For how we live.
Two large cohorts link purpose in life to lower mortality and lower Alzheimer's risk. Whether purpose protects health, or health sustains purpose, is what the studies cannot fully separate.
A cohort with serial MRI and autopsy data found earlier menopause tracked faster cognitive decline and white matter damage. The per-year coefficients are very small.
A ten-person phase 1 study measured whether oral rapamycin reaches the central nervous system in early Alzheimer's. It did not — and several disease biomarkers rose over eight weeks.
The committee that decides what Israel's national insurance covers added new cancer and depression drugs to the 2026 list — and turned down an early Alzheimer's treatment because of what it would have cost.
A 614-donor autopsy study tied advanced CTE to dementia independently of other brain disease. A separate imaging report in three former athletes hints at a test for the living. The caveats on both are heavy.
The approved tests are for patients already showing cognitive decline. Used on the worried well, a positive result mostly signals a risk that may never become disease — and no treatment follows from it.
Autopsy studies show educated brains carry the same disease but express it as dementia later. That is the concept's strength — and the reason it resists being turned into a to-do list.
The link between puzzles and a sharper old age is real in the data and largely the wrong way round: the earliest changes of dementia quietly reduce the very activities that later look protective.
A standing commission estimates that eliminating 14 risk factors could prevent or delay 45% of dementia across a whole population. What that number means for one person is a different and much weaker claim.
University of Florida researchers identify excess glycan production as a driver of Alzheimer's pathology, and find oral glucosamine worsened cognition in mice and tracked with faster decline.
Buntanetap showed dose-dependent cognitive benefit in biomarker-positive patients with mild disease. The company's announcement does not say what happened in the full 351-patient population.
Researchers profiled nearly 356,000 nuclei from post-mortem hippocampi across five groups. Chromatin accessibility in neurogenic cells was already altered in people with preclinical Alzheimer's pathology.
A 220,000-person cohort found opposite associations for two neurodegenerative diseases depending on the type and distance of greenery. Two other February papers ask who can actually use it.
Three February papers push plasma p-tau217 past detection: clock models estimating years to symptom onset, four assays compared head to head, and a real-world audit of what the result changes.
A 131,821-person cohort followed for up to 43 years and a dose-response meta-analysis of 450,000 people converge on roughly two to three cups — and diverge sharply above it.
In 85 people with mild cognitive impairment, transient beta-band events recorded at rest differed years before diagnosis. The sample is small and the finding has not been replicated.
The biomarker effect reported at CTAD is large and sustained over two years. The sample is seven, the design is open dose-escalation, and imaging was available for three.
A small longitudinal study found reduced spindle activity over the temporal lobes in early Alzheimer's — and that lower temporal spindle density tracked with faster decline over up to seven years.
At a Mayo Clinic cohort of 252 patients, 40% of amyloid-negative people tested positive. The manufacturer says it has found a manufacturing problem and put the product on hold.
Bristol Myers Squibb found 'irregularities' in how a small number of ADEPT-2 sites executed the study, excluded their patients, and is enrolling more. Alzheimer's-related psychosis still has no approved treatment.
Semaglutide moved Alzheimer's biomarkers without moving the clinic. A separate liraglutide trial missed its primary endpoint on brain metabolism. Together they close a decade-old hypothesis — or at least narrow it.
Sequencing hundreds of single neurons from 15 donors with CTE and 4 with repetitive head impacts but no CTE, researchers found the genomic damage tracked the disease, not the exposure.