Kei Cho (Professor of Neuroscience) Henry Wellcome LINE and MRC Centre for Synaptic Plasticity How does Aβ influence synaptic plasticity? How does Aβ regulate postsynaptic proteins? Synaptic Plasticity: Pathways towards and away from Amyloid-peptide-mediated synaptic dysfunction MRC Medical Research Council Centre for Synaptic Plasticity
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Kei Cho (Professor of Neuroscience) Henry Wellcome LINE and MRC Centre for Synaptic Plasticity How does Aβ influence synaptic plasticity? How does Aβ regulate.
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Kei Cho (Professor of Neuroscience)
Henry Wellcome LINE and MRC Centre for Synaptic Plasticity
How does Aβ influence synaptic plasticity?
How does Aβ regulate postsynaptic proteins?
Synaptic Plasticity: Pathways towards and away from Amyloid- peptide-mediated synaptic dysfunction
MRCMedicalResearchCouncil
Centre for Synaptic Plasticity
Synaptic Plasticity and Alzheimer’s Disease
Cerebral elevation and accumulation of A1-42 peptide in many aspects of AD mediated pathogenesis.
Oligomeric forms of A1-42 in the extracellular space correlates with cognitive decline and synaptic alterations (impairment of LTP, inflammation, fibrillization)
Synaptic Transmission
The role of AThe role of A in synaptic in synaptic plasticityplasticity
AA
LTP
LTD
Intracellular
Extracellular
?
A oligomers PlasmaMembrane
Signal cascades
?Output
Neurotoxicity, Cell death, Atrophy,
Synaptic dysfunction
Target and Strategy
Using a combination of biochemistry, molecular biology and electrophysiology, the project will explore whether soluble A regulates enzymes and postsynaptic protein-protein interactions involved in LTP and LTD.
Molecules of interest include PSD-95, GRIP1, PICK1, AMPARs, caspase and neuronal calcium sensors.