Topic
Progressive neurodegenerative disease and the most common cause of dementia, historically characterised by amyloid-beta plaques and tau tangles in brain tissue.
MIT researchers used a genome-wide CRISPR screen to tie APOE4's myelin damage to suppressed Wnt signaling in human oligodendrocytes. The result gives drug researchers a named pathway to test, though the evidence so far comes from cultured cells and mice.
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Penn researchers found little tau in the parts of one donated brain where aducanumab had cleared amyloid plaques. The finding comes from one patient, so it fits a lasting protective effect of amyloid removal but cannot establish one.
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UC Santa Cruz researchers say the peptide P3, long thought harmless, can form clumps faster than amyloid beta and may damage brain cells. The claim comes from a commentary that highlights research, so P3's role in Alzheimer's disease is still a hypothesis.
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Two researchers won the 2026 chemistry Nobel for asymmetric synthesis, a way to make only one mirror-image form of a molecule. One lab using it says mixed Alzheimer's trial results for resveratrol may trace to two forms of the compound.
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UCL researchers report a mesh of 2-micrometre channels that carried labelled tau and amyloid beta toward the brain surface in mice, in an unreviewed preprint. They are a candidate exit for the proteins that build up in Alzheimer's, so far untested in a living human brain.
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Toronto and UCSF researchers report that older women with higher levels of 16 menopause-linked molecules were 15 percent likelier to develop Alzheimer's. The authors see menopause as a window for early-warning testing, though the evidence so far is a correlation.
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University of Arizona researchers argue that older brains move memory work from the hippocampus to the frontal cortex as an adaptive reorganization. The paper reinterprets earlier studies and adds no new data, so the idea still awaits a direct test.
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UW-Madison researchers linked higher blood levels of the gut-made compound ImP to faster cognitive decline in nearly 1,200 people. Evidence that ImP causes harm so far comes from mice, so lowering it to slow dementia is still an idea for the future.
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Lund University scans of more than 1,000 people show Alzheimer's reorganizes brain connectivity along a path distinct from normal aging. If the result replicates, brain-wide connectivity could join amyloid and tau as a way trials judge whether a drug helps.
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Mount Sinai researchers report APOE4 turns brain pericytes into scar-making cells, and blocking TGF-beta reversed the change in aged mice. That gives drug developers a vascular target in carriers of the strongest known genetic risk factor for Alzheimer's.
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University of Missouri researchers found four weeks of daily low-dose rapamycin raised brain blood flow only in healthy APOE4 carriers aged 45 to 65. That makes perfusion a measurable target for prevention trials, though a month of scans cannot show that fewer people go on to develop dementia.
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Washington University researchers report that a CXCR3-blocking antibody halved brain T cells and spared 40% more memory-region tissue in tauopathy mice. Tau levels never fell, evidence the immune reaction to tau does much of the killing.
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University of Florida researchers linked glucosamine use to a 25% higher chance of mild cognitive impairment becoming dementia in patient records. The team calls it an association that a clinical trial must test.
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Emory researchers link 5,000 IU a day to better cognitive screening scores in people with mild cognitive impairment and sleep disturbance. The exposure sits above the recommended safety ceiling.
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Mississippi State's kinetic model of copper and zinc speeding amyloid-beta clumping matches atomic force microscopy data, the university says. Its two simulated anti-plaque strategies could guide lab work if the fit holds on data the equations were not tuned to.
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UCSF researchers tied 16 blood proteins that shift with menopausal hormones to a 15% higher Alzheimer's risk in nearly 12,000 older women. Those women were in their 60s and 70s, so a menopause screening test would need a study that follows the same women from midlife.
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Standard gene models leave out short open reading frames, so a Salk team built a search database that includes them and pointed it at existing proteomics data from postmortem frontal cortex samples.
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Mount Sinai researchers report that APOE4 turns vessel-support cells into scar-forming ones, and that blocking TGF-beta reversed it in aged mice. Both reversals so far are in aged mice and in stem-cell-derived human tissue.
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A 2024 analysis of nearly 9 million US death certificates put taxi and ambulance drivers last among 443 occupations for Alzheimer's deaths. The essay that extends that finding to map specialists is asking a question the data cannot answer.
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UC San Diego researchers report that catestatin, an endogenous piece of chromogranin A, lowered amyloid, tau and neuroinflammation in mice while improving memory and motor scores. Which of those effects drives the others is still open.
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