Paul A St. John


Cell Biology, University of Arizona

Associate Professor of Cell Biology & Anatomy

Dr. St. John has had a long-term research interest in the cell biology and developmental regulation of neurotransmitter receptors, with a particular focus on nicotinic acetylcholine receptors in both neurons and muscle. Chance findings have led Dr. St. John in recent years to shift his primary focus to the molecular and cellular events involved in the pathogenesis of Alzheimer’s disease (AD). A variety of studies in the past 10-15 years has strongly implicated the naturally occurring amyloid- ß (A ß ) peptide as causing or contributing to AD. How A ß might cause AD is not clear, however, and that is the focus of Dr. St. John’s research. Understanding the role of A ß in AD is complicated by the fact that A ß spontaneously aggregates to generate different physical forms, called “assembly forms.” Dr. St. John’s laboratory examines the interaction and effects of the different assembly forms of A ß with cultured hippocampal neurons and glial cells. Their work has revealed striking differences between A ß assembly forms in their binding to neurons, which may be a first step in the pathogenesis of the disease, and further differences in the subcellular location of A ß binding sites and the ability to trigger apoptosis. Current experiments in the laboratory are designed to identify the binding partner(s) for A ß on CNS neurons, with the goal of discovering treatments or agents that interfere with such binding and could be considered candidates for the development of disease therapies.

Phone: (520) 626-2553