Texas A&M researcher receives $2.17 million federal grant to study early brain changes linked to Alzheimer’s disease

Dr. Jianrong Li, a professor and researcher in the Texas A&M University College of Veterinary Medicine and Biomedical Sciences (VMBS), has received a $2.17 million grant from the National Institute on Aging, part of the National Institutes of Health, to examine how support cells in the brain help protect nerve cells and what happens when that protection begins to break down.

Li’s project focuses on early brain changes that may occur long before Alzheimer’s disease is typically diagnosed, offering researchers a new way to understand how the disease begins and progresses.  

“We’re studying the brain’s support system, especially glial cells and myelin, and how their dysfunction may contribute to aging and Alzheimer’s disease,” Li said. “Most of Alzheimer’s disease research focuses on neurons, but neurons rely heavily on the supporting system for energy supply, insulation and immune regulation.”

The brain’s support system

Neurons are often compared to electrical wires because they carry signals throughout the brain, but they cannot function on their own. To work properly, they depend on support cells called glial cells, which help regulate energy use, protect neurons, and keep the brain in balance.

One important type of glial cell is the oligodendrocyte. These cells produce myelin, a fatty coating that surrounds nerve fibers and helps signals move quickly and smoothly through the brain.

“Neurons need metabolic support and energy, as well as insulation — which is provided by myelin,” Li said.  

When myelin is healthy, brain cells communicate effectively. When it becomes damaged, signals can slow down or fail, disrupting communication in the brain. This type of damage is well known in diseases such as multiple sclerosis, but growing evidence suggests that myelin may also be affected early in Alzheimer’s disease.

“If the supporting system weakens, neurons can become dysfunctional,” Li said.

Why BIN1 matters in Alzheimer’s disease

Alzheimer’s disease is often diagnosed after memory loss and other symptoms become noticeable.

“By the time Alzheimer’s disease is diagnosed, it is already late — significant changes have already occurred in the brain,” Li said. “That’s why we’re interested in early disease mechanisms and how the support system changes.”

To study these early changes, Li’s team focused on isolating how BIN1 affects myelin-producing cells at specific stages, allowing scientists to better understand how disruptions in the brain’s support system may influence neurons long before widespread damage develops.

BIN1 — a multifunctional protein that acts as a bridge inside cells, helping transport materials and maintain cell membrane structure — has drawn increasing attention from scientists because of its strong link to late-onset Alzheimer’s disease, the most common form of the condition. Large genetic studies have shown that people with certain changes in the BIN1 gene have a much higher risk of developing Alzheimer’s disease later in life.

What makes BIN1 especially important, Li said, is where it is active in the brain. While many Alzheimer’s-related genes affect neurons directly, BIN1 is highly expressed in oligodendrocytes. This suggests that genetic risk for Alzheimer’s disease may act through the brain’s support system rather than neurons alone.

“BIN1 is highly expressed in the myelin-producing cells, but what it does in those cells has not been explored,” Li said.

Despite BIN1’s strong link to Alzheimer’s disease, scientists still know relatively little about how the gene functions in myelin-producing cells. Li’s study aims to fill that gap by examining how changes in BIN1 affect myelin structure and, in turn, the health of axons — the long extensions of neurons that allow brain cells to communicate.

By studying BIN1 in oligodendrocytes rather than neurons, Li hopes to better understand how early damage to the brain’s insulation system may make neurons more vulnerable over time, setting the stage for later disease progression.

Protecting axons and brain communication

Another major focus of the study is axon integrity, which refers to the health of axons — long extensions of neurons that carry signals from one brain cell to another and allow the brain to communicate and form networks. Because many axons depend on myelin for protection and efficient signal transmission, damage to that system can leave axons weaker and more vulnerable over time.

“When axons degenerate, you lose synapses, which is how neurons communicate with each other,” Li said.

Loss of synapses disrupts communication in the brain and is closely linked to cognitive decline. By examining how BIN1 affects myelin and axons together, Li hopes to better understand how early changes in the brain’s support system may contribute to the breakdown of neural connections seen in Alzheimer’s disease.

Why federal funding is key

The size of the federal grant reflects both the urgency of Alzheimer’s research and the novelty of Li’s approach, which allows her team to examine brain support cells with a level of precision and scale that would not be possible otherwise.

“This work is novel and significant because myelin involvement in Alzheimer’s disease has not been well studied,” Li said.

Support from the National Institute on Aging allows Li’s team to use advanced models and tools to isolate changes in specific cell types over time, helping researchers answer questions that have remained unanswered in Alzheimer’s research. 

While there is still no cure for Alzheimer’s disease, Li hopes this research will help reshape how scientists think about the condition and how future treatments are developed, ultimately providing a clearer picture of how Alzheimer’s disease begins — and how it might one day be slowed or prevented.

“The more we understand early disease mechanisms, the better we can develop strategies for prevention or intervention,” she said.