Tau PET Misses Early AD Pathology, Primary Age-Related Tauopathy
The largest autopsy-confirmed study of tau PET to date finds that the scans cannot identify early Alzheimer’s disease or PART.
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?
New data from cultured cells suggest tau snarling into tangles may be a stepwise process. Tau first oligomerized and condensed into liquid droplets, which remained soluble. When tau had lost its N-terminus, however, the protein solidified into beta sheets. Truncated tau is common in the aging brain, hinting this could be a key factor in vivo as well.
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