, which works out to roughly 110 grams for a 160-pound adult, and possibly more if you are training intensely. Some experts recommend up to 1 gram per pound for strength and longevity goals, since hitting a protein target every day is hard and a higher target builds in a buffer.
Which recommendation should you start with?
The one that matches your biology, which is not necessarily the one that appears most often.
Omega-3s and B vitamins can sometimes be relatively simple gaps to correct. Strength training, aerobic exercise, and improving nutrition tend to require bigger and more sustained behavior change. Good brain health plans usually contain both kinds: quick wins, and habits you build into your life for years.
But even the most common recommendations are not automatically your top five. Someone with insulin resistance may need to focus heavily on metabolic health. Someone with low B12 needs a different plan. Someone with poor cardiovascular fitness, elevated ApoB, inadequate protein intake, or poor sleep has another set of priorities.
That is why BetterBrain starts by looking at the whole picture: your bloodwork, cardiovascular and metabolic health, nutrition, exercise, sleep, cognition, health history, and, where appropriate, genetics. Then you can take what science says about healthy brain aging and decide where to focus first.
The bottom line
The five recommendations above come up constantly because they address things that matter for almost every brain. Which of them belongs at the top of your plan is a question your biology answers.
If you have not seen your full picture yet, that is the place to start. Blueprint includes 50+ biomarkers, a consultation of up to 90 minutes with a brain health expert, and a personalized action plan ranked by impact. $89 with insurance, $399 cash pay.
Already a BetterBrain client? Open your protocol to see the science behind each technique and the recommendations most relevant to you.
Frequently asked questions
What is the best exercise for brain health?
The best-supported combination is aerobic exercise plus strength training. Aerobic activity supports the cardiovascular and metabolic systems the brain depends on, and randomized trials suggest modest cognitive benefits. Resistance training preserves muscle, mobility, and physical function, and a 2025 meta-analysis of 58 randomized trials found improvements in global cognition among older adults who trained. The most effective exercise in practice is the one you can sustain consistently.
Does strength training help your brain?
Research suggests it can. A 2025 network meta-analysis of 58 randomized trials found resistance training improved global cognitive scores in older adults. The broader case is indirect but strong: strength training preserves muscle mass, metabolic health, and physical function, all of which are interconnected with how well the brain ages. A common goal is training the major muscle groups a few times per week.
Should I take omega-3 supplements for brain health?
It depends on your starting point. Trial evidence suggests modest cognitive benefits mostly in people with low fish intake or mild cognitive impairment, while the two largest trials in generally healthy adults found no cognitive benefit from supplementation. If you regularly eat fatty fish, you may have little reason to supplement. Understanding your diet and biomarkers first is more useful than defaulting to a capsule.
Do B vitamins help memory?
Only in certain situations. Correcting a true B12 or folate deficiency is important, and in the VITACOG randomized trial, B vitamins slowed brain atrophy in adults with mild cognitive impairment, especially those with high homocysteine. But across 11 randomized trials of roughly 22,000 people with adequate levels, routine supplementation did not improve cognition. Testing your levels tells you which group you are in.
How much protein do you need for healthy aging?
Needs vary with age, activity, body size, and health, but a commonly used target is at least 0.7 grams of protein per pound of body weight daily, roughly 110 grams for a 160-pound adult. Some experts suggest up to 1 gram per pound for strength and longevity goals. Adequate protein supports the muscle maintenance and recovery that keep you active and independent.
How do I know which brain health habit to prioritize?
Start from your biology rather than from a generic list. Blood pressure, metabolic markers, nutrient levels, cardiovascular fitness, and sleep all change what deserves attention first. A comprehensive assessment that reads these together, the way BetterBrain's does, can rank actions by likely impact for you specifically, so you spend effort where it counts.

pTau-217: What the Alzheimer's Blood Test Can and Can't Tell You
pTau-217: What the Alzheimer's Blood Test Can and Can't Tell You
A simple blood draw can now flag Alzheimer's-related changes in the brain years before any symptom appears. For some people that is welcome news, an early window to act. For others it raises a harder question they are not sure how to answer: would they even want to know. Either way, the decision deserves more than a headline.
pTau-217 is the reason this is suddenly everywhere. On August 24, 2026, CNN reported that the FDA had cleared Elecsys pTau217, a new blood test from Roche and Eli Lilly, and a new study in JAMA suggests it may help estimate future cognitive risk in people who have no symptoms yet. The New York Times, meanwhile, focused on the confusion and distress these results can cause.
The test itself is not new to us. BetterBrain began offering direct-to-consumer, expert-supported pTau-217 testing in 2024. In April 2025, physician and scientist Eric Topol called it "one of the most exciting advances in neurology for decades", and that same month BetterBrain was featured in Nature's coverage of the rise of Alzheimer's blood tests. Our takeaway from that feature was as much about responsibility as access. Making a powerful test easier to get is only useful if people also get the context, guidance and support to understand the result.
What is pTau-217?
Tau is a protein found inside brain cells. In Alzheimer's disease, tau undergoes abnormal changes and can eventually form tangles that interfere with how those cells work.
The "p" stands for phosphorylated, meaning a phosphate group has attached to the tau protein. The number 217 points to the precise location where that change happened.
When Alzheimer's-related biology begins developing in the brain, levels of pTau-217 in the blood tend to rise. And although the name refers to tau, blood pTau-217 is especially good at tracking the buildup of amyloid plaques, another hallmark of Alzheimer's. Until recently, that kind of information generally required an expensive PET scan or a spinal tap.
Why pTau-217 matters for early detection
Alzheimer's-related brain changes can begin 15 to 20 years before memory problems show up, and pTau-217 may become abnormal during this preclinical period. That makes it one of the most promising tools we have for identifying Alzheimer's-related pathology before symptoms start, which is exactly when there is the most time to act.
Does an elevated pTau-217 result mean I have Alzheimer's?
No. An elevated pTau-217 result is a signal, not a diagnosis.
It suggests that Alzheimer's-related biological changes may be present and that your risk of developing cognitive symptoms is higher. It cannot tell you with certainty whether you will develop symptoms, or when. A negative result is reassuring, but it does not guarantee you will never develop Alzheimer's. It points to a lower likelihood of significant Alzheimer's-related pathology at the time you were tested.
This distinction between detection and prediction sits at the center of the current debate.
What the JAMA study actually found
In July, a JAMA study of nearly 2,700 cognitively healthy older adults found that higher pTau-217 levels were associated with faster cognitive decline and a greater chance of developing cognitive impairment. Among participants with very high levels, researchers estimated a 38% risk of cognitive impairment within five years and a 78% risk within ten years.
Those numbers understandably drew attention. But they were group-level estimates from selected research cohorts whose average age was about 70, and the researchers cautioned that the ten-year figure rested on a relatively small number of people followed for that long. It is meaningful information. It is not a personalized countdown.
Are all Alzheimer's blood tests the same?
Not quite. Several are now available, and each gives a slightly different view of Alzheimer's-related biology. Some measure pTau-217 alone, others combine it with additional markers, and each laboratory method comes with its own reference ranges and cutoffs. That makes the specific test an important part of understanding the result.
The first Alzheimer's blood test cleared by the FDA, in May 2025, measures the ratio of pTau-217 to an amyloid marker. Later that year the FDA cleared Elecsys pTau181, designed mainly to help rule out Alzheimer's-related pathology. In August 2026 it cleared PrecivityAD2, which combines several amyloid and tau measurements, followed by the newly cleared Elecsys pTau217, which measures pTau-217 alone.
These FDA clearances apply to tests used as part of a broader clinical evaluation for people who are experiencing cognitive concerns. The results are meant to be read alongside symptoms, cognitive testing, health history and other clinical information.
BetterBrain uses Quest's AD-Detect pTau-217 test, a laboratory-developed assay that uses different technology from both the newly cleared Elecsys test and the ALZpath test used in many published studies. Because each platform measures pTau-217 differently, each result is interpreted using the reference range established for that specific assay. We use the reference range provided by Quest, then interpret the result alongside cognitive testing, kidney function, other biomarkers, health history and lifestyle.
What a pTau-217 result does not tell you
Here is the part of the conversation that often gets missed. We agree with The New York Times that handing someone a frightening result without enough support can cause real distress. That does not mean the test cannot provide useful information. It means the information needs a fuller picture around it.
A pTau-217 result tells us about one part of Alzheimer's biology. It does not tell us why one person with elevated pathology develops symptoms while another stays cognitively healthy for years, and it says nothing about the many other factors shaping that person's brain health.
Those other factors carry real weight. The 2024 Lancet Commission estimated that addressing 14 modifiable risk factors across life could potentially prevent or delay around 45% of dementia cases at the population level. The U.S. POINTER randomized trial found that a program combining exercise, nutrition, cognitive and social activity, and regular health monitoring improved cognition in older adults at elevated risk. And a long-term observational study found that a healthier midlife lifestyle was associated with a lower incidence of cognitive impairment across pTau-217 levels and APOE4 status. Pathology is not the whole story. The real answers come from looking at all of your numbers together.
What should you do with a pTau-217 result?
Unlike LDL cholesterol or blood pressure, pTau-217 is not a marker you improve through one clearly established intervention. It is primarily a measurement tool.
