Microglia Make Tau, Spelling Their Demise in Tauopathies
When carrying a pathogenic tau variant, microglia were bad at phagocytosis, barely made TREM2, and spat out neurotoxic proteins.
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When carrying a pathogenic tau variant, microglia were bad at phagocytosis, barely made TREM2, and spat out neurotoxic proteins.
As flies age, mitochondrial damage in their neurons somehow ages glia, which, in turn, cause lipid droplets to pile up on other, healthy glia.
The enzyme cleaves off three amino acids at a time with a twist of the substrate, and a helping hand from a β-strand.
The astrocytic receptor enforces distancing among glial cells. Free from this constraint, they better contain plaques.
A new study challenges this idea, finding that in mice, clearance of an injected dye slowed during sleep and anesthesia.
When the nuclear RNA-binding proteins NONO and SFPQ accumulate, adenosine-to-inosine editing of RNA runs amok. This spoils transcripts for axonal, synaptic, and mitochondrial proteins.
FDA qualification would streamline the use of plasma NfL to select asymptomatic carriers of pathogenic frontotemporal dementia mutations for enrollment in prevention trials.
Scientists correlated the PET signal in PSP patients with tau deposits in postmortem brain; the signal arises from neurons and oligodendrocytes.
People born in the 1970s had 15 percent more surface area in their cortices than those born in the 1930s.
Equipped with ApoE3-Christchurch, microglia made short work of tau fibrils, and spewed fewer inflammatory cytokines.
Lecanemab will soon have maintenance dosing and subcutaneous formulations available; FDA advisory committee will consider donanemab June 10.
An adeno-associated virus that binds the transferrin receptor delivered β-glucocerebrosidase throughout the mouse brain.
APOE4 carriers who also have a glycine-to-glutamic-acid substitution in the extracellular matrix protein were much less likely to develop Alzheimer’s disease.
Blood and other in vitro assays will need to meet the same standards as medical devices, including demonstrating diagnostic accuracy.
By age 65, nearly all people who carry two copies of APOE4 harbor neuropathological or biomarker evidence of AD pathology.