Recent research from Kindai University reveals that the widely available amino acid arginine shows potential in reducing damage associated with Alzheimer’s disease (AD). In animal models, the supplement appears to inhibit the aggregation of harmful amyloid beta (Aβ), a protein linked to the progression of the disease. The study suggests that arginine could pave the way for more accessible therapeutic options for those affected by AD.
Alzheimer’s disease is a progressive disorder that leads to the degeneration of nerve cells, and it is a leading cause of dementia globally. Current treatment options, including antibody-based drugs targeting Aβ, have shown limited effectiveness and can be costly. This underscores the urgent need for safer and more affordable alternatives.
A study published on November 21, 2025, in the journal Neurochemistry International, highlights how oral arginine functions as a “safe chemical chaperone.” The research team, led by Graduate Student Kanako Fujii and Professor Yoshitaka Nagai from the Department of Neurology at Kindai University, along with Associate Professor Toshihide Takeuchi, found that arginine significantly reduced Aβ aggregation in both fruit flies and mice.
Initial laboratory experiments demonstrated that arginine inhibits the formation of Aβ42 aggregates in a concentration-dependent manner. Subsequent trials in established AD models showed a marked decrease in Aβ accumulation and its associated neurotoxic effects. Professor Nagai stated, “Our study demonstrates that arginine can suppress Aβ aggregation both in vitro and in vivo. What makes this finding exciting is that arginine is clinically safe and inexpensive, making it a highly promising candidate for repositioning as a therapeutic option for AD.”
In tests involving mice, arginine not only reduced amyloid plaque formation but also lowered insoluble Aβ42 levels in the brain. Behavioral assessments indicated improved performance in treated mice, alongside a decrease in pro-inflammatory cytokine gene expression, which is closely linked to neuroinflammation and AD progression. These findings suggest that arginine’s benefits extend beyond simply preventing aggregation; they also encompass broader neuroprotective and anti-inflammatory effects.
The study emphasizes the potential of drug repositioning—utilizing existing compounