Dr. Nengwei Hu

Dr Nengwei Hu graduated with a first class honours degree in Medicine and a PhD in Neurophysiology in 2005 from Sun Yat-sen University. He started his postdoctoral training at Trinity College Dublin in 2005 and advanced to the position of Senior Research Fellow in the Department of Pharmacology & Therapeutics at TCD in 2013. His research focused on synaptic dysfunction mechanisms and novel therapeutic targets for neurodegenerative diseases, with a particular emphasis on Alzheimer's disease. Dr Hu began his role as an Assistant Professor in the Discipline of Pharmacology & Therapeutics in January 2024.

  Age related diseases   Ageing, memory and other cognitive processes   Ageing, stroke, dementia   Neurodegeneration   Neuropsychology

Our research focuses on synaptic dysfunction mechanisms and novel therapeutic targets for Alzheimer's disease (AD). Having reported that amyloid ß dimer is the smallest form to cause synaptic plasticity disruption (Brain, 2008), we subsequently discovered that glutamate receptor subtypes, particularly GluN2B (PNAS, 2009) and mGluR5 (Nat Commun, 2014) are potential therapeutic targets for AD. Recently, we found that tau from AD patient cells also disrupts synaptic plasticity, providing a better understanding of AD pathophysiology (Cell Rep, 2018a). Apart from that, we developed stimulation protocols to reliably induce long-term depression of synaptic transmission in hippocampus in vivo (Nat Commun, 2014; Cell Rep, 2018b; Sci Rep, 2018; Neurobiol Dis, 2019; Transl Psychiatry, 2022; J Alzheimers Dis, 2022). This development enables researchers to study the two major forms of neuroplasticity, long-term potentiation and long-term depression at glutamatergic synapses, providing an in vivo means to uncover cellular and molecular processes underlying learning and memory in health and disease. Having previously reported that amyloid ß facilitates hippocampal long-term depression (Nat Commun, 2014; Cell Rep, 2018b; Transl Psychiatry, 2022), my group recently discovered that hippocampal long-term depression but not long-term potentiation triggers tau phosphorylation in live rats under the condition of ageing (J Alzheimers Dis, 2022) or amyloid ß treatment (AD/PD2023 poster). Our ongoing study is focusing on: 1. Age and activity dependent Aß-tau interactions; 2. The physiological or pathological role of phospho-tau promoted by long-term depression and related behaviour.