If your level is elevated, the next step is to understand the complete picture. That may include further clinical evaluation, establishing a cognitive baseline, considering confirmatory testing, assessing eligibility for clinical trials or approved treatments when appropriate, and addressing the modifiable factors that contribute to overall dementia risk. Research into using pTau-217 to monitor treatment response is promising, though there is still a lot to learn about this relatively new test.
Why BetterBrain never offers pTau-217 alone
When we started BetterBrain, we were driven by personal experiences with Alzheimer's in our own families. We learned firsthand that brain health is not about one marker or one intervention. So we do not simply order a pTau-217 test and email you the result. We think that would be irresponsible.
We pair pTau-217 with more than 50 other brain-relevant biomarkers in our Essentials Panel, a cognitive assessment and a detailed look at your health history and lifestyle. We look under the hood for modifiable risk drivers across vascular, metabolic, inflammatory, hormonal and nutritional health. A trained clinical expert then walks you through the findings, explains what they do and do not mean, and builds a personalized action plan focused on the areas where you have the most opportunity to improve. If a result calls for more evaluation, we help you identify the right clinical next step alongside your existing doctor.
The real power does not come from one blood test. It comes from combining early detection with a much broader understanding of your biology, then turning that into meaningful action. Knowledge can be powerful, but only when you know what to do with it.
Learn about pTau-217 testing with BetterBrain, or start your brain health journey to see the full picture.
Frequently asked questions
What is pTau-217?
pTau-217 is a form of the tau protein, measurable in blood, that tends to rise as Alzheimer's-related biology develops in the brain. It is particularly good at tracking amyloid plaque buildup, a hallmark of Alzheimer's disease.
Does an elevated pTau-217 result mean I have Alzheimer's?
No. An elevated result suggests Alzheimer's-related changes may be present and that risk is higher, but it is a signal, not a diagnosis. It cannot confirm whether or when someone will develop symptoms.
Are all Alzheimer's blood tests the same?
No. Some measure pTau-217 alone and others combine it with additional markers, and each laboratory method has its own reference ranges. The specific test used is an important part of interpreting the result.
Can you lower your pTau-217?
pTau-217 is not a marker you improve through one established intervention the way you might lower LDL cholesterol. It is primarily a measurement tool. The action lives in the modifiable risk factors around it, such as vascular, metabolic and lifestyle health.
Who should consider pTau-217 testing?
It is often considered by people who want early insight into Alzheimer's-related risk, including those with a family history. It is most useful when the result is interpreted alongside cognitive testing, other biomarkers, health history and lifestyle, not in isolation.
How much does pTau-217 testing cost with BetterBrain?
The pTau-217 test is $299, offered as an add-on to a Blueprint assessment. It isn't sold on its own, and insurance doesn't cover it. See the full breakdown, including where it's available, on our pTau-217 cost page.

VERVE-102: A One-Time Gene Edit for Cholesterol, and Why It's a Brain Story | BetterBrain
One shot to lower cholesterol for life: what PCSK9 gene editing means for your brain
The short version: In the Heart-2 trial, a single infusion of a gene editing therapy called VERVE-102 lowered LDL cholesterol by up to 62% and kept it down for as long as 18 months. It is a phase 1b result in 35 people with inherited high cholesterol, so it is years away from a pharmacy. The part that matters to you now is the target. High LDL in midlife is one of the 14 modifiable dementia risk factors named by the Lancet Commission, and the particle count underneath it, ApoB, is something you can measure this month.
Most people learn their cholesterol is high at an annual physical, get told to watch it, and never find out what the number is actually doing. It is doing something to your brain.
That connection is why a cardiology result got our attention. In May 2026, researchers reported that a single infusion of a gene editing medicine lowered LDL cholesterol substantially, and that the reduction held for up to 18 months. The results were presented at the European Atherosclerosis Society Congress and published in the New England Journal of Medicine.
It is early research in a small, specific group of patients. But the biology it targets is among the most studied in all of cardiovascular medicine, and it runs straight to your brain.
What VERVE-102 actually did
Heart-2 is a phase 1b trial. The interim analysis covered 35 participants, average age 52, all with heterozygous familial hypercholesterolemia, premature coronary artery disease, or both, and all already on the maximum statin dose they could tolerate.
Each received one infusion, at doses from 0.3 to 1.0 mg/kg. The results, per Lilly's May 25, 2026 release:
- PCSK9 protein fell by 51% to 88%, depending on dose.
- LDL cholesterol fell by 9% to 62%. At the highest dose, the drop was 62%, or 78 mg/dL in absolute terms.
- Reductions were sustained, with durability observed for up to 18 months after a single treatment.
- There were no dose-limiting toxicities and no treatment-related serious adverse events. Side effects were mostly low-grade infusion reactions and fatigue. All 35 participants received their full dose and none withdrew.
One infusion. Effects still holding a year and a half later.
How PCSK9 works, in plain language
Your liver clears LDL cholesterol out of your blood using surface proteins called LDL receptors. Think of them as docking ports: the more ports available, the more LDL particles get pulled out of circulation.
PCSK9 is a protein that destroys those ports. More PCSK9 activity means fewer receptors, which means more LDL staying in your bloodstream.
Here is the part that makes this target unusually well understood. Some people are born with naturally low-functioning PCSK9 genes. They have markedly lower LDL across their entire lives and substantially lower rates of heart disease, with no apparent downside. Turning PCSK9 down is not a theory. It is a protective pattern that already exists in nature and has been studied for two decades.
Drugs that lower PCSK9 have been approved for years. What is new here is the delivery. VERVE-102 uses base editing, a precise form of gene editing, to make a single change to the PCSK9 gene inside liver cells. The goal is to do once, permanently, what existing drugs do by repeated injection.
The honest caveats
This headline is easy to over-read. The careful version:
It is a phase 1b trial. That stage is designed mainly to test safety and look for early signals in a small number of people. It has not been shown to prevent heart attacks, strokes, or cognitive decline. A phase 2 trial is the next step, with enrollment planned by the end of 2026.
It is a specific patient group. Everyone enrolled had an inherited form of very high cholesterol or early coronary artery disease and needed aggressive LDL lowering despite maximum oral therapy. These are not general-population results.
Gene editing is a young field. The PCSK9 mechanism is exceptionally well characterized, which is reassuring. Making a permanent edit to a gene is still new, and the long-term safety record takes years to build. Approval, if it comes, will likely start with very high-risk patients such as those with familial hypercholesterolemia, and the price is likely to be high.
It is years away. Nobody should be adjusting their plan today on the expectation that this arrives soon.
Why cholesterol is a brain story, not only a heart story
Brain health is whole-body health, and few things connect the two as directly as lipids.
ApoB is the number underneath LDL
You have probably heard of LDL cholesterol. ApoB is the more precise measurement sitting beneath it.
Every LDL particle carries exactly one ApoB protein. So LDL-C tells you how much cholesterol is being carried inside LDL particles, while ApoB tells you how many particles there actually are. Since it is the particles that lodge in artery walls and start plaque, ApoB is the better predictor of risk. When the two numbers disagree, ApoB is the one to trust.
Among BetterBrain clients, 86% come back with a suboptimal ApoB. It is the single most commonly out-of-range marker we see, and most people have never had it measured.
The Lancet Commission added LDL to the dementia list in 2024
The blood vessels feeding your brain are subject to the same lipid-driven damage as the ones feeding your heart, and that vascular damage is one of the major pathways of cognitive decline.
This is no longer a fringe position. In its 2024 update, the Lancet Commission on dementia prevention added high midlife LDL cholesterol as one of 14 modifiable risk factors, based on cohort studies covering more than a million participants plus a Mendelian randomization meta-analysis of 27 studies. The Commission attributes 7% of preventable dementia to high LDL alone, and links nearly half of dementia cases to the 14 factors combined.
High cholesterol in your forties and fifties is now formally a brain risk factor, not only a heart one.
If you carry APOE4
People who carry an APOE4 variant tend to run higher LDL, and APOE4 is the strongest common genetic risk factor for Alzheimer's disease. That combination is one reason lipid management is a core part of what we do, and one reason knowing your genotype can change what you prioritize rather than just giving you something to worry about.
The bigger picture
Between therapies like this one and the medications already on the shelf, the tools for managing cardiovascular disease are getting very good, and they will keep improving. But adding years to your life is only worth so much if your brain is not working well for those years. That is the conversation most people are not having yet, and it is the one that matters most to us.
What this means for you, right now
You do not have to wait for a therapy that is years away. The target itself, your lipid health, is measurable and movable today.
- Get ApoB tested, not just standard cholesterol. A routine lipid panel gives you total cholesterol, LDL, HDL, and triglycerides. ApoB counts the particles actually driving damage and is rarely ordered unless you ask for it. It is one of the most informative single markers for both heart and brain health.
- Treat lipids as a lifelong number, not a yearly one. The PCSK9 story works precisely because it lowers exposure over decades. Risk accumulates the same way. Small, steady improvements compound in your favor, and starting earlier is worth more than starting perfectly.
- Use the levers you already have. Diet, regular movement, and, where your physician recommends them, proven lipid-lowering medications all work today. Statins and existing PCSK9 inhibitors are not placeholders waiting for gene editing. They are the current standard of care.
