Kei Cho

Research Interests

Prof. Cho is interested in physiologicaland pathophysiological synaptic plasticity in the hippocampus, specifically focusing on the mechanism of synapse weakening in the brain and to identify potential therapeutic targets for neurodegenerative disease and associated mental illness. Synapses undergo pathophysiological weakening by the aggregation of amyloidbeta, hyperphosphorylated Tau and aberrant regulation of RNAbinding proteins. Prof. Cho is studying the biological processes that lead to the weakening of synapses and their progressive loss in neurodegenerative disease and identifying / validating molecular targets for the design of new treatments that can slow down or stop neurodegeneration.

Most significant discovery

Prof Cho uncovered the molecular mechanisms of physiological and pathophysiological synapse weakening, identifying a key role for caspases, often associated with apoptosis, which mediate cleavage of Akt-1 and activation of GSK3b and downstream long-term depression in synaptic transmission (LTD). Subsequently, Cho identified amyloid-beta and tau phosphorylation (pTau)-mediated pathological synapse dysfunction and discovered a potential therapeutic target for rescue effect from neurodegeneration.

Educational Interests

• Memory mechanisms in health and disease
• Neuroscience literature-based research
project
• Laboratory research project in
Neuroscience

Top 4 Publications

• Jo, J., et al 2011. Nat Neurosci. 14; 545-547

• Hughes et al., 2020. Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation defific and rat neuronal cell death. Commun Biol. 3(1):79.

• Regan, P., et al 2021. Regulation of synapse weakening through interactions of Tau with PACSIN1. J Neurosci. 41(34): 7162-7170

• Kim et al 2023. Mimicking hypomethylation of FUS requires liquid-liquid phase separation to induce synaptic dysfunctions. Acta Neuropathol. Comms 11, 199.

Methods / Expertise

• Electrophysiology
• Multiphotonconfocal imaging
• Neurobiology
• AI-based drug target search