08/27/2026
The New York Times recently published an article questioning the value of Alzheimer’s biomarkers such as p-tau217 in people who have no cognitive symptoms. The premise is essentially this: Why test for Alzheimer’s-related pathology before symptoms appear if there is little or nothing you can do about it—doesn’t that just create worry?
Wait a minute, this is 2026, not 1976! That premise is outdated—we ALL know that there is plenty that can be done to reduce risk for cognitive decline, and as I’ve noted in the past, for anyone who has begun PreCODE or ReCODE while asymptomatic, and followed it appropriately, the chance of developing dementia is so low that we have not documented a single case. Moreover, this approach improves overall health, reduces inflammation, improves energy, reduces depression symptoms (https://pmc.ncbi.nlm.nih.gov/articles/PMC12838874/ ), enhances detox, and often ends the need for drugs such as antihypertensives or statins or anti-diabetes drugs.
The article went on to say that having a high p-tau does not guarantee that one will go on to develop Alzheimer-related dementia. Of course there is no guarantee, just as for every other screening test in medicine—having a high cholesterol does not guarantee that you’ll have a myocardial infarction, but we still want to know our lipid status in order to reduce our risk; and having a high hemoglobin A1c does not guarantee you will develop diabetes-related cardiovascular disease or retinal disease or renal disease, but every responsible physician tests hemoglobin A1c, so that we can avoid diabetes and its complications. The same reasoning holds true for everything from Pap smears to PSAs to cancer blood tests, and on and on.
Furthermore, the evidence that p-tau217 is indeed an important predictor of future cognitive impairment continues to grow. In 2026, it was reported that cognitively unimpaired older adults with high p-tau217 levels had an estimated 78% risk of developing cognitive impairment over 10 years. Other recent research has shown that changes in p-tau217 can help estimate when Alzheimer’s symptoms may emerge. Some groups have even recommended that elevated p-tau217 be considered diagnostic of Alzheimer’s. Therefore, just as for every other screening test, it alerts us to begin an optimal treatment or prevention program. And as we, and many others now, have shown since 2014, a precision medicine approach like ReCODE or PreCODE provides just that.
Finally, the article noted that drugs are in trial—the same drugs that have failed to improve cognition in patients with Alzheimer’s—to determine whether these are effective at prevention. Why would anyone with normal cognition take a drug with side effects of brain microhemorrhage, brain swelling, brain atrophy, and occasionally death, when there are such healthier ways to prevent cognitive decline?
Waiting for symptoms to appear (and even worse, doing nothing and assuming “it’s just normal aging”) is an antiquated approach. Biomarkers offer better outcomes by identifying Alzheimer’s pathophysiology in its early stages. To the author of this misguided article, please wake up, it is 2026 and as we have demonstrated time and time again, there is now so much that can be done to prevent and reverse cognitive decline, especially for those of us who do not delay. Therefore, measuring biomarkers like p-tau 217 is just like measuring lipids or hemoglobin A1c or hs-CRP—potentially lifesaving.
