Physiological Method for Early Detection of Synaptic Vulnerability in Alzheimer’s Disease Model Animals


Multiple factors will cause or contribute to synaptic dysfunction in Alzheimer’s disease. The excessive production or accumulation of amyloid beta peptide has been documented to have deleterious effects on synaptic activity by various mechanisms. Many scaffolding proteins like mGluR proteins, Shank, Homer and postsynaptic density 95 are known to form complexes at synaptic terminals, and amyloid beta accumulation at synaptic terminals leads to disruption of these scaffolding protein interactions. Synaptic changes occur prior to the detection of brain plaques and behavioral changes associated with cognitive deterioration in Alzheimer’s disease. Alzheimer’s disease is recognized as a disease of synaptic failure. This project proposes the development of an optical imaging method for detection of early changes in synaptic function occurring in animal models of Alzheimer’s disease.

Funding to Date



Foundational Genetics, Other Areas of Investigation


Riqiang Yan, Ph.D

Srdjan D. Antic, M.D.