School of Psychology

The amyloid cascade hypothesis proposes that Alzheimer’s disease (AD) is caused by the abnormal production and deposition amyloid-β in the brain leading to dementia.  A recent revision to this hypothesis has highlighted the important role played by intermediate Aβ oligomers in early-stage synaptic and cognitive dysfunction in Alzheimer’s Disease before extracellular amyloid plaques develop. This revised hypothesis predicts that the very earliest stages of amyloid-induced cognitive dysfunction are a result of a breakdown in synaptic plasticity processes and the subsequent disruption to neural network activity that encodes and retrieves information. Little is known as to how amyloid production influences network activity within the brain, therefore the main aim of my project is to build upon preliminary work that shows amyloid production disrupts network activity within the hippocampus and between the hippocampus and key regions contributing to memory using the Tg2576 mouse model of amyloid pathology. Following this I will examine how exercise-induced plasticity in the hippocampus influences network properties in APP over expressing mice.