Plaques Kick Neocortical Neurons into Overdrive, Entangling Tau
A new study casts neuronal hyperexcitability as the link between Aβ aggregation in the neocortex and tau pathology in the medial temporal lobe.
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A new study casts neuronal hyperexcitability as the link between Aβ aggregation in the neocortex and tau pathology in the medial temporal lobe.
In AD brain, microglia make less of the full-length protein. Loss of INPP5D releases the brakes on inflammation, and may spur microglial phagocytosis.
The patient, an APOE4 homozygote with severe cerebral amyloid angiopathy, developed vascular inflammation and bleeding throughout her brain.
Growth-associated protein 43 in the CSF identified people who accumulated tangles fastest. These spread through connected brain regions.
In CD8+ T cells and monocytes, DNA was more accessible in people with AD and even more so in ApoE4 carriers.
ApoE2 reported as raising risk for progressive supranuclear palsy, a rare tauopathy.
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.
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?