- Look at the whole vascular picture. ApoB, Lp(a), triglycerides, blood pressure, and HbA1c interact. One number in isolation rarely tells you what to do first.
ApoB is one of the 50+ biomarkers in the BetterBrain panel, alongside homocysteine, hs-CRP, Lp(a), HbA1c and the rest of the vascular and metabolic markers. See everything we test.
Common questions
Is PCSK9 gene editing available now?
No. VERVE-102 is in phase 1b trials. A phase 2 trial is planned to begin enrolling by the end of 2026, and broad availability is years out. If it is approved, the first patients are likely to be people with familial hypercholesterolemia or other very high-risk conditions.
What is the difference between ApoB and LDL cholesterol?
LDL-C measures the amount of cholesterol carried inside LDL particles. ApoB measures the number of those particles, because each one carries exactly one ApoB protein. Two people can have the same LDL-C with very different particle counts. When the two disagree, ApoB is the better predictor of cardiovascular and cerebrovascular risk.
Does lowering cholesterol reduce dementia risk?
The 2024 Lancet Commission identified high midlife LDL cholesterol as one of 14 modifiable dementia risk factors and attributes 7% of preventable dementia to it. That is an association drawn from large cohort and genetic studies, not proof that lowering LDL prevents dementia in any individual. What is well established is that lipid-driven damage to blood vessels is one of the major pathways of cognitive decline, and that the vessels feeding your brain are affected the same way as the ones feeding your heart.
Should I get an ApoB test?
ApoB is not part of a standard lipid panel and usually has to be requested. It is most informative if you have a family history of early heart disease or dementia, if your LDL and triglycerides do not line up, if you carry an APOE4 variant, or if you simply want a clearer read than total cholesterol gives you. Discuss it with your physician or your Brain Health Coach.
Does BetterBrain test ApoB?
Yes. ApoB is included in the BetterBrain biomarker panel, which covers 50+ markers selected for their connection to brain health, across metabolic, cardiovascular, hormonal, inflammation, and nutrient categories. Blueprint is $89 with insurance and $399 without, and includes a cognitive assessment and an up-to-90-minute session with a Brain Health Coach who turns the results into a personalized action plan.
The bottom line
A one-time gene editing infusion produced large, durable reductions in LDL cholesterol in an early trial, by copying a protective genetic pattern that already exists in nature. It is not available, it is not proven to prevent anything yet, and it will not be in a clinic near you for years.
What is available is the target. Your lipid numbers are one of the few brain risk factors you can measure precisely, act on immediately, and improve over decades. Whatever arrives in five or ten years, the decades in between are the ones you protect now.

Fasting Insulin and Brain Health: The Metabolic Marker Most Physicals Skip
Key takeaways
- Fasting insulin usually moves before fasting glucose. Glucose tells you the result. Insulin tells you the effort behind it.
- In BetterBrain's dashboard, optimal fasting insulin is below 6 mcIU/mL. The fair range runs from 6 to 19.6.
- Higher fasting insulin has been associated with roughly double the Alzheimer's risk in adults 65 and older, with the strongest association in people who did not have diabetes.
- Metabolic syndrome has been associated with a 24% higher risk of young-onset dementia, with a dose response as components accumulate.
- These are observational findings. They establish association, not cause.
- Most standard panels stop at glucose and HbA1c. Fasting insulin is inexpensive and is included in BetterBrain's Essentials panel.
For most people, metabolic health shows up as one line on a lab report. Fasting glucose, 94 mg/dL, flagged normal, nothing to discuss, see you next year.
That reading is accurate. But fasting glucose is also one of the last things to change. Your body can spend years quietly working to hold that number in range, and the work it does to hold it is where the brain story actually starts.
What is fasting insulin?
Fasting insulin measures how much insulin your pancreas is releasing to keep your blood sugar steady after an overnight fast.
Insulin is the hormone that moves glucose out of your bloodstream and into your cells. A fasting insulin test tells you how much of that hormone your body needs to hold a normal blood sugar level while you are not eating. A low number means your cells are responding easily. A higher number means your body is working harder to reach the same result.
In your BetterBrain dashboard, the optimal range for fasting insulin is below 6 mcIU/mL. Above 6, and into the fair range of 6 to 19.6, the picture starts to shift.
The distinction that matters: glucose tells you the result, insulin tells you the effort behind it.
Why your glucose can look normal for years
When cells stop responding well to insulin, the pancreas compensates by producing more of it. Glucose can stay in range through that entire process, sometimes for years, while insulin climbs in the background.
This is why a single normal glucose reading is an incomplete picture. It is a true measurement of an outcome, not a measurement of how much work went into producing that outcome.

Fasting insulin can rise years before glucose looks abnormal.
What the research says about insulin and the brain
Older adults: Alzheimer's risk roughly doubled
In a study published in Neurology, researchers tracked 683 adults aged 65 and older for nearly 3,700 person-years. Alzheimer's risk roughly doubled among people with hyperinsulinemia, and the association was strongest in people who did not have diabetes.
That last detail is the important one. The association was not explained by diabetes being present.
Midlife: the same pattern, six years later
In the ARIC cohort, adults aged 45 to 64 had fasting insulin measured at baseline. Six years later, higher baseline insulin predicted greater decline in delayed word recall and verbal fluency.
The authors described insulin resistance as a potentially modifiable midlife risk factor. That phrase matters because it points at what you can do about it.
A note on complexity
Very low fasting insulin has also been associated with risk in some long follow-up studies, so the relationship is not a straight line. This is exactly why we read insulin alongside glucose, HbA1c, and the rest of the domain rather than treating any single number as a verdict.
What is actually happening in your brain
Your brain is roughly 2% of your body weight and uses about 20% of your resting energy, almost all of it from glucose. Getting that fuel where it needs to go depends on insulin signaling working.
A systematic review of 23 imaging studies covering 5,308 participants found that insulin resistance was associated with reduced glucose uptake in the brain across 22 of 23 studies. The regions involved, the parietotemporal cortex, posterior cingulate, and precuneus, are the same areas that show reduced metabolism in Alzheimer's disease. Some of those associations appeared in people who were cognitively normal at the time of scanning.
Cells that respond poorly to insulin have a harder time pulling in fuel. Consequently, the parts of your brain with the highest energy demand are the ones affected first.
Metabolic syndrome and dementia risk: when the components stack
A 2025 study in Neurology followed nearly 2 million Korean adults aged 40 to 60 for an average of 7.8 years.
Metabolic syndrome, defined as three or more of excess belly fat, high blood pressure, elevated fasting glucose, elevated triglycerides, and low HDL, was associated with a 24% higher risk of young-onset dementia. Each component added to the effect, and participants with all five had roughly 70% higher risk.
Two things worth noting: the association was stronger in people in their 40s than in their 50s, and stronger in women (34%) than in men (15%).
This is observational research, which establishes association, not cause. It is one national population, and the researchers could not account for APOE status. What it does establish clearly: the direction of the effect, a dose response across components, and earlier timing than most people assume.
The metabolic health domain: which markers we read together
When we assess metabolic health at BetterBrain, it is one of the ten health domains we track. We read a group of markers together rather than checking any one off in isolation:
GroupMarkersWhat it tells youGlucose controlFasting glucose, HbA1c, fasting insulinHow easily your body manages fuelLipid loadTriglycerides, ApoBHow much lipid your system is carryingLiver stressALT, ASTHow much metabolic work your liver is absorbingNutrient statusVitamin D, B12, folateWhether you have the raw materials to make and use energy
Any one of these can look unremarkable on its own. Read together, they tell you something a single value can't: whether your body is handling fuel comfortably, or working hard to look like it is.
What you can do
Test your fasting insulin, not just glucose. Most standard panels stop at fasting glucose and HbA1c. Fasting insulin tends to move first, it is inexpensive, and it is included in the 50+ biomarkers in the BetterBrain Essentials panel.
Move after you eat. A short walk in the hour after a meal meaningfully blunts the glucose rise. This is one of the higher-return habits in the metabolic domain because it costs almost nothing. One BetterBrain client liked the idea enough to build a free app for it, called Exercise Snacks for Health & Wellbeing.
Build meals around protein and fiber before the starch. Same food, different order, measurably flatter glucose response. Vegetables and protein first, then the carbohydrate portion.
Finish eating three to four hours before bed. Late meals land against a window when insulin sensitivity is at its lowest. Moving dinner earlier is one of the easiest and most impactful techniques to manage glucose spikes.
Retest and see it move. Fasting insulin and triglycerides respond within weeks. HbA1c takes two to three months to reflect a real change. Knowing which to watch first keeps you from concluding too early that nothing is happening.
Frequently asked questions
Can you have insulin resistance with normal blood sugar?
Yes. When cells stop responding well to insulin, the pancreas compensates by producing more of it, which can hold glucose in the normal range for years. Fasting glucose is typically one of the last metabolic markers to change, which is why a normal reading does not rule out insulin resistance.
What is a good fasting insulin level?
In BetterBrain's dashboard, the optimal range for fasting insulin is below 6 mcIU/mL, with a fair range of 6 to 19.6. Reference ranges vary between labs, and fasting insulin should be interpreted alongside fasting glucose and HbA1c rather than on its own.
