Mind the GAP—Synaptic Protein in CSF Signals Tau Spread
Growth-associated protein 43 in the CSF identified people who accumulated tangles fastest. These spread through connected brain regions.
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Growth-associated protein 43 in the CSF identified people who accumulated tangles fastest. These spread through connected brain regions.
Last summer saw a first: the traditional approval of a disease-modifying Alzheimer's therapy. Solid progress on biomarkers, and a flourishing of basic research, made for a good year.
Axons touch arterioles, releasing glutamate that makes smooth muscle cells relax. This increases cerebral blood flow in mice.
A U.K. Biobank analysis generated 15 risk factors for young-onset dementia. Many factors also correlated with late-onset disease.
In people on Entresto, Aβ42 and Aβ40 shot up over six months. The Aβ42/40 ratio fell by a third.
In AD brain, microglia make less of the full-length protein. Loss of INPP5D releases the brakes on inflammation, and may spur microglial phagocytosis.
A new study casts neuronal hyperexcitability as the link between Aβ aggregation in the neocortex and tau pathology in the medial temporal lobe.
Researchers wrangled gene expression, epigenetic, and spatial transcriptomic data on 32 million brain cells into the most detailed picture of the mouse brain yet.
A new method tags individual cells in a tissue slice with a DNA barcode. This allows isolated cells to be mapped to their original location.
PET tracers for the two main proteopathies of FTD, tau and TDP-43, are now in trials, while AI-enabled analysis of FDG-PET scans discriminates between diseases.
Scientists have identified potential fluid and imaging markers that could discriminate between the two main proteopathies of FTD, tau and TDP-43.
Second Holloway Summit Showcases Intense Search for FTD Biomarkers At Holloway Summit, FTD Imaging Shows New Vista To enable clinical trials in frontotemporal dementia, scientists need biomarkers that distinguish its several underlying pathologies. At a r
Whether expressing two copies of APOE3 or -E4 with this variant, mice had less tauopathy, gliosis, atrophy. One copy of Christchurch partially protected.
Cell-type-specific polygenic risk scores single out microglia as influencers of Aβ and tau pathology, as well as cognitive decline.
Proteins in human blood flag organ-specific accelerated aging and disease risk. For cognition, 49 proteins better predicted decline then did plasma p-tau 181.
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