Long COVID and Dementia: The Link Is Still Elusive
While memory problems plague some people with lingering COVID symptoms, researchers do not yet understand what is going wrong in their brains.
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While memory problems plague some people with lingering COVID symptoms, researchers do not yet understand what is going wrong in their brains.
In sleep-deprived mice, TREM2 signaling activated microglia in a dysfunctional way, hobbling their endolysosomes and keeping them from digesting Aβ plaques.
The antibody slowed decline by 35 percent, met secondary endpoints, will likely be approved. Major question: How to avoid severe ARIA.
Scientists devised fresh approaches for curbing tau tangles that might better reach the protein inside cells, or target several pathologies at once.
Data from TRIAD cohort cast activated microglia, egged on by ApoE4, as harbingers of tau pathology and neurodegeneration. Data from BioFinder hint that other microglia restrain these processes.
In Alzheimer’s, Parkinson’s, and Lewy body dementia, phospholipid and cholesterol homeostasis are disrupted early on. Scientists are bringing new methods to bear on the problem.
Safety and cerebrospinal fluid tau data from the six-month Phase 1 trial are now published.
cGAS and STING initiate a type I interferon response, which weakens neurons’ resilience to tau pathology.
The antisense oligonucleotide targets extremely rare variants of the superoxide dismutase 1 gene.
Scientists showed how pooling microglia from different donors, then putting them through cutting-edge analyses, can link genetic variation to functional change.
At AD/PD, scientists zeroed in on endolysosomal mechanisms in microglia that may contribute to neurodegenerative disease. Blending omics with cellular studies leads them from genes and function.
Lilly’s Phase 3 antibody remternetug resembles donanemab, but without pesky antidrug antibodies; Prothena’s Phase 1 PRX012 may need fewer injections.
Analysis of cerebrospinal fluid from the Parkinson’s Progression Markers Initiative identifies PD with high sensitivity and specificity.
The microglial receptor activates an antiviral signaling cascade. The virus downregulates TREM2 expression after infecting microglia.
Clusterin latches onto dimers of CD33 on the microglial cell surface, setting off inhibitory signaling that squelched phagocytosis.
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