Flipping the Script: Could Myelin Degeneration Drive Amyloidosis?
Myelin breakdown in the Alzheimer’s brain is thought to be a consequence of plaques, but a new study in mice suggests it may be a cause.
6473 RESULTS
Sort By:
Myelin breakdown in the Alzheimer’s brain is thought to be a consequence of plaques, but a new study in mice suggests it may be a cause.
The APP/PS1 double knock-ins begin to deposit amyloid in the brain by 3 months of age.
Across a three-decade span, there was no difference in amyloid pathology, but younger cohorts had healthier cerebrovasculature.
In mice, the neuronal transcription factor NPAS4 recruits DNA repair machinery to active promoters; without it, double-strand DNA breaks accumulate.
Authors say the evidence that physical activity improves cognition in healthy people is inconclusive. Others disagree.
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.
Multiplex analyses spy a new microglial subtype that surrounds Aβ plaques, and a type of neuron resilient to neurofibrillary tangles.
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.