Internationally recognized UTSA researcher studies complex contributors of Alzheimer’s disease

FEBRUARY 22, 2023 — The development of Alzheimer’s disease is a complex web.

Amyloid plaques are believed to be the critical driver of Alzheimer’s disease. To date, Alzheimer’s research has primarily focused on amyloid development in and around the brain.

The build-up of the protein is consistent with the onset and progression of Alzheimer’s, and many researchers believe the plaque prevent brain cells from properly functioning.

But UTSA researcher George Perry doesn’t buy it.

“Being correlated and being causative are not the same thing,” said Perry, UTSA’s Semmes Foundation Distinguished University Chair in Neurobiology. “Instead, many who study Alzheimer’s have confused causality with association.”

“I think all the disease related proteins we study in neurodegenerative diseases are how you maintain successful aging.”

Aging is a normal process. The body, including the brain, is altered throughout the aging process with billions of neurons adjusting, adapting and evolving. Some changes, Perry explained, may appear abnormal but they are needed to keep the brain healthy. Amyloid is an example.

“It’s a key adjustment protein related to the aging process. Alzheimer’s is the result of this normal process failing,” Perry explained. “Amyloid is a piece of the brain’s response to aging, and I think all the disease related proteins we study in neurodegenerative diseases are how you maintain successful aging.”

Perry’s research focuses on the mechanism and physiological consequences of Alzheimer’s at the cellular level. He and his research collaborators have found that oxidative damage—an imbalance in oxygen reacting with the body’s defenses—is the initial diagnostic tool to examine cells in determining the cause or nature of Alzheimer’s disease.

The team is working to determine the sequence of events leading to the neuronal oxidative damage and the source of the increased oxygen radicals that scientists observe during cognitive decline.

“Biology doesn’t have good or bad things. It depends on the context. Free radicals and amyloid aren’t either bad or good. Everyone develops amyloid and oxidative stress in their late 30s, whether or not they will develop Alzheimer’s. Surprisingly amyloid reduces oxidative stress by blocking free radical formation. Based on the antioxidant activity of amyloid, we predicted over 20 years ago that amyloid removal would not benefit patients,” Perry said.

Alzheimer’s has no cure. However, prevention and lifestyle modification can greatly reduce risk, Perry noted. The multidisciplinary studies of UTSA’s Brain Health Consortium are essential to benefiting patients and families living with Alzheimer’s disease.

“How many chronic age-related diseases are cured? Few if any. Arthritis? Heart disease? The best medicine can do is to slow them down,” Perry said.

— Ari Castañeda