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P75 NEUROTROPHIN RECEPTOR SIGNALING THROUGH THE RHOA/ROCK PATHWAY CONTRIBUTES TO ALZHEIMER’S DISEASE TAUOPATHY
Liao Kangand 2 co-authors
Peking University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-388
Presentation
Date TBA
Board: PS02-07PM-388
Event Information
Poster Board
PS02-07PM-388
Poster
View posterAbstract
Hyper-phosphorylated tau-derived intracellular paired helical filaments (PHF) is one of the major pathology of Alzheimer’s disease (AD). Previous studies have found that knock-out (KO) of p75 neurotrophin receptor (p75NTR) had protection effects on Aβ plaque-induced neuropathology in 5xFAD mouse model of AD amyloidosis. However, the role of p75NTR in tau-associated AD pathology remains unclear. In the present study, we introduce different p75NTR mutations, including KO and signaling-deficient variants lacking the death domain (dDD) or transmembrane Cys259 (C259A) into the P301S mouse model of AD tauopathy. We show that learning and memory deficits as well as degeneration in P301S is ameliorated by introduction of dDD mutations but not C259A. Cell death and synaptic loss are also significantly rescued by the introduction of dDD mutation. In addition, we find that the introduction of KO and dDD mutations but not C259A, reduces the levels of PHF and gliosis in hippocampus of P301S mice. To obtain a comprehensive understanding of p75NTR’s role in AD tauopathy, we introduce the Rho-signaling-deficient mutations of p75NTR and find that this mutation also ameliorates tau-related pathology in P301S both histologically and in behavior. Currently, we are working on understanding more about the mechanisms of this protection effect.
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