Do Tau Fibrils Form Via Droplets?
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.
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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.
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.
Mice missing microglia develop astrogliosis and neurodegeneration by middle age. Giving them healthy microglia prevents or reverses pathology.
Nixing an endosomal targeting sequence shields APP from BACE1, reducing Aβ and pathologic C-terminal fragments in mice.
Injected into the cerebrospinal fluid, a viral vector delivers the lysosomal protein into the human brain. In mice, a protein transport vehicle delivered into the blood does the same.
A panel of eight plasma proteins identified people who were on the path to Parkinson’s. Could this help select participants for prevention trials?
With limited guidance, physicians will have to navigate questions about whom to treat, when to stop, and how to manage safety.
C05-05 binds α-synuclein deposits in the mouse, marmoset, and human brain. Uptake in the PD midbrain correlated with motor symptom severity.
All 11 committee members voted that the antibody was effective for people with MCI or mild AD dementia, with its benefits outweighing risks.
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