In Down's Syndrome, Blood P-Tau217 Detects Plaques and Tangles
In young adults with Down’s, plasma phospho-tau217 correlated with amyloid and tau PET positivity. With great accuracy.
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In young adults with Down’s, plasma phospho-tau217 correlated with amyloid and tau PET positivity. With great accuracy.
The same endothelial cell response is found in various models of brain disease.
A tetravalent IgG1 prompts TREM2 to cluster, boosting the receptor’s activation 100-fold. Treated mice had fewer plaques, better memories.
The Parkinson’s-related proteins promoted pathological hyperphosphorylation of α-synuclein.
Analysis of 168 metabolites in one blood sample foretold 10-year risk of developing common disorders.
Blocking glycolysis triggers microglia to crank up lipid metabolism, boosting ATP production and improving phagocytosis. In Alzheimer’s disease, the opposite happens.
While GFAP seems a sensitive biomarker of Aβ plaque removal, NfL might respond more slowly.
Sans SYK, mice struggle to mobilize disease-associated microglia or reign in amyloid or myelin fragments.
The antibody removed less plaque than expected and did not slow cognitive decline, according to top-line data. Detailed data to come at CTAD.
In two primary tauopathies, fragments containing tau’s microtubule-binding region drop in the CSF as they accumulate in the brain.
ApoE2 was detected in cerebrospinal fluid of ApoE4 carriers with Alzheimer’s disease who received a virus expressing the protective allele.
The assay captures α-sheet structure. It detected AD with 99 percent accuracy, including among healthy people who later became cognitively impaired.
CSF monocytes increasingly crank out the chemokine CXCL16, while T cells up its receptor, CXCR6. The same cross-talk unfolded among microglia and T cells around plaques.
In fly tauopathy model, dsRNA triggers inflammation and neuron death. In Alzheimer’s, dsRNA accumulates in the brain.
Brain-derived forms of tau distinguished people with Alzheimer's from those with other neurodegenerative diseases.
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