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18 stories from Planck Standard. Latest: July 25, 2026.
Researchers compared 142 people with exceptional memory against 89 typical peers and found no genetic advantage — not in APOE, not in polygenic risk scores, not even in rare protective variants.
Buck Institute researchers report that neurons carrying the rare APOE2 variant accumulate less DNA damage and resist cellular aging — and that adding APOE2 protein protected high-risk APOE4 neurons too.
Biogen's diranersen missed its main goal in a Phase 2 trial but reduced tau pathology and showed signs of slowing decline, enough to push it toward a Phase 3 study.
Penn State researchers discovered that a lattice-like skeleton just beneath a neuron's surface controls what the cell absorbs — and when it weakens, harmful Alzheimer's proteins flood in.
A study in mice finds that tau — infamous for the tangles it forms in dementia — is essential during a brief window for turning fresh experiences into durable memories, reframing how scientists think about the protein.
Researchers at King's College London have identified 'karyoptosis,' a form of cell death in which a neuron's nucleus shrinks and shatters under the strain of toxic proteins — a process far more common in diseased brains than healthy ones.
ETH Zurich researchers traced dementia to a malfunctioning protein clustering around brain cells' power plants, then showed an experimental molecule, Compound 10, could blunt the damage.
A Boston Children's Hospital team found that microglia accumulate the same mutations that fuel blood cancers — and instead of cancer, they may stoke the inflammation that kills neurons.
Compounds fusing vitamin K with retinoic acid were three times better than natural vitamin K at turning stem cells into neurons, pointing to a possible new front against Alzheimer's and Parkinson's.
Breakthrough treatment restored brain's natural cleanup system and cleared toxic proteins, with elderly mice behaving like healthy younger animals.
Engineered nanoparticles restored brain cleanup systems and cleared toxic proteins, with elderly treated mice later behaving like healthy younger animals.
Researchers raised levels of the gene-regulating protein Sox9 in star-shaped support cells called astrocytes, triggering the brain to clear toxic amyloid plaques 'like a vacuum cleaner' and preserving memory in mice with established disease.
Researchers enhance Sox9 protein in astrocytes to help brain clear harmful plaques while preserving memory in mouse studies.
University of Illinois researchers published the first technology to simultaneously map thousands of neural connections, revealing previously unknown wiring in the mouse brain and opening a new path to understanding Alzheimer's.
Scientists discover brain immune cells destroy smell-related nerve fibers after detecting abnormal signals, offering potential for earlier diagnosis.
A previously unknown waste-removal pathway running along the middle meningeal artery could explain how the brain disposes of amyloid proteins and what goes wrong in Alzheimer's disease.
New research reveals that lecanemab clears amyloid plaques by activating microglia through its Fc fragment, a finding that is reshaping Alzheimer's treatment strategy and pointing toward more potent next-generation therapies.
Researchers at KU Leuven and VIB discovered that lecanemab works not by binding amyloid plaques directly but by activating the brain's own immune cells through the antibody's Fc fragment, pointing toward a new class of Alzheimer's therapies that could be more effective and have fewer side effects.