Implicated in ARIA: Perivascular Macrophages and Microglia
These immune cells spew free radicals and inflammatory cytokines that damage blood vessels, contributing to edema and brain bleeds.
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These immune cells spew free radicals and inflammatory cytokines that damage blood vessels, contributing to edema and brain bleeds.
These are the first deaths reported from clinical use of lecanemab. One was APOE4 homozygote; both developed severe ARIA-E and seizures.
A study links 161 PSEN 1 mutations to age of onset and disease progression. Good news for variant calling, and for developing γ-secretase modulators.
Are Alzheimer’s Blood Tests Ready for Primary Care? Living Among Us: People Whose Alzheimer’s Is Already Being Prevented First Success Stories From Alzheimer’s Secondary Prevention Trial Liraglutide Trial Was Negative Four Years Ago, Still Negative Today
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.
Case studies from the Dominantly Inherited Alzheimer Network trial show amyloid immunotherapy can prevent tangles and cognitive decline in some mutation carriers.
On gantenerumab, some people with dominantly inherited AD mutations remain plaque- and tangle-free, and cognitively healthy, years after their expected age of onset.
Plasma p-tau217/tau217, alone or with Aβ42/40, identified people with amyloid pathology more accurately than did expert clinical assessment.
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 postmortem analyses of athletes who had repetitive head injuries, neurofibrillary tangles were more common than α-synuclein fibrils in the substantia nigra.
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.
In cultured cells, mutant human tau that was forced together formed liquid droplets. When tau was missing its N-terminus, the droplets hardened into insoluble aggregates.