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Xinglin Lecture Series No. 212 - Ningbo University 40th Anniversary & 30th Anniversary of the Merger of Three Campuses

Author: Date: 2026-04-07

Lecture Title: Age and Activity Dependent Aβ-Tau Interactions

Time: 14:00–15:30, Thursday, April 9, 2026

Venue: Smart Classroom 404, Zhichen Building, Medical School

Speaker: Professor Nengwei Hu

Moderator: Professor Qinwen Wang

Biography:

Professor Hu leads the Neuropharmacology Research Group in the Department of Pharmacology and Therapeutics at Trinity College Dublin, Ireland. His laboratory focuses on the synaptic mechanisms underlying cognitive dysfunction and explores novel therapeutic targets for neurodegenerative tauopathies, particularly Alzheimer's disease.

Professor Hu was the first to report that β-amyloid dimers represent the minimal form of amyloid-β that disrupts synaptic plasticity (Brain, 2008). Subsequent studies identified glutamate receptors (PNAS, 2009; Nat Commun, 2014; Cell Rep, 2018a; JAD, 2022) and the integrated stress response (Transl Psychiatry, 2022; JAD, 2022; Brain Commun, 2024) as potential therapeutic targets. After demonstrating the synaptotoxic effects of extracellular tau protein (Cell Rep, 2018b), his team recently revealed that these effects are mediated by the microtubule-binding region of tau (Acta Neuropathol, 2025).

A key technical breakthrough from Professor Hu’s team is the establishment of a reliable method for inducing hippocampal long-term depression (LTD) in vivo—a form of synaptic plasticity whose role in cognitive function remains incompletely understood. Validated through both electrical stimulation (Nat Commun, 2014; Sci Rep, 2018; Neurobiol Dis, 2019; JAD, 2022; Transl Psychiatry, 2022; Brain Commun, 2024) and optogenetic techniques (Cell Rep, 2018a), this approach enables researchers to simultaneously investigate both major forms of synaptic plasticity, LTP and LTD, in vivo, providing a crucial tool for elucidating the cellular and molecular mechanisms of learning and memory under physiological and pathological conditions.

Research - Talks -
Talks

Xinglin Lecture Series No. 212 - Ningbo University 40th Anniversary & 30th Anniversary of the Merger of Three Campuses

Author: Date: 2026-04-07

Lecture Title: Age and Activity Dependent Aβ-Tau Interactions

Time: 14:00–15:30, Thursday, April 9, 2026

Venue: Smart Classroom 404, Zhichen Building, Medical School

Speaker: Professor Nengwei Hu

Moderator: Professor Qinwen Wang

Biography:

Professor Hu leads the Neuropharmacology Research Group in the Department of Pharmacology and Therapeutics at Trinity College Dublin, Ireland. His laboratory focuses on the synaptic mechanisms underlying cognitive dysfunction and explores novel therapeutic targets for neurodegenerative tauopathies, particularly Alzheimer's disease.

Professor Hu was the first to report that β-amyloid dimers represent the minimal form of amyloid-β that disrupts synaptic plasticity (Brain, 2008). Subsequent studies identified glutamate receptors (PNAS, 2009; Nat Commun, 2014; Cell Rep, 2018a; JAD, 2022) and the integrated stress response (Transl Psychiatry, 2022; JAD, 2022; Brain Commun, 2024) as potential therapeutic targets. After demonstrating the synaptotoxic effects of extracellular tau protein (Cell Rep, 2018b), his team recently revealed that these effects are mediated by the microtubule-binding region of tau (Acta Neuropathol, 2025).

A key technical breakthrough from Professor Hu’s team is the establishment of a reliable method for inducing hippocampal long-term depression (LTD) in vivo—a form of synaptic plasticity whose role in cognitive function remains incompletely understood. Validated through both electrical stimulation (Nat Commun, 2014; Sci Rep, 2018; Neurobiol Dis, 2019; JAD, 2022; Transl Psychiatry, 2022; Brain Commun, 2024) and optogenetic techniques (Cell Rep, 2018a), this approach enables researchers to simultaneously investigate both major forms of synaptic plasticity, LTP and LTD, in vivo, providing a crucial tool for elucidating the cellular and molecular mechanisms of learning and memory under physiological and pathological conditions.