John Capodilupo

Professor

Email 
[email protected]

Office 
232 Henry Hall

Phone 
(616) 331-3019

COURSES TAUGHT

BMS 202 - Human Anatomy and Physiology
BMS 202L - Laboratory in Human Anatomy and Physiology
BMS 208 - Human Anatomy
BMS 250 - Anatomy and Physiology I Laboratory
BMS 290 - Human Physiology
BMS 291 - Laboratory in Human Physiology
BMS 309 - Human Anatomy Cadaver Laboratory
BMS 310 - Basic Pathophysiology
BMS 365 - Exercise Physiology
BMS 375 - Biology of Human Aging
BMS 427 - Neuroanatomy
BMS 428 - Neuroscience
BMS 495 - Capstone

EDUCATION

Ph.D. (1994) Wayne State University School of Medicine
M.S. (1991) Wayne State University School of Medicine
B.S. (1987) Mercy College of Detroit

RESEARCH INTERESTS

We are examining a molecule called GAP-43 which is a brain protein that is expressed in a wide variety of species including humans and has been shown to become biochemically altered in the process of learning and memory.  Specifically, levels of phosphorylated forms of GAP-43 have been shown to increase following a controversial paradigm of learning and memory in several animals including rat, mouse and rabbit.  We are interested to see if any differences in the profile of GAP-43 are associated with dementing illnesses that severely disrupt memory and learning.  Since human brain tissue is difficult to obtain, we utilize brain tissue from a genetically altered mouse engineered to resemble Alzheimer’s disease, a human neurodegenerative disorder characterized by profound cognitive impairment.  Therefore, to test the hypothesis that the profile of  phosphorylated isoforms of GAP-43 are changed in the brains of a mouse used to model Alzheimer’s disease, GAP-43 will be examined by 1 and 2 dimensional SDS polyacrylamide gel electrophoresis.  Isoforms of mouse brain GAP-43 will be detected by immunocytochemistry  and silver staining and, further, quantified by computerized densitometry.  Alterations in quantities of phosphorylated forms of GAP-43 might result from a pathological biochemical processes.  Revealing molecular defects generates potential targets for the development of possibly more effective drugs to combat dementia.



Page last modified August 16, 2021