Do Rod-Shaped Microglia Dampen Hyperexcitability in ALS?
These microglia formed soon after overexpressing TDP-43 in a transgenic mouse. The cells pruned excitatory synapses, cooling circuits and extending lifespan.
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?
The antibody becomes the second amyloid immunotherapy to receive traditional FDA approval, joining Leqembi.
New candidate OXD-2314 binds 3R and 4R forms of tau and has begun Phase 1. The pan-tau tracer APN-1607 begins Phase 3 for progressive supranuclear palsy, a 4R tauopathy.
To modulate synapses, Aη weakens ion flux through glutamate receptors and strengthens their non-ionotropic signaling. This dual action is a first, say scientists.
In mouse models of amyloidosis, CD8+ T cells trigger myelin pathology by rousing microglia and confusing oligodendrocytes.
The innate immune protein C1q can’t leave neurons alone. Already implicated in synaptic pruning, now it appears to be sneaking into neuronal ribosomes as well. There, it cozies up to mRNA and forms liquid droplets. In aging mice, C1q slows the pace of neuronal protein production. Does this contribute to neurodegeneration?
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