Aggregation and accumulation of proteins in the brain are common features of diverse age-related neurodegenerative diseases. Each of these neurodegenerative diseases is associated with abnormalities in the folding of a different protein leading to protein aggregation and ultimately to neuronal death. We use different transgenic mouse models which develop several lesions similar to those seen in AD. Specifically we are interested in the question of how Aβ protein aggregates and forms plaques in vivo and what might trigger the initiation of plaque formation along with the pathology that accompanies it. The methods we use in the lab range from biochemistry, molecular biology, stereotaxic approaches and microscopy (including 2-Photon microscopy).