Using an array of receptors to sense neurons in peril, microglia make matters worse by taking bites out of the struggling cells.
Using single-nuclei or cell sorting, three separate research groups sequenced RNA from human postmortem brains. They unveiled AD-associated gene-expression signatures, but disease-related transcriptomes from human microglia were quite different from those in mice.
A person's blood phospho-tau level, combined with his or her APOE genotype and scores on executive function and memory tests, outperforms the clinician in predicting dementia within the next four years.
In the plaque-ridden mouse brain, microglia that had taken up Aβ activated a unique gene-expression profile. It faded after microglia were moved to plaque-free environs.
Scientists know that both genetic and environmental risk factors contribute to sporadic Parkinson’s disease, and that one suspected environmental culprit is manganese...
At a conference in Heidelberg, researchers proposed that Aβ oligomers trigger local translation of tau in cytosol and dendrites, and that targeting this aberrant tau may preserve synapses.
Unlike iPSC-derived neurons, those created directly from fibroblasts reflect the donor's age and disease status. Epigenetic modifications appear to make the difference.
While the FDA weighs aducanumab’s marketing license application, Alzheimer’s researchers agree that the agency’s own statistician correctly assessed the data as weak. Most prefer that one more trial be done.
A “mammalian-wide interspersed repeat-natural antisense transcript” blocks translation of tau mRNA. Other MIR-NATS may act on α-synuclein and APP.
Activating the G protein-coupled receptor PAC1R in the mouse brain prompts the proteasome to clear tangles.
A large multinational epidemiology study finds only small and inconsistent associations.
When pulsed through the skull, ultrasound restored synaptic signaling, neurogenesis, and memory, in old mice.
Downregulation of a chemokine receptor traps T cells in the meninges. Glymph drainage slows, amyloid burden rises.
Treatments that promote neurogenesis and elevate BDNF act as exercise does to improve memory in mouse models of Alzheimer’s disease.
Take a three-dimensional tour of the plaques and tangles of mouse and human brains as they develop Alzheimer’s disease-related pathology.