Is fasting insulin included in a standard blood panel?
Usually not. Most standard panels stop at fasting glucose and HbA1c. Fasting insulin generally has to be requested specifically. It is included in BetterBrain's Essentials panel of 50+ biomarkers.
Does insulin resistance affect the brain?
Research as associated insulin resistance with reduced glucose uptake in the brain. A systematic review of 23 imaging studies covering 5,308 participants found this association in 22 of the 23 studies, in the parietotemporal cortex, posterior cingulate, and precuneus. Some of those associations appeared in people who were cognitively normal at the time of scanning. These are observational findings.
How quickl can fasting insulin improve?
Fasting inslin and triglycerides can respond within weeks. HbA1c reflects roughly two to three months of glucose exposure, so it takes longer to show a real change. Knowing which marker moves first prevents you from concluding too early that nothing is working.
What is metaolic syndrome?
Metabolic synrome is defined as having three or more of the following: excess belly fat, high blood pressure, elevated fasting glucose, elevated triglycerides, and low HDL cholesterol. A 2025 study of nearly 2 million adults associated it with a 24% higher risk of young-onset dementia, with risk increasing as more components were present.
The bottom line
Metabolic health is not a number you pass or fail. It is a set of markers that move together, and it is the domain where what you do this month shows up in your labs this quarter.
If you have not seen your full metabolic picture, that is a good place to start. Blueprint includes 50+ biomarkers, a consultation of up to 90 minutes with a brain health expert, and a personalized action plan ranked by impact. $89 with insurance, $399 cash pay.
Already have your results? View your metabolic markers to see where you sit and which techniques your Brain Health Coach recommends first.
.webp)
How to Personalize Your Brain Health Plan With Your Own Data
How to Personalize Your Brain Health Plan With Your Own Data
Most brain health advice is useful, but it is also designed for the average person.
Sleep more. Move often. Eat a nutritious diet. Manage stress. Build strength.
These fundamentals matter. But they cannot tell you which risk factors deserve the most attention, what may be changing in your body, or whether your current routine is producing the results you want.
Personalized brain health guidance uses your own labs, health history, sleep, activity, habits, and goals to help determine where to focus first.
BetterBrain members can now bring more of that information into My Vault, the health data home inside the BetterBrain platform. You can upload previous lab results, connect wearable data, and import relevant health context from an AI assistant such as ChatGPT, Claude, or Gemini.
All three tools are available free across BetterBrain accounts.
Why Does Generic Brain Health Advice Have a Ceiling?
General health advice tells you what tends to help people on average. It cannot tell you which intervention is likely to matter most for you.
Two people can follow the same routine and have very different needs because they begin with different:
- Biomarker levels
- Genetics and family histories
- Sleep patterns
- Activity levels
- Medical histories
- Medications and supplements
- Diets, habits, and goals
One person may need to focus on improving sleep consistency. Another may already sleep well but have an elevated cardiovascular risk marker that deserves more attention. A third may be exercising regularly but not recovering adequately.
That is why personalization matters. It helps turn broad recommendations into clearer priorities.
Research has also found that multidomain brain health interventions tailored to individual risk profiles can produce better cognitive outcomes than general health information alone. You can read the randomized controlled trial published in Nature Medicine here.
What Is Personalized Brain Health Guidance?
Personalized brain health guidance applies current research to information about your own health.
Instead of simply telling everyone that sleep is important, personalized guidance can consider:
- How much you are actually sleeping
- Whether your sleep duration or consistency is changing
- How your sleep relates to your activity and recovery
- Whether your current protocol appears to be helping
- Which other risk factors may deserve attention
Personalization does not replace the fundamentals. It helps identify which fundamentals matter most for you, where to begin, and what to monitor over time.
How Does My Vault Help Personalize Your Brain Health Plan?
My Vault brings several sources of health information together inside your BetterBrain account.
You can use it to:
- Upload previous laboratory results
- Connect sleep and activity data from a wearable
- Import relevant health context from another AI assistant
Together, these tools give BeBe, BetterBrain’s AI brain health coach, a more complete picture of your health and goals.
Upload Past Lab Results and Track Changes Over Time
A single laboratory result is only a snapshot. The trend often provides more useful context.
If you have previous results stored in a patient portal, computer folder, email, or paper file, you can upload them to My Vault as a PDF or image. BetterBrain can extract the biomarker results and display them alongside your current numbers.
Tracking results over time can help you understand:
- Whether a biomarker is moving in the desired direction
- Whether a change is new or part of a longer pattern
- How your results respond to changes in your routine
- Whether an intervention appears to be working
- Which markers may deserve further discussion with your clinician
For example, a cholesterol result may appear acceptable when viewed alone. But seeing several years of results together could reveal that the number has been steadily increasing or improving.
Your brain health plan should respond to what is changing, not just what appeared on one test.
Link Your Wearable Data
Questionnaires capture what you remember. Wearables can capture what is happening each day.
If you use a fitness tracker or smartwatch, you can connect it to BetterBrain through the BeBe app and Apple Health. You choose which information you want to share, and you can change the permissions or disconnect the integration at any time.
Depending on your device and permissions, wearable data may provide useful context about:
- Sleep duration
- Sleep consistency
- Daily movement
- Exercise
- Heart rate
- Recovery patterns
- Changes in routine
This can make guidance more specific.
Instead of receiving another reminder that sleep is important, you may be able to see that your sleep duration is adequate but inconsistent, or that your activity has declined over the past several weeks.
The goal is not to obsess over every daily number. It is to recognize meaningful patterns that may otherwise be easy to miss.
Import Your AI Memory
Many people already use ChatGPT, Claude, or Gemini to discuss their health, routines, goals, and preferences.
You may have already told an AI assistant about:
- Your health history
- Current symptoms or concerns
- Injuries
- Medications and supplements
- Family medical history
- Exercise habits
- Diet
- Sleep
- Health goals
- How you prefer advice to be delivered
- Strategies you have already tried
You can now bring that context into BetterBrain instead of starting from the beginning.
Visit Import AI Memory inside My Vault. You will see a prompt that you can open or paste into the AI assistant you use. The assistant will organize the relevant information it knows about you. You can then review the response and paste it into BetterBrain.
The process takes about a minute.
Once imported, BeBe can begin with more context about your history, preferences, goals, and previous efforts.
How Is BeBe Different From ChatGPT, Claude, or Gemini?
General AI assistants draw from broad knowledge across an enormous range of subjects. Their responses are also largely shaped by what you choose to tell them in each conversation.
BeBe is built specifically for brain health. It is grounded in brain health research that has been reviewed and interpreted by BetterBrain’s scientists and clinicians.
BeBe can then apply that specialized knowledge to information within your BetterBrain account, including:
- Your laboratory history
- Wearable sleep and activity data
- Health profile
- Current brain health protocol
- Uploaded documents
- Coaching insights
- Imported health context
- Personal goals and preferences
The distinction is specialized brain health science combined with your personal data.
A general assistant may repeat common recommendations. BeBe is designed to help you understand how the evidence relates to your own risks, results, and priorities.
Is My Health Information Private?
Your imported information stays private to your account and is used to personalize your guidance.
You control what you upload, what wearable information you share, and whether you want to delete information later. Wearable permissions can also be changed or turned off at any time.
Only import information you are comfortable storing in your BetterBrain account.
How Do I Get Started With My Vault?
You do not need to complete everything at once.
Start with whichever option is easiest:
- Upload one previous lab report.
- Connect your wearable through the BeBe app and Apple Health.
- Import relevant health context from ChatGPT, Claude, or Gemini.
- Review your health profile and current protocol.
- Ask BeBe what patterns or priorities stand out.
All three personalization tools are available with a free Self Directed BetterBrain account.
Members who want to go further can also purchase laboratory testing through Blueprint or enroll in the BetterBrain Coaching Program.
Frequently Asked Questions About Personalized Brain Health Guidance
What is personalized brain health guidance?
Personalized brain health guidance applies scientific evidence to information about your individual labs, health history, sleep, activity, habits, risk factors, and goals. It helps identify which actions may deserve the most attention for you.
What is BetterBrain My Vault?
My Vault is the health data home within your BetterBrain account. It allows you to upload lab reports and other files, complete your health profile, record your current protocol, connect wearable data, and import relevant health context from another AI assistant.
Why should I upload previous lab results?
Previous results help establish a trend. Comparing multiple tests over time can show whether a biomarker is improving, worsening, or remaining stable.
What wearable data can BetterBrain use?
Available data depends on your device and Apple Health permissions. It may include sleep, activity, exercise, heart rate, and other daily health metrics.
Can I control which wearable information I share?
Yes. You choose which Apple Health categories to share and can update your permissions or disconnect the integration later.
What does importing AI memory mean?
Importing AI memory means asking ChatGPT, Claude, or Gemini to summarize relevant information it already knows about your health, preferences, habits, and goals. You can review that response before pasting it into BetterBrain.
Does BetterBrain automatically access my ChatGPT or Claude conversations?
No. You choose what to export, review the response, and manually paste it into BetterBrain.
How long does it take to import AI memory?
The process typically takes about a minute. BetterBrain provides a prompt that helps your existing AI assistant organize the relevant information.
