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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.
These microglia formed soon after overexpressing TDP-43 in a transgenic mouse. The cells pruned excitatory synapses, cooling circuits and extending lifespan.
Ratio of 3R/4R tau in extracellular vesicles identified people with behavioral variant FTD and PSP. Vesicle TDP43 identified bvFTD and ALS.
In mice, the innate immune protein slips into neurons, where it interacts with the translation machinery.
In people with FTLD-TDP-43 Type C, TDP-43 and annexin A11 twist into heteromeric amyloid filaments. Could there be others?
