Original story: UT Health San Antonio Newsroom
By Claire Kowalick
SAN ANTONIO (April 21, 2026)
Alzheimer’s is a highly heritable disease with about 60% of the risk coming from a person’s genes. The other 40% of the risk remains less well-studied and may, in part, come from environmental stressors.
The University of Texas at San Antonio was recently awarded a highly competitive Alzheimer’s Association research grant to investigate the gene-environment interaction and how it may contribute to an increased risk for Alzheimer’s disease. The grant will begin in April and provides $200,000 to fund the study over the next three years.
“We are trying to incorporate as many genetic variants and environmental stressors as we can to have a robust model that mimics late-onset Alzheimer’s disease, as opposed to other preclinical work that shows early onset, highly aggressive, non-physiological models,” said principal investigator Juan Pablo Palavicini, PhD, assistant professor in the Department of Cellular and Integrative Physiology in the Joe R. and Teresa Long School of Medicine. He is also a researcher with the Sam and Ann Barshop Institute for Longevity and Aging Studies.
Circadian disruption as an environmental stressor
Palavicini is teaming with Kevin B. Koronowski, PhD, assistant professor in the Department of Biochemistry and Structural Biology in the Long School of Medicine and researcher with the Barshop Institute, to primarily study the effects of circadian rhythm disruption as an environmental stressor and its effects on human phosphorylated-tau proteins.
The aggregation of tau proteins and amyloid plaques are well-known hallmarks of Alzheimer’s disease and other dementias.
“In modern society, it’s difficult to reduce environmental stressors like disrupted sleep schedules and diet. That is the whole point of our study. We don’t yet know all the potential consequences of this disruption,” Koronowski said.
Story continues:
UT San Antonio team studies circadian disruption’s role in Alzheimer’s disease