Are the My Vault personalization tools free?
Yes. Uploading previous labs, connecting wearable data, and importing AI memory are available across BetterBrain accounts, including free Self Directed accounts.
Does BeBe replace a doctor?
No. BeBe provides educational brain health guidance and helps you understand your data and potential priorities. It does not replace medical diagnosis, treatment, or care from a licensed healthcare professional.
Get immediate insights with a 3 minute assessment
Start nowGrey Matters: What 6 months of lifting weights does to your hippocampus
Is Resistance Training Best for Brain Health?
Bottom line: When researchers compared aerobic exercise, resistance training, mind-body practices like yoga, and combined programs for their effect on cognitive function in older adults, resistance training came out on top.
Last week we covered the GPLD1 pathway - how aerobic exercise prompts your liver to release protective signals that repair your blood-brain barrier. That's a powerful mechanism, and the evidence for aerobic exercise and brain health is strong.
But a body of research has been quietly building on a different type of exercise entirely. And a comprehensive 2025 network meta-analysis just made the case for strength training impossible to ignore.
What the research found:
The analysis, published in Frontiers in Aging Neuroscience, pulled data from dozens of randomized controlled trials involving cognitively healthy older adults. Resistance training produced the strongest overall effect on global cognition, with an effect size considered moderate to large in cognitive research (where meaningful improvements are notoriously difficult to achieve).
A parallel 2025 systematic review examined actual brain imaging alongside cognitive testing. The findings: at least two resistance training sessions per week, sustained for at least six months, were associated with measurable increases in cortical thickness in two critical brain regions.
The hippocampus (your brain's primary memory formation center) and the prefrontal cortex (involved in planning, complex reasoning, and self-control). These are precisely the regions most vulnerable to aging and most associated with early cognitive decline.
Why this matters:
These weren't just improvements in test scores. These were structural changes in brain tissue, visible on MRI scans. Six months of consistent strength training literally changed the physical structure of participants' brains.
The Exact Dose Your Brain Needs
Looking for the research-backed protocol? Here's what the evidence supports.
The Science:
Building new brain cells
When your skeletal muscles contract under load, they secrete signaling proteins called myokines into your bloodstream. One well-studied myokine, irisin, crosses the blood-brain barrier and has been shown to increase new brain cell formation in the hippocampus, your brain's memory center. So when you're working out and think you're building muscle, know that your exercise and the myokine reaction is also building new cells in your brain at the same time. The work you're doing in the weight room is literally growing your hippocampus.
Improving insulin sensitivity
Resistance training also improves how your muscles respond to insulin, contributing to better metabolic health throughout your body. This matters enormously for your brain because brain insulin resistance is increasingly understood as a central mechanism in Alzheimer's disease, some researchers even call it "type 3 diabetes." When you lift weights, you're not just managing blood sugar. You're protecting your brain from one of the most well-established pathways to cognitive decline.
Getting Started
Frequency: At least two sessions per week. Some studies suggest three sessions produces greater effects, following a dose-response pattern.
Duration: Six months minimum for structural brain changes to appear on imaging. This isn't a quick fix. It's a sustained practice.
Form matters more than weight: Good form is non-negotiable. Controlled movements through a full range of motion - no jerking, no momentum, no compromising your body position to move heavier weight. Poor form not only increases injury risk, it reduces the actual muscle stimulus you're trying to create. If you can't maintain good form for 8-12 reps, the weight is too heavy. Drop it down.
If you're new to resistance training, consider working with a trainer for even just a few sessions to learn proper form on basic movements. That upfront investment pays dividends in both safety and effectiveness.
Intensity: Moderate intensity works best - approximately 50 to 70% of your maximum. In practical terms, this means lifting a weight you can complete 8 to 12 controlled repetitions with, where the final 2 to 3 reps require genuine effort.
BetterBrain Tip: You don't need a gym membership to start. Bodyweight exercises (squats, push-ups, lunges), resistance bands, or even filled water bottles work. The goal is progressive challenge over time, gradually increasing difficulty as you get stronger. Start where you are, build gradually, and prioritize consistency over perfection.
Learn more about building a sustainable strength training practice on the BetterBrain Portal.
How to Track Your Progress
So how do you know if your strength training routine is working for your brain? Here are the markers that respond:
Insulin Sensitivity: Resistance training improves how your cells respond to insulin. You can track this through fasting insulin levels and HbA1c (which shows your average blood sugar control over three months). Better insulin sensitivity is directly associated with better cognitive function.
Inflammatory Markers: Consistent strength training reduces systemic inflammation. Track hs-CRP and homocysteine to see objective evidence of this anti-inflammatory effect. Lower inflammation means better brain protection.
Metabolic Health Markers: Strength training improves multiple metabolic markers including glucose control, lipid profiles (like VLDL-C), and overall metabolic function. These improvements happen through muscle-mediated pathways that complement what aerobic exercise does.
Why this matters: These biomarkers provide concrete evidence that your training is working. Seeing these numbers improve is powerfully motivating and shows you that the effort you're putting in is producing real results.
The case for combining aerobic and resistance training:
Last week's newsletter covered how aerobic exercise works through the GPLD1 pathway - your liver releasing signals during movement that repair your blood-brain barrier. That's one powerful mechanism.
This week's research shows strength training works through entirely different pathways: muscle-derived signaling proteins (myokines), improved insulin sensitivity, and hormonal changes that protect brain structure.
These are complementary, not redundant. Research on combined programs shows that doing both produces greater cognitive benefit than either alone.
If you're currently doing aerobic exercise regularly (great - keep that GPLD1 pathway active), adding just two strength sessions per week hits the research-backed minimum for the mechanisms we covered today.
Both are rated Essential in your BetterBrain protocol. And now you know why!
VERVE-102: A One-Time Gene Edit for Cholesterol, and Why It's a Brain Story | BetterBrain
One shot to lower cholesterol for life: what PCSK9 gene editing means for your brain
The short version: In the Heart-2 trial, a single infusion of a gene editing therapy called VERVE-102 lowered LDL cholesterol by up to 62% and kept it down for as long as 18 months. It is a phase 1b result in 35 people with inherited high cholesterol, so it is years away from a pharmacy. The part that matters to you now is the target. High LDL in midlife is one of the 14 modifiable dementia risk factors named by the Lancet Commission, and the particle count underneath it, ApoB, is something you can measure this month.
Most people learn their cholesterol is high at an annual physical, get told to watch it, and never find out what the number is actually doing. It is doing something to your brain.
That connection is why a cardiology result got our attention. In May 2026, researchers reported that a single infusion of a gene editing medicine lowered LDL cholesterol substantially, and that the reduction held for up to 18 months. The results were presented at the European Atherosclerosis Society Congress and published in the New England Journal of Medicine.
It is early research in a small, specific group of patients. But the biology it targets is among the most studied in all of cardiovascular medicine, and it runs straight to your brain.
What VERVE-102 actually did
Heart-2 is a phase 1b trial. The interim analysis covered 35 participants, average age 52, all with heterozygous familial hypercholesterolemia, premature coronary artery disease, or both, and all already on the maximum statin dose they could tolerate.
Each received one infusion, at doses from 0.3 to 1.0 mg/kg. The results, per Lilly's May 25, 2026 release:
- PCSK9 protein fell by 51% to 88%, depending on dose.
- LDL cholesterol fell by 9% to 62%. At the highest dose, the drop was 62%, or 78 mg/dL in absolute terms.
- Reductions were sustained, with durability observed for up to 18 months after a single treatment.
- There were no dose-limiting toxicities and no treatment-related serious adverse events. Side effects were mostly low-grade infusion reactions and fatigue. All 35 participants received their full dose and none withdrew.
One infusion. Effects still holding a year and a half later.
How PCSK9 works, in plain language
Your liver clears LDL cholesterol out of your blood using surface proteins called LDL receptors. Think of them as docking ports: the more ports available, the more LDL particles get pulled out of circulation.
PCSK9 is a protein that destroys those ports. More PCSK9 activity means fewer receptors, which means more LDL staying in your bloodstream.
Here is the part that makes this target unusually well understood. Some people are born with naturally low-functioning PCSK9 genes. They have markedly lower LDL across their entire lives and substantially lower rates of heart disease, with no apparent downside. Turning PCSK9 down is not a theory. It is a protective pattern that already exists in nature and has been studied for two decades.
Drugs that lower PCSK9 have been approved for years. What is new here is the delivery. VERVE-102 uses base editing, a precise form of gene editing, to make a single change to the PCSK9 gene inside liver cells. The goal is to do once, permanently, what existing drugs do by repeated injection.
The honest caveats
This headline is easy to over-read. The careful version:
It is a phase 1b trial. That stage is designed mainly to test safety and look for early signals in a small number of people. It has not been shown to prevent heart attacks, strokes, or cognitive decline. A phase 2 trial is the next step, with enrollment planned by the end of 2026.
It is a specific patient group. Everyone enrolled had an inherited form of very high cholesterol or early coronary artery disease and needed aggressive LDL lowering despite maximum oral therapy. These are not general-population results.
Gene editing is a young field. The PCSK9 mechanism is exceptionally well characterized, which is reassuring. Making a permanent edit to a gene is still new, and the long-term safety record takes years to build. Approval, if it comes, will likely start with very high-risk patients such as those with familial hypercholesterolemia, and the price is likely to be high.
