Researchers show new drug rescues memory loss in mouse model of Alzheimer’s

In a recent breakthrough in Alzheimer’s disease research, scientists at Auburn University have studied a new drug, troriluzole, that can prevent brain changes that lead to memory loss and cognitive decline in a mouse model of the disease. The study, published in the Journal of Neurochemistryis the first to show how troriluzole can target early-stage alterations associated with Alzheimer’s disease, offering new hope for potential treatments.

Dr. Miranda Reed, a professor in the department of drug discovery and delivery at Auburn University and principal investigator of the study, noted that “by examining how drug treatments can intervene early in the disease process, we aim to develop therapies that could prevent or even cure Alzheimer’s disease.”

“This study also highlights how scientific advances can transform our understanding of complex diseases like Alzheimer’s,” said Dr. Michael Gramlich, assistant professor of biophysics and another principal investigator on the study.

A new path in Alzheimer’s disease research

Alzheimer’s disease affects millions of people worldwide, causing progressive memory loss, confusion, and eventually an inability to perform basic tasks. Despite decades of research, no cure has yet been found. Alzheimer’s disease is characterized by the accumulation of amyloid plaques and tau protein tangles in the brain, which disrupt neuronal communication.

In the early stages, excessive levels of the neurotransmitter glutamate cause damaging overactivity in synapses, the connections between nerve cells.

The study, led by Auburn University researchers Dr. Miranda Reed and Dr. Michael Gramlich, examined how the new drug troriluzole can maintain normal brain function in mice genetically engineered to mimic the early stages of Alzheimer’s disease.

The results were compelling: Troriluzole not only reduced harmful glutamate levels, but also improved memory and learning in mice, suggesting maintenance of healthy brain function.

“Our research demonstrates that by targeting synaptic activity early, we could prevent or slow the progression of Alzheimer’s disease. This could revolutionize the way we approach the treatment of this disease,” the two researchers noted.

How does troriluzole work?

In the Auburn study, mice treated with troriluzole showed significantly reduced synaptic glutamate levels and decreased brain hyperactivity. These molecular changes led to tangible improvements: the treated mice performed better on memory tests, such as navigating mazes, indicating that their cognitive functions had been restored.

“These results are promising because they suggest that troriluzole can protect the brain at a fundamental level, starting with molecular changes and improving cognitive abilities,” Dr. Reed said. “It’s like fixing an engine before it completely breaks down.”

This research is a collaboration between Auburn University’s College of Science and Mathematics, Harrison College of Pharmacy and the Center for Neuroscience Initiative, as well as private researchers and students. The team’s combined expertise in neuroscience and pharmacology was essential to the success of the study.

“This collaboration combines basic science and pharmaceutical research to address one of the most complex neurological problems of our time,” said Dr. Gramlich. “Our work not only advances the scientific understanding of Alzheimer’s disease, but also offers a potential new treatment that could improve the lives of millions of people around the world.”

Although the results in mice are encouraging, the researchers stress the need for further studies to determine how troriluzole works at different stages of disease progression.