Amyloid, Not Vascular Disease, May Drive White-Matter Hyperintensities
These imaging abnormalities grew the most in people with many plaques or cerebral amyloid angiopathy pathology, irrespective of cardiovascular risk.
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These imaging abnormalities grew the most in people with many plaques or cerebral amyloid angiopathy pathology, irrespective of cardiovascular risk.
Scientists report that when the TREM2 fragment binds transgelin-2, it weakens phosphorylation of tau in neurons.
At Leiden conference, scientists discussed how shifting cells toward “specialized pro-resolving mediators” could counter inflammation.
The Alzheimer’s risk allele locks microglia in a state of homeostasis. They ignore amyloid plaques and neurofibrillary tangles.
An antibody copying the effects of the protective ApoE variant prevents tau hyperphosphorylation in the mouse eye and brain.
A cholesterol metabolite magnifies pathology in a tauopathy mouse. Microglia need cholesterol to rein in amyloid. ApoE4 jams the fat's export from neuron to glia.
We all know oligodendrocytes maintain myelin. According to scientists at the 2nd Symposium on Lipids in Diseases, they need microglia to do it.
At a conference on lipids in the brain, scientists reported how unsaturated fatty acids might worsen or ameliorate the effects of proteinopathies.
Cutting (or Slippery?) Edge: Lipids in Neurodegeneration Science Does the Brain Use Microglia to Maintain Its Myelin? Cracking the Cholesterol-AD Code: Metabolites and Cell Type Can Flipping a Lipid Switch Protect the Brain? The average human brain contai
CMS has lifted restrictions that allowed beneficiaries one scan per lifetime as part of a clinical study. Approval of immunotherapies was a key factor.
A comparative snRNA-Seq study of three regions from AD, PSP, and FTD brains identifies subtypes of neurons and glia hit hard in each disorder.
The oligomers beckon microglia and astrocytes to prune dendrites. This correlates with cognitive decline.
A consortium of pharma companies mined data from 50,000 people in the U.K. Biobank to turn up thousands of new gene-protein connections.
Reported in 21 papers, a collaborative effort describes brain-wide gene expression, epigenetics, morphology, and activity at single-cell resolution.
Resilient and vulnerable interneurons mark different stages of Alzheimer's. Gene regulation crumbles in late stages. Microglial states change with epigenomic shifts.
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