New Atlas Catalogues Regulatory RNA Changes in Alzheimer’s
Survey of post-translationally modified and noncoding RNA identified more than 25,000 differences between AD and control brain.
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Survey of post-translationally modified and noncoding RNA identified more than 25,000 differences between AD and control brain.
In AD brain, cells ramp up expression of herpes virus proteins. In cultured neurons, these proteins boost p-tau, which then suppresses viral proteins.
In mice, eliminating the NPC1 gene from microglia recapitulated aspects of the lysosomal storage disorder.
In lab animals, lithocholic acid replicates life-extending benefits of caloric restriction.
Dennis Selkoe offers a closing response.
In postmortem tissue, nearly half of AD patients had HCMV infections in the brain and gut. In cerebral organoids, HCMV triggered accumulation of Aβ and p-tau212.
With age, this coupling erodes, making synapses sluggish. Rekindling it lessens synaptic deficits and memory loss in old mice.
Scott Small offers a closing argument.
Dennis Selkoe replies to Scott Small.
Scott Small reacts to a recent perspective paper and the discussion it engendered.
In mice, crippling PSEN2 worsened amyloid deposition, synaptic dysfunction, and deficit in working memory.
A Tolstoy-inspired method identifies AD variants that exert similar effects, pinpointing causal AD proteins—six known, plus a new one, RET.
As levels of the deacetylase wane with age, more APP gets processed in endosomes, worsening amyloid pathology.
Report probes predictors of dementia, the benefits of early detection, and people’s motivation to seek testing and treatment.
Lipids, amino acids, carbohydrates, and other molecules in the CNS linked to genetic variants, some of which upped the risk for neurodegenerative disease.
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