A recent study has revealed that troriluzole may prevent early-stage brain changes in a mouse model of Alzheimer’s disease.
The research found that troriluzole lowers harmful glutamate levels, helping to preserve memory and cognitive abilities.
This discovery suggests that early intervention with troriluzole could slow or even stop the progression of Alzheimer’s, offering fresh hope for future treatments.
However, additional studies are required to assess its effectiveness across various stages of the disease.
In a recent advancement in Alzheimer’s research, scientists at Auburn University have investigated troriluzole, a drug that may prevent the brain changes that lead to memory loss and cognitive decline in an animal model of the disease.
Published in the Journal of Neurochemistry, this study is the first to show how troriluzole can target early-stage brain alterations linked to Alzheimer’s, providing hope for potential treatment options.
Dr. Miranda Reed, a professor in Auburn University’s Department of Drug Discovery and Delivery, and the study’s lead researcher, commented, “By exploring how drug interventions can act early in the disease process, we aim to develop therapies that might prevent or even cure Alzheimer’s.”
“This study also underscores how scientific progress can change our understanding of complex diseases like Alzheimer’s,” added Dr. Michael Gramlich, an assistant professor of biophysics and a co-researcher of the study.
Alzheimer’s disease affects millions globally, causing a gradual decline in memory, confusion, and eventually, the inability to complete basic tasks.
Despite extensive research, a cure remains elusive. The disease is marked by the buildup of amyloid plaques and tau tangles in the brain, which hinder neuron communication.
In the early stages, excessive glutamate—a neurotransmitter—triggers damaging overactivity at synapses, the connections between neurons.
In their research, Auburn University scientists Dr. Reed and Dr. Gramlich examined how troriluzole, a novel drug, helps maintain normal brain function in genetically modified mice designed to model early Alzheimer’s.
Their findings are notable: troriluzole not only lowered harmful glutamate levels but also enhanced memory and learning in these mice, suggesting that healthy brain function was preserved.
“Our study shows that targeting synaptic activity early in the disease could prevent or slow Alzheimer’s progression, potentially changing the treatment landscape,” the researchers stated.
In the Auburn study, mice treated with troriluzole exhibited a significant drop in synaptic glutamate levels, along with a reduction in brain hyperactivity.
These molecular changes translated into real-world benefits: the treated mice outperformed their untreated counterparts in memory tests, such as navigating mazes, suggesting that their cognitive functions were restored.
“These results are promising because they show that troriluzole can safeguard the brain at a fundamental level, starting with molecular shifts that lead to better cognitive abilities,” explained Dr. Reed. “It’s similar to fixing an engine before it completely breaks down.”
The research was a collaborative effort involving Auburn University’s College of Science and Mathematics, the Harrison College of Pharmacy, the Center for Neuroscience Initiative, and contributions from private researchers and students. This team’s combined expertise in neuroscience and pharmacology was critical to the study’s success.
“This collaboration merges basic science with pharmaceutical research to address one of the most challenging neurological disorders of our time,” Dr. Gramlich highlighted.
“Our work not only advances scientific knowledge of Alzheimer’s but also provides a potential new treatment that could improve the lives of millions globally.”
Although the results in mice are encouraging, the researchers stress the importance of further studies to understand how troriluzole functions at different stages of Alzheimer’s progression.