It is years away. Nobody should be adjusting their plan today on the expectation that this arrives soon.
Why cholesterol is a brain story, not only a heart story
Brain health is whole-body health, and few things connect the two as directly as lipids.
ApoB is the number underneath LDL
You have probably heard of LDL cholesterol. ApoB is the more precise measurement sitting beneath it.
Every LDL particle carries exactly one ApoB protein. So LDL-C tells you how much cholesterol is being carried inside LDL particles, while ApoB tells you how many particles there actually are. Since it is the particles that lodge in artery walls and start plaque, ApoB is the better predictor of risk. When the two numbers disagree, ApoB is the one to trust.
Among BetterBrain clients, 86% come back with a suboptimal ApoB. It is the single most commonly out-of-range marker we see, and most people have never had it measured.
The Lancet Commission added LDL to the dementia list in 2024
The blood vessels feeding your brain are subject to the same lipid-driven damage as the ones feeding your heart, and that vascular damage is one of the major pathways of cognitive decline.
This is no longer a fringe position. In its 2024 update, the Lancet Commission on dementia prevention added high midlife LDL cholesterol as one of 14 modifiable risk factors, based on cohort studies covering more than a million participants plus a Mendelian randomization meta-analysis of 27 studies. The Commission attributes 7% of preventable dementia to high LDL alone, and links nearly half of dementia cases to the 14 factors combined.
High cholesterol in your forties and fifties is now formally a brain risk factor, not only a heart one.
If you carry APOE4
People who carry an APOE4 variant tend to run higher LDL, and APOE4 is the strongest common genetic risk factor for Alzheimer's disease. That combination is one reason lipid management is a core part of what we do, and one reason knowing your genotype can change what you prioritize rather than just giving you something to worry about.
The bigger picture
Between therapies like this one and the medications already on the shelf, the tools for managing cardiovascular disease are getting very good, and they will keep improving. But adding years to your life is only worth so much if your brain is not working well for those years. That is the conversation most people are not having yet, and it is the one that matters most to us.
What this means for you, right now
You do not have to wait for a therapy that is years away. The target itself, your lipid health, is measurable and movable today.
- Get ApoB tested, not just standard cholesterol. A routine lipid panel gives you total cholesterol, LDL, HDL, and triglycerides. ApoB counts the particles actually driving damage and is rarely ordered unless you ask for it. It is one of the most informative single markers for both heart and brain health.
- Treat lipids as a lifelong number, not a yearly one. The PCSK9 story works precisely because it lowers exposure over decades. Risk accumulates the same way. Small, steady improvements compound in your favor, and starting earlier is worth more than starting perfectly.
- Use the levers you already have. Diet, regular movement, and, where your physician recommends them, proven lipid-lowering medications all work today. Statins and existing PCSK9 inhibitors are not placeholders waiting for gene editing. They are the current standard of care.
- Look at the whole vascular picture. ApoB, Lp(a), triglycerides, blood pressure, and HbA1c interact. One number in isolation rarely tells you what to do first.
ApoB is one of the 50+ biomarkers in the BetterBrain panel, alongside homocysteine, hs-CRP, Lp(a), HbA1c and the rest of the vascular and metabolic markers. See everything we test.
Common questions
Is PCSK9 gene editing available now?
No. VERVE-102 is in phase 1b trials. A phase 2 trial is planned to begin enrolling by the end of 2026, and broad availability is years out. If it is approved, the first patients are likely to be people with familial hypercholesterolemia or other very high-risk conditions.
What is the difference between ApoB and LDL cholesterol?
LDL-C measures the amount of cholesterol carried inside LDL particles. ApoB measures the number of those particles, because each one carries exactly one ApoB protein. Two people can have the same LDL-C with very different particle counts. When the two disagree, ApoB is the better predictor of cardiovascular and cerebrovascular risk.
Does lowering cholesterol reduce dementia risk?
The 2024 Lancet Commission identified high midlife LDL cholesterol as one of 14 modifiable dementia risk factors and attributes 7% of preventable dementia to it. That is an association drawn from large cohort and genetic studies, not proof that lowering LDL prevents dementia in any individual. What is well established is that lipid-driven damage to blood vessels is one of the major pathways of cognitive decline, and that the vessels feeding your brain are affected the same way as the ones feeding your heart.
Should I get an ApoB test?
ApoB is not part of a standard lipid panel and usually has to be requested. It is most informative if you have a family history of early heart disease or dementia, if your LDL and triglycerides do not line up, if you carry an APOE4 variant, or if you simply want a clearer read than total cholesterol gives you. Discuss it with your physician or your Brain Health Coach.
Does BetterBrain test ApoB?
Yes. ApoB is included in the BetterBrain biomarker panel, which covers 50+ markers selected for their connection to brain health, across metabolic, cardiovascular, hormonal, inflammation, and nutrient categories. Blueprint is $89 with insurance and $399 without, and includes a cognitive assessment and an up-to-90-minute session with a Brain Health Coach who turns the results into a personalized action plan.
The bottom line
A one-time gene editing infusion produced large, durable reductions in LDL cholesterol in an early trial, by copying a protective genetic pattern that already exists in nature. It is not available, it is not proven to prevent anything yet, and it will not be in a clinic near you for years.
What is available is the target. Your lipid numbers are one of the few brain risk factors you can measure precisely, act on immediately, and improve over decades. Whatever arrives in five or ten years, the decades in between are the ones you protect now.
Grey Matters: Your liver is quietly protecting your brain
Your Liver Is Talking to Your Brain
(And Exercise Is the Conversation)
Bottom line: Researchers at UC San Francisco just discovered that when you exercise, your liver releases an enzyme called GPLD1 that travels to your brain and repairs one of the most critical mechanisms of aging: a leaky blood-brain barrier.
We've said it before: exercise is probably the most important thing you can do for your brain. But we know that statement, repeated often enough, without context, starts to feel like background noise. So here's more on the mechanisms.
The problem most people don't know exists:
Your brain is surrounded by a remarkable security system called the blood-brain barrier. Think of it as an extremely selective bouncer at an exclusive club. It lets in what your brain needs (oxygen, glucose, essential nutrients) and keeps out inflammatory molecules and toxins.
For most of your life, this barrier does its job beautifully. But with age, it becomes leaky. Inflammatory molecules start seeping into brain tissue, creating chronic, low-grade inflammation that researchers increasingly recognize as an early feature of cognitive decline.
Think of it less like a sudden breach and more like slow rust. Over years and decades, it adds up.
What the UCSF team discovered:
Neurologist Saul Villeda and his team spent years studying what happens in the brains of older animals that exercise regularly. The benefits were clear: better memory, less inflammation, more new brain cells. What wasn't understood was how.
In a study published in Cell in February 2026, they found the answer. And it starts not in your brain, not in your muscles, but in your liver.
When you exercise, your liver releases an enzyme called GPLD1 into your bloodstream. GPLD1 travels to the blood vessels forming your blood-brain barrier and repairs the age-related damage, essentially making the barrier behave like it did years earlier.
What this means:
The UCSF team tested this pathway in older mice and saw consistent results: less barrier leakiness, lower brain inflammation, and better memory performance. In Alzheimer's disease models, GPLD1 treatment reduced amyloid plaques by approximately 30%.
The researchers are clear: mouse studies don't always translate to humans.
But two pieces of evidence suggest the mechanism likely translates: active older adults already show elevated GPLD1 in their blood, and the same TNAP buildup the enzyme targets has been identified in human blood-brain barrier tissue. Human studies are planned within five years.
This is one of the reasons why movement is rated as Essential in BetterBrain's coaching program.
Technique Spotlight
Looking for the actual prescription for brain-protective movement? Here's what the evidence supports.
The Science:
GPLD1 is released during exercise, not stored permanently. The blood-brain barrier benefits aren't something you can bank with a few intense weeks of training and coast on for months. The protective signal requires steady, ongoing input.
This aligns perfectly with what we already know from population studies: brain health benefits of exercise accrue most reliably in people who move consistently over years, not in those who exercise intensely for short bursts. The GPLD1 pathway offers a molecular explanation for that pattern.
Getting Started:
The dose that evidence supports is 150 minutes of moderate-intensity aerobic activity per week, distributed across multiple sessions. That breaks down to approximately 30 minutes, five times per week, at an effort level where you can hold a conversation but wouldn't want to sing.
A brisk walk meets this threshold. So does swimming, cycling, dancing, or water aerobics. The specific activity matters far less than the consistency.
If you're doing less than 150 minutes per week: Any increase from your current baseline carries benefit. The dose-response curve is favorable at every level. People who go from sedentary to 60 minutes per week gain more cognitive benefit, proportionally, than people going from 120 to 180 minutes.
Starting somewhere and building gradually over months is the actual prescription. Research on previously sedentary adults shows measurable brain changes within three months of consistent walking.
BetterBrain Tip: Pick activities you genuinely enjoy. The best exercise routine is the one you'll actually do next week, next month, and next year. Movement doesn't have to mean suffering through workouts you hate. Turn on music you love, walk with a friend, or dance in your living room. Consistency comes from enjoyment, not willpower.
