Organization of Aβ Plaques and Tau Tangles Illuminated in AD Brain
Plaques comprise different-sized fibrils and cell membrane components, while tangles have distinct fibril structures segregated into intra- and extracellular compartments.
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Plaques comprise different-sized fibrils and cell membrane components, while tangles have distinct fibril structures segregated into intra- and extracellular compartments.
The ability to quickly detect cerebral amyloid angiopathy and ARIA would make amyloid immunotherapy safer, but research in this area is just beginning.
Scientists at AAIC said ARIA-E resembles inflammation related to cerebral amyloid angiopathy. The prime suspect? The complement cascade.
A crop of new PET tracers that bind α-synuclein aggregates shows promise in tissue samples and in animal models. Will they prove potent enough for brain imaging?
First data from the Longitudinal Early-Onset Alzheimer’s Disease Study hints at what might cause this type of AD and how it unfolds.
In mice, curbing a hepatic hydrolase boosted protective epoxy fatty acids in the brain, which stimulated microglia to clear amyloid.
In contrast to phospho-tau species that mirror amyloid, CSF MTBR-tau-243 reflects tau-PET. It fell upon treatment with an antibody against tau’s midsection.
Between basic researchers and clinicians, momentum is growing to test BACE inhibition again. This time, at low doses.
Alzheimer’s researchers got their first look at data from the positive Phase 3 trial. Many expect this antibody to become the third approved immunotherapy for AD.
Donanemab Data Anchors Upbeat AAIC Give BACE Inhibitors a Second Chance? CSF MTBR-tau-243 Tracks Tangles, Plummets in Response to Antibody Cohort LEADS Toward Better Understanding of Sporadic Early Onset AD Spying on α-Synuclein Inclusions: PET Tracers In
While each disease features distinct proteomes in the brain, cerebrospinal fluid, and blood, some proteins overlap. They are more dysregulated in familial than in sporadic AD.
In cells from people with Down’s syndrome, and in mouse models of DS and Alzheimer’s, excess β-CTF binds vacuolar ATPase, hobbling lysosomal acidification.
Two interference screens netted a thousand proteins that affect tau oligomerization. The affected pathways? Mitochondrial malfunction, and UFMylation.
The panel of six marker candidates includes proteins involved in lipid processing and metabolism in microglia.
A trio of studies report that missense variants in SORL1 that disrupt its trafficking or dimerization are highly likely to cause Alzheimer's disease in carriers, strengthening the case for SORL1 being a familial AD gene.