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In dementia with Lewy bodies, basic scans are used in routine diagnosis. Multimodal imaging and new PET tracers for affected neurotransmitters of pathological deposits in the brain and gut are entering research settings.
Provocative new data suggest that glial engulfment of synapses dampens network hyperexcitability early in disease. Key mediators: TREM2 and phosphatidylserine.
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.
Researchers identify where proteases snip the microglial receptor TREM2 to release its extracellular domain: exactly at the site of a rare AD risk variant.
At a conference on lipids in the brain, scientists reported how unsaturated fatty acids might worsen or ameliorate the effects of proteinopathies.
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.
At Leiden conference, scientists discussed how shifting cells toward “specialized pro-resolving mediators” could counter inflammation.
A new study defined the location and expression profile of this astrocyte subtype, pegging the protein myocilin as a marker.
Most participants in AD research studies and trials are non-Hispanic whites. At a conference in St. Louis, scientists discussed strategies to include diverse populations.
Across several studies, black/African Americans and Hispanic or Latino people had lower amyloid positivity rates than whites. Scientists are studying why.
Scientists at AAIC said ARIA-E resembles inflammation related to cerebral amyloid angiopathy. The prime suspect? The complement cascade.
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
They can be neutralized by lecanemab, an anti-amyloid antibody designed to mop up Aβ protofibrils.
Phase 1b results tease that the small molecule PRI-002 might curb cognitive decline. Phase 2 is slated for early 2024.
Children lacking a gene needed for clearing away tired mitochondria develop a rare neurodegenerative disorder.
