Finally, a Diagnostic Marker for Lewy Body Disease?
α-Synuclein seed amplification assays identify people with LBD. They may outperform clinical diagnosis, and hint that dementia with Lewy bodies might be overdiagnosed.
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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.
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 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.
While memory problems plague some people with lingering COVID symptoms, researchers do not yet understand what is going wrong in their brains.
Scientists devised fresh approaches for curbing tau tangles that might better reach the protein inside cells, or target several pathologies at once.
Data from TRIAD cohort cast activated microglia, egged on by ApoE4, as harbingers of tau pathology and neurodegeneration. Data from BioFinder hint that other microglia restrain these processes.
In Alzheimer’s, Parkinson’s, and Lewy body dementia, phospholipid and cholesterol homeostasis are disrupted early on. Scientists are bringing new methods to bear on the problem.
cGAS and STING initiate a type I interferon response, which weakens neurons’ resilience to tau pathology.
Scientists showed how pooling microglia from different donors, then putting them through cutting-edge analyses, can link genetic variation to functional change.