When Autophagy Stops, Microglia Sour into Senescence
Backed up, the cells never transitioned into a disease-associated state, shirking their plaque compaction and synapse protection duties.
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Backed up, the cells never transitioned into a disease-associated state, shirking their plaque compaction and synapse protection duties.
Three reviews, two perspectives, and four comments discuss recent advances and opportunities for dementia research.
More evidence that presynaptic tau may spread from neuron to neuron.
Mendelian randomization identified HDL cholesterol and systolic blood pressure as modifiable risk factors.
Arranged in bundles and lattices within a plaque, Aβ42 fibrils were intermixed with extracellular vesicles of different shapes and sizes. Their origin remains unknown.
Transplanting a human cerebral organoid containing microglia into a mouse brain allows the cells to thrive in something close to their natural environment.
Multiplex analyses spy a new microglial subtype that surrounds Aβ plaques, and a type of neuron resilient to neurofibrillary tangles.
They can be neutralized by lecanemab, an anti-amyloid antibody designed to mop up Aβ protofibrils.
An amino acid change in this ApoE receptor-binding protein may have bestowed 20 years of resilience to a brother and sister carrying the presenilin Paisa mutation.
The D2 dopamine receptor agonist reduced agitation behaviors in Phase 3 trials of dementia due to AD.
Scientists celebrated LaDu's scientific and academic career at Chicago memorial.
Bound up in vesicles extracted from Alzheimer's brain, tau filaments adopt their characteristic back-to-back C-shape. A mystery molecule is involved in tying them down.
The public database includes information about the structure, polarity, and stability of both pathogenic and functional amyloid folds.
One study links early menopause to tangles in early AD, another finds a sex difference in the brain's stress response. Could hormones fuel women’s higher risk of dementia?
A deletion in the gene for a lysosomal ion channel popped out of a genomic analysis of LBD risk. So did rare structural variants in other FTD and ALS genes.
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