Alzheimer’s disease (AD) arises through the aggregation of amyloid-β (a cleavage product of APP) and tau protein throughout the brain. The build-up of these proteins can result in harmful changes to neuronal functioning and health, including dysfunction of mitochondria, which are responsible for energy production within the cell, and changes to the way neurons communicate with each other at synapses. My project aims to express AD-causing mutant forms of APP and tau proteins in primary neuronal cultures to generate a sped- up model for neurodegeneration in AD. Upon validating these models with regards to neuronal health and production of neurotoxic proteins, the models will then be used to investigate the changes to mitochondria morphology and proteins controlling this. Using a mixture of protein biochemistry, immunofluorescence imaging and potentially electrophysiology, I will detect changes that occur when either or both of these neurotoxic proteins are expressed to dissect each proteins’ role in mitochondrial dysfunction. Further to this, the cellular localization, surface expression and activity of synaptic proteins including AMPA receptors and CB1 receptors will be investigated following expression of these neurotoxic proteins. This work could help to find new points of intervention to slow dementia in AD.