In Vivo Models for Golgi Fragmentation and the Molecular Pathogenesis of Alzheimer’s Disease


The Golgi apparatus is required for normal function of all cells. This proposal is aimed at determining whether reversal of Golgi fragmentation by overexpression of a key Golgi protein (called GRASP55) in the mouse brain can modulate the behavioral, molecular and histological features of two mouse models of Alzheimer’s disease.

Funding to Date



Studies of Alternative Neurodegenerative Pathways, Translational


Sam Gandy, M.D., Ph.D.

Yanzhuang Wang, Ph.D.