Nothing to Sneeze At: Viruses Raise Risk of Neurodegenerative Disease
Twelve severe viral illnesses boosted risk up to 15 years after infection.
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Twelve severe viral illnesses boosted risk up to 15 years after infection.
New studies report that transdifferentiated neurons from AD patients retain signatures of aging. They also model lysosomal dysfunction, tau phosphorylation, and cell death.
The panel of six marker candidates includes proteins involved in lipid processing and metabolism in microglia.
The comprehensive survey of brain-wide gene expression over the lifespan flagged glial cells in white matter as potential drivers of aging.
In mice, curbing a hepatic hydrolase boosted protective epoxy fatty acids in the brain, which stimulated microglia to clear amyloid.
Compared to AD, tau tangles in PART accumulated slowly, and only in the medial temporal lobe. Cognition slipped subtly, and no amyloid amassed over three years.
A retrospective study found an increased risk of brain bleeds in people who received blood from someone else with such bleeds, hinting at a soluble agent. Aβ?
The transmembrane protein tempers an enzyme that destroys lipids comprising myelin. Sans TMEM106b, lipid levels drop, and the myelin may be compromised.
Acetylation of lysine residues unique to 4R tau hinders protofibril folding. The findings might explain selective 3R tau deposition in Pick’s disease.
CMS has lifted restrictions that allowed beneficiaries one scan per lifetime as part of a clinical study. Approval of immunotherapies was a key factor.
Functional variants of AD GWAS hits found in enhancers of myeloid genes.
Adding palmitate makes an estrogen receptor linger at the synapse, curbing α-synuclein aggregation, motor deficits, and faulty memory. In mice.
Faulty lipid metabolism is being blamed for supercharging tau phosphorylation. Restoring lipid efflux protects the mouse brain.
Cryo-EM reveals a common conformational progenitor for tau filaments found in Alzheimer’s disease and chronic traumatic encephalopathy.
In the dura, these lymphocytes release interleukin 17, activating perivascular macrophages. They curb cerebral blood flow, and mice become forgetful.
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