At the Heart of Alzheimer’s in Down’s: Cerebrovascular Disease
Few people with Down's syndrome have cardiovascular risk factors, yet most develop cerebrovascular disease. Will this complicate anti-amyloid immunotherapy?
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Few people with Down's syndrome have cardiovascular risk factors, yet most develop cerebrovascular disease. Will this complicate anti-amyloid immunotherapy?
Two men with loss-of-function variants in their APOE4 alleles escaped amyloid pathology. One was in his 90s.
Swapping allele expression in astrocytes lowered amyloid load, lessened gliosis, and improved memory. This works even after amyloidosis is in full swing.
Scientists at AAIC debated discrepant results, updated a model of the biomarker-efficacy relationship, and debuted the CenTauR scale for tau PET.
At AAIC 2023, scientists tied clinical success to drug exposure, speed of plaque clearance, amyloid negativity.
DNA from leaky mitochondria unleash the cGAS-STING cascade, triggering interferon responses in the brain.
A section of the protein folds on itself to form five layers. Three V-shaped layers cradle each other. This differs from the double-spiral fold in people with FTD/ALS.
The newly proposed scheme uses only amyloid and tau for diagnosis and staging. It establishes parallel tracks for fluid or imaging markers, and recognizes a clinical stage zero.
α-Synuclein seed amplification assays identify people with LBD. They may outperform clinical diagnosis, and hint that dementia with Lewy bodies might be overdiagnosed.
Twelve people heterozygous for this protective variant were still sharp seven years after their expected age of AD onset. One had fewer tangles than expected.
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.
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