Learn more about building a sustainable movement practice on the BetterBrain App.
Tracking What Movement Does for Your Brain
So how do you know if your exercise routine is working? Here are the biomarkers that respond to consistent movement:
Inflammatory Markers: We've covered these before (hs-CRP, homocysteine), and exercise is one of the most powerful tools for lowering them. Consistent aerobic activity reduces systemic inflammation throughout your body, including your brain. Levels of hs-CRP often drop measurably within weeks of starting a regular exercise routine.
Insulin Sensitivity:Regular movement improves how your cells respond to insulin, which matters enormously for brain health. Better insulin sensitivity is associated with better cognitive function and slower cognitive decline. You can track this through markers like fasting insulin and HbA1c.
Metabolic Markers: Exercise improves multiple metabolic markers including glucose control (HbA1c), lipid profiles (VLDL-C), and overall metabolic health. These improvements happen through complementary pathways - aerobic exercise primarily through increased blood flow and metabolic efficiency, resistance training through muscle-mediated insulin sensitivity.
Why this matters: These aren't just numbers on a lab report. They're concrete evidence that your brain is responding to the work you're putting in. Tracking them provides motivation to maintain the habits that are actually making a difference.
The case for combining aerobic and resistance training:
Aerobic exercise works primarily through increased blood flow to your brain and improved metabolic efficiency (including the GPLD1 pathway we just discussed). Resistance training works through different mechanisms: improved insulin sensitivity, hormonal changes, and metabolic benefits from increased muscle mass. (More on this in future newsletters!)
These are partially complementary pathways, and research on combined programs shows that doing both produces greater cognitive benefit than either alone.
If you're currently doing one but not the other, that gap is worth exploring. The Move section of your BetterBrain protocol covers both aerobic and resistance training, and both are rated Essential for brain health.
hs-CRP: The Biomarker Most Likely to Flag Silent Inflammation in Brain Health
What hs-CRP measures
CRP or C-reactive protein is made by your liver in response to inflammation anywhere in your body. The "hs" stands for "high-sensitivity," which means the test can detect very low levels of CRP that the standard CRP test cannot.
Standard CRP is designed to spot acute inflammation, like an active infection or a recent injury. The values it flags are high enough to indicate something is actively wrong right now. hs-CRP is designed to spot chronic low-grade inflammation, the kind that does not feel like anything but is associated with long-term risk for cardiovascular disease, type 2 diabetes, and cognitive decline.
For brain health, the chronic low-grade version is the one we care about.
Chronic systemic inflammation is associated with neuroinflammation, the inflammatory state of the brain itself. The mechanism is not fully understood, but the body of evidence is large. People with higher long-term hs-CRP have higher rates of cognitive decline, faster brain atrophy on imaging, and elevated risk of Alzheimer’s disease.
Inflammation does not directly cause Alzheimer’s, but it appears to be one of the upstream conditions that lets the underlying pathology progress more quickly. Lowering it is one of the few interventions where the evidence is consistent across cardiovascular, metabolic, and cognitive outcomes.
What the numbers mean
- Optimal: under 1.0 mg/L
- Borderline: 1.0 to 3.0 mg/L
- High: above 3.0 mg/L
Most standard labs flag a result only when it crosses 3.0 mg/L or higher. The 1.0 to 3.0 range is where a meaningful number of clients are quietly running elevated. Their primary care has waved it off as "in range." However, for brain health purposes, this is not optimal.
The biomarkers that pair with hs-CRP
A single hs-CRP value is informative but more useful with other biomarkers to understand the whole picture. The markers we look at alongside it:
Homocysteine. Elevated homocysteine is associated with both inflammation and methylation problems. If hs-CRP and homocysteine are both elevated, the inflammation is likely driven in part by nutrient gaps.
ApoB and Lp(a). Cardiovascular markers. Elevated hs-CRP plus elevated ApoB is a particularly bad combination for vascular brain health.
HbA1c and Fasting Insulin. Metabolic markers. Glycemic dysfunction drives systemic inflammation. If hs-CRP is elevated, look here next.
Ferritin. Iron storage. Elevated ferritin can indicate underlying inflammation, separate from iron status.
The picture you assemble from these markers tells you whether the inflammation is metabolic, vascular, nutrient-driven, or something else.
What you can do about it
The interventions that consistently move hs-CRP often overlap with the same levers that support long-term cognitive health: sleep, glycemic control, omega-3 status, dental health, gut health, and visceral fat reduction. Because hs-CRP can be influenced by several systems at once, the right next step is not to try everything at once. It is to identify the most likely driver in your case, based on your other markers, symptoms, habits, and what you are already doing consistently.
For BetterBrain clients with elevated hs-CRP, the coaching protocol usually starts with the highest-leverage area their panel reveals. If hs-CRP is elevated alongside high HbA1c, the first priority may be blood sugar regulation. If it is elevated alongside high homocysteine, the starting point may be methylated B-complex and a closer look at folate, B12, and B6 intake. The goal is not to guess. It is to use the panel to identify the most likely driver and prioritize the change most likely to move the needle.
The Bottom Line
hs-CRP is one of the most useful brain-health markers in routine bloodwork, and one of the most commonly missed. If you have not had a high-sensitivity version of CRP measured in the past year, it is worth checking.
If you'd like the full panel with coach interpretation, BetterBrain Blueprint covers hs-CRP alongside 50+ other markers and starts at $89 with insurance.
pTau-217: What the Alzheimer's Blood Test Can and Can't Tell You
pTau-217: What the Alzheimer's Blood Test Can and Can't Tell You
A simple blood draw can now flag Alzheimer's-related changes in the brain years before any symptom appears. For some people that is welcome news, an early window to act. For others it raises a harder question they are not sure how to answer: would they even want to know. Either way, the decision deserves more than a headline.
pTau-217 is the reason this is suddenly everywhere. On August 24, 2026, CNN reported that the FDA had cleared Elecsys pTau217, a new blood test from Roche and Eli Lilly, and a new study in JAMA suggests it may help estimate future cognitive risk in people who have no symptoms yet. The New York Times, meanwhile, focused on the confusion and distress these results can cause.
The test itself is not new to us. BetterBrain began offering direct-to-consumer, expert-supported pTau-217 testing in 2024. In April 2025, physician and scientist Eric Topol called it "one of the most exciting advances in neurology for decades", and that same month BetterBrain was featured in Nature's coverage of the rise of Alzheimer's blood tests. Our takeaway from that feature was as much about responsibility as access. Making a powerful test easier to get is only useful if people also get the context, guidance and support to understand the result.
What is pTau-217?
Tau is a protein found inside brain cells. In Alzheimer's disease, tau undergoes abnormal changes and can eventually form tangles that interfere with how those cells work.
The "p" stands for phosphorylated, meaning a phosphate group has attached to the tau protein. The number 217 points to the precise location where that change happened.
When Alzheimer's-related biology begins developing in the brain, levels of pTau-217 in the blood tend to rise. And although the name refers to tau, blood pTau-217 is especially good at tracking the buildup of amyloid plaques, another hallmark of Alzheimer's. Until recently, that kind of information generally required an expensive PET scan or a spinal tap.
Why pTau-217 matters for early detection
Alzheimer's-related brain changes can begin 15 to 20 years before memory problems show up, and pTau-217 may become abnormal during this preclinical period. That makes it one of the most promising tools we have for identifying Alzheimer's-related pathology before symptoms start, which is exactly when there is the most time to act.
Does an elevated pTau-217 result mean I have Alzheimer's?
No. An elevated pTau-217 result is a signal, not a diagnosis.
It suggests that Alzheimer's-related biological changes may be present and that your risk of developing cognitive symptoms is higher. It cannot tell you with certainty whether you will develop symptoms, or when. A negative result is reassuring, but it does not guarantee you will never develop Alzheimer's. It points to a lower likelihood of significant Alzheimer's-related pathology at the time you were tested.
This distinction between detection and prediction sits at the center of the current debate.
What the JAMA study actually found
In July, a JAMA study of nearly 2,700 cognitively healthy older adults found that higher pTau-217 levels were associated with faster cognitive decline and a greater chance of developing cognitive impairment. Among participants with very high levels, researchers estimated a 38% risk of cognitive impairment within five years and a 78% risk within ten years.
Those numbers understandably drew attention. But they were group-level estimates from selected research cohorts whose average age was about 70, and the researchers cautioned that the ten-year figure rested on a relatively small number of people followed for that long. It is meaningful information. It is not a personalized countdown.
Are all Alzheimer's blood tests the same?
Not quite. Several are now available, and each gives a slightly different view of Alzheimer's-related biology. Some measure pTau-217 alone, others combine it with additional markers, and each laboratory method comes with its own reference ranges and cutoffs. That makes the specific test an important part of understanding the result.
The first Alzheimer's blood test cleared by the FDA, in May 2025, measures the ratio of pTau-217 to an amyloid marker. Later that year the FDA cleared Elecsys pTau181, designed mainly to help rule out Alzheimer's-related pathology. In August 2026 it cleared PrecivityAD2, which combines several amyloid and tau measurements, followed by the newly cleared Elecsys pTau217, which measures pTau-217 alone.
