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TARGETING OF TUBULIN-ALPHA 4A POLYGLUTAMYLATION TO MODULATE TAU-MICROTUBULE INTERACTIONS AND PREVENT TAU HYPERPHOSPHORYLATION IN ALZHEIMER'S DISEASE
Diana Peristichand 4 co-authors
University Medical Center Hamburg-Eppendorf, Center for Molecular Neurobiology
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-364
Presentation
Date TBA
Board: PS02-07PM-364
Event Information
Poster Board
PS02-07PM-364
Poster
View posterAbstract
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by cognitive decline, memory impairment, and histological hallmarks such as neurofibrillary tangles. Tau, a microtubule-associated protein (MAP), dissociates from microtubules (MTs) upon a pathological hyperphosphorylation observed in AD, leading to toxic aggregation and formation of intracellular neurofibrillary tangles. The interaction between Tau and MTs is influenced by tubulin isotypes and tubulin post-translational modifications, including polyglutamylation. Tubulin-alpha 4a (Tuba4a), a highly polyglutamylated tubulin isotype, has been identified as a key factor in Tau-MT interaction. Loss of Tuba4a polyglutamylation impairs Tau binding to MTs, reduces Tau phosphorylation, and rescues Tau hyperphosphorylation-induced aggregation in tauopathy mouse models. This study aims to explore therapeutic strategies targeting Tuba4a polyglutamylation to disrupt Tau-MT interaction using cellular in vitro models. Furthermore, behavioral tests in transgenic human Tau mouse models will assess the general behavioral phenotype as well as the cognitive rescue potential of Tuba4a polyglutamylation loss at different time points. This project seeks to develop targeted treatments to prevent Tau hyperphosphorylation and aggregation, offering potential therapeutic avenues for AD and related tauopathies.
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