Second Holloway Summit Showcases Intense Search for FTD Biomarkers
Scientists have identified potential fluid and imaging markers that could discriminate between the two main proteopathies of FTD, tau and TDP-43.
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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.
Cryo-EM identified TAF15 filaments at the heart of protein aggregates in some FTD cases. Should FDT-FUS be renamed FTD-FET?
In the dura, these lymphocytes release interleukin 17, activating perivascular macrophages. They curb cerebral blood flow, and mice become forgetful.
Cryo-EM reveals a common conformational progenitor for tau filaments found in Alzheimer’s disease and chronic traumatic encephalopathy.
Each associates with distinct AD risk variants, brain atrophy, and disease severity.
C2N’s PrecivityAD2 and ALZpath Inc.’s p-tau217 immunoassay identify people with AD with good accuracy.
For a diagnostic test, specificity and sensitivity fall a little shy. Using two cut points might solve the problem.
Adding palmitate makes an estrogen receptor linger at the synapse, curbing α-synuclein aggregation, motor deficits, and faulty memory. In mice.
This clarification comes after geriatricians argued that diagnosing AD in people without symptoms is premature, and the NIH pulled its name.
Faulty lipid metabolism is being blamed for supercharging tau phosphorylation. Restoring lipid efflux protects the mouse brain.
Signaling within microglia requires dozens of substrates of γ-secretase. Without the enzyme, the cells barely react to plaques in mice.