Alzheimer disease (AD) is the most prevalent devastating neurodegenerative disorder in the world, estimated to currently affect over 35 million people and to contribute to ~63% of all dementia cases. As life expectancy continues to increase, a dramatic rise in the incidence of AD is anticipated, with the number of people suffering from this debilitating disease expected to double every 20 years.

The sequential cleavage of APP by β- and γ-secretases, results in the release of amyloid-β (Aβ) peptides, which are generally accepted as the primary culprits in the pathogenesis of AD.

Our research interests include understanding APP biology, i.e., to unravel the protein network and the mechanisms involved in Aβ generation by structural and functional analyses, and investigating the molecular events of amyloid aggregation, gain of toxicity, and the causes of neuronal dysfunction. Our primary aim is to identify novel targets to develop pharmacological strategies for prevention and therapy.

i) APP biology

ii) Amyloid aggregation

iii) Functions of APLPs

iv) Biomarkers for AD