Human Cell Models Reveal Two Sides to α-Synuclein Inclusions
Dynamic, lipid-rich inclusions of α-synuclein appear toxic, while stable, fibril-rich aggregates seem to protect neurons.
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Dynamic, lipid-rich inclusions of α-synuclein appear toxic, while stable, fibril-rich aggregates seem to protect neurons.
A new strategy, which marries nanobodies or misfolded tau to a ubiquitin ligase RING domain, tags tangles for disposal.
The consortium has cranked out dozens of mouse models of late-onset AD for the research community. Strains carry humanized Aβ and tau, and a growing list of risk variants.
This super-sized isoform resists phosphorylation and aggregation, and occurs in cerebellum and brainstem, regions largely spared from tau pathology.
The indefatigable Colombian neurologist leaves behind a legacy of Alzheimer’s prevention research, which, at the time of his passing, stands on the cusp of success.
Kynurenine curbs lactate production in astrocytes, which then fail to nourish neurons. Shutting down kynurenine production rescued cognition in AD mouse models.
How—or even if—a newly spotted AluYb8 element raises risk of neurodegenerative disease has become a question of intense interest. Centenarians, it seems, are spared.
As immunotherapies enter care, scientists explore when to stop them, how amyloid removal relates to cognitive benefit, and whether fluid markers will track both plaque and tangles responses.
Plaques and their surrounding cells and neurites occupy 6 percent of cortical volume. Their removal could account for shrinkage during amyloid immunotherapy.
Contrary to media stories, results of a small trial, which finished four years ago, did not demonstrate protection against cognitive decline or against brain shrinkage in people with Alzheimer’s.
During non-REM sleep, waves of activity that wash slowly across the cortex help consolidate memories. Tau pathology in the frontal cortex breaks them up.
In people who fended off cognitive slippage despite a hefty load of plaques and tangles, astrocytes cranked up choline and polyamine synthesis.
The largest autopsy-confirmed study of tau PET to date finds that the scans cannot identify early Alzheimer’s disease or PART.
Synapses of fast-spiking interneurons nestle in holes within dense extracellular matrix. These ‘cages’ corral glutamate, so it won’t spark excitotoxicity.
Knocking out this immunoglobulin receptor makes microglia fit to fight. An anti-PILRA antibody does the same.
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