Alzheimer’s Disease is characterized by extracellular Beta-Amyloid (βA) Plaques. Beta-Amyloid are produced by the sequential cleavage of amyloid precursor protein by Y-secretase. Arc, a ~50 kDa IEG protein, may regulate Y-secretase activity. For this study, Unilaminar Vesicles acted as Cell Membranes, as FCS studies were done to quantify Arc’s interactions with lipids. HEK cells were transfected with EGFP-Arc to identify expression and association on cell surface and within the cytosol using N&B method. My findings support the model of inactivated Arc in the cytosol being directed to the plasma-membrane where activation and self-association leads to scaffolding, allowing Arc to interact with PS1 ultimately leading to activity-dependent generation of βA to facilitate Alzheimer’s Disease.
Rajeev Ranjan Jha
Share this Post