These FDA clearances apply to tests used as part of a broader clinical evaluation for people who are experiencing cognitive concerns. The results are meant to be read alongside symptoms, cognitive testing, health history and other clinical information.
BetterBrain uses Quest's AD-Detect pTau-217 test, a laboratory-developed assay that uses different technology from both the newly cleared Elecsys test and the ALZpath test used in many published studies. Because each platform measures pTau-217 differently, each result is interpreted using the reference range established for that specific assay. We use the reference range provided by Quest, then interpret the result alongside cognitive testing, kidney function, other biomarkers, health history and lifestyle.
What a pTau-217 result does not tell you
Here is the part of the conversation that often gets missed. We agree with The New York Times that handing someone a frightening result without enough support can cause real distress. That does not mean the test cannot provide useful information. It means the information needs a fuller picture around it.
A pTau-217 result tells us about one part of Alzheimer's biology. It does not tell us why one person with elevated pathology develops symptoms while another stays cognitively healthy for years, and it says nothing about the many other factors shaping that person's brain health.
Those other factors carry real weight. The 2024 Lancet Commission estimated that addressing 14 modifiable risk factors across life could potentially prevent or delay around 45% of dementia cases at the population level. The U.S. POINTER randomized trial found that a program combining exercise, nutrition, cognitive and social activity, and regular health monitoring improved cognition in older adults at elevated risk. And a long-term observational study found that a healthier midlife lifestyle was associated with a lower incidence of cognitive impairment across pTau-217 levels and APOE4 status. Pathology is not the whole story. The real answers come from looking at all of your numbers together.
What should you do with a pTau-217 result?
Unlike LDL cholesterol or blood pressure, pTau-217 is not a marker you improve through one clearly established intervention. It is primarily a measurement tool.
If your level is elevated, the next step is to understand the complete picture. That may include further clinical evaluation, establishing a cognitive baseline, considering confirmatory testing, assessing eligibility for clinical trials or approved treatments when appropriate, and addressing the modifiable factors that contribute to overall dementia risk. Research into using pTau-217 to monitor treatment response is promising, though there is still a lot to learn about this relatively new test.
Why BetterBrain never offers pTau-217 alone
When we started BetterBrain, we were driven by personal experiences with Alzheimer's in our own families. We learned firsthand that brain health is not about one marker or one intervention. So we do not simply order a pTau-217 test and email you the result. We think that would be irresponsible.
We pair pTau-217 with more than 50 other brain-relevant biomarkers in our Essentials Panel, a cognitive assessment and a detailed look at your health history and lifestyle. We look under the hood for modifiable risk drivers across vascular, metabolic, inflammatory, hormonal and nutritional health. A trained clinical expert then walks you through the findings, explains what they do and do not mean, and builds a personalized action plan focused on the areas where you have the most opportunity to improve. If a result calls for more evaluation, we help you identify the right clinical next step alongside your existing doctor.
The real power does not come from one blood test. It comes from combining early detection with a much broader understanding of your biology, then turning that into meaningful action. Knowledge can be powerful, but only when you know what to do with it.
Learn about pTau-217 testing with BetterBrain, or start your brain health journey to see the full picture.
Frequently asked questions
What is pTau-217?
pTau-217 is a form of the tau protein, measurable in blood, that tends to rise as Alzheimer's-related biology develops in the brain. It is particularly good at tracking amyloid plaque buildup, a hallmark of Alzheimer's disease.
Does an elevated pTau-217 result mean I have Alzheimer's?
No. An elevated result suggests Alzheimer's-related changes may be present and that risk is higher, but it is a signal, not a diagnosis. It cannot confirm whether or when someone will develop symptoms.
Are all Alzheimer's blood tests the same?
No. Some measure pTau-217 alone and others combine it with additional markers, and each laboratory method has its own reference ranges. The specific test used is an important part of interpreting the result.
Can you lower your pTau-217?
pTau-217 is not a marker you improve through one established intervention the way you might lower LDL cholesterol. It is primarily a measurement tool. The action lives in the modifiable risk factors around it, such as vascular, metabolic and lifestyle health.
Who should consider pTau-217 testing?
It is often considered by people who want early insight into Alzheimer's-related risk, including those with a family history. It is most useful when the result is interpreted alongside cognitive testing, other biomarkers, health history and lifestyle, not in isolation.
How much does pTau-217 testing cost with BetterBrain?
The pTau-217 test is $299, offered as an add-on to a Blueprint assessment. It isn't sold on its own, and insurance doesn't cover it. See the full breakdown, including where it's available, on our pTau-217 cost page.
Grey Matters: One coach’s most effective brain health strategies
Meet Ana Hernandez, RD: Brain Health Coach
Ana is a Registered Dietitian with over 20 years of experience helping people build habits that stick. A New Mexico native and mom of two teenage sons, she believes that understanding why we make the choices we do is just as important as knowing what to do. Her approach is collaborative, helping clients build routines that support clarity, emotional steadiness, and long-term well-being in the context of real life.
What draws Ana to working with BetterBrain clients is the opportunity to support her clients in a truly holistic way. "The mind and body are not separate systems. Helping clients understand that nurturing their brain is also a way of tending to the whole body is preventative medicine at its best!"
A transformative Coaching Program journey
"One of my clients came to our first appointment completely overwhelmed. She was raising four children, supporting a mother with dementia, and working two jobs. We started simply: ordering the BetterBrain essentials labs. In our second session, after the results came back, they helped us identify clear opportunities for action. She reinitiated key medications she had stopped taking, we worked on supporting her circadian rhythm for better sleep quality, and we made small, non-restrictive shifts to her nutrition.
Over seven weeks and five appointments, her energy and focus have shown subtle but real improvement. Her habits around sleep, movement, and technology use are small but compounding. That compounding creates psychological momentum, and that momentum becomes its own motivation. It is a powerful reminder of how much consistent, small shifts can do."
Ana's Top Recommendations
"I go to Body Jam twice a week. It's a Les Mills dance fitness class that blends hip hop, Latin, and street dance into a high-energy group workout set to current music. Reconnecting with this kind of movement from my childhood has been genuinely life-changing.
It brings together so many of the things we know protect the brain: friendship, joy, flow state, cardiovascular challenge, and something researchers call collective effervescence, that intense sense of energy, unity, and shared emotion that happens when people move together toward a common purpose."
In our BetterBrain portal the technique summary for the practice is "Dance is unique in that it simultaneously integrates motor coordination, balance, memory, and emotional expression, activating multiple brain regions at once. Longitudinal research consistently shows that regular dancers have a significantly lower risk of dementia compared to non-dancers. One landmark study found up to a 76% reduction.
If you want to protect your brain, add challenge and joy to your movement routine, I believe Dance is hard to beat.
A mindset shift that makes a big difference
“Our brains have a negativity bias. We are wired to scan for what is not working. Add in the information overload of modern life, and motivation can fade fast even when real progress is happening.
In every coaching session, I start by reviewing the small things that went well: a habit that stuck, a moment of feeling better, a choice that aligned with a value. This is not just feel-good coaching. Recognizing and naming wins activates the brain’s reward circuitry, reinforcing the neural pathways that make a behavior more likely to repeat. That is neuroplasticity in action.
I also remind clients that the knowing-doing gap is real for everyone. Motivation is a state that fluctuates. Progress is not linear. Normalizing that, and building in a daily practice of noticing even the smallest forward movement, helps recalibrate the brain away from deficit and toward momentum.
When clients feel stuck, I ask: what is one thing, however small, that went better this week? Start there.”
Her go-to brain-boosting ritual
“Most mornings or evenings I take what I call an AWE walk, and it has become one of my most anchoring practices.
Awe is a complex emotional state that arises when we encounter something vast, beautiful, or beyond our current understanding, something that challenges the way we see the world. We tend to think of awe as rare: the first time you stood at the edge of the Grand Canyon, or watched the Northern Lights. Those experiences are profound, but most of us cannot access them daily.
What science is revealing is that we do not need grand spectacles. Awe is available in small doses, every day. I find it in the way the sunset colors the Sandia Mountains, the first blooms appearing on a tree, or the way wildflowers may bloom in strange places. Researchers call this “everyday awe,” and its effects on our biology are measurable and meaningful.”
A 2020 study published in Emotion by Virginia Sturm and colleagues at UC San Francisco found that participants who took weekly awe walks for eight weeks reported greater positive emotions, less distress, and showed increases in positive affect compared to a control group who took ordinary walks. The awe walkers also showed reductions in self-reported stress, and the researchers observed changes in how participants oriented their attention, shifting from inward rumination to outward curiosity.
Dacher Keltner’s lab at UC Berkeley has similarly found that awe reduces levels of pro-inflammatory cytokines, the same markers linked to chronic stress, cognitive decline, and depression. Awe also quiets the default mode network, the brain region most associated with worry and self-referential thought, which is why it tends to produce that distinctive feeling of calm clarity.
Researchers also describe a “small self” effect: when we encounter something larger than ourselves, our problems shift in scale. Stress becomes more manageable. Perspective returns. And none of it requires a trip to a national park. It just requires slowing down enough to actually look.
The simplest practice: on your next walk, look up. Notice the sky, the sunset, the flowers, the glistening of the snow on the sidewalk. Your brain will thank you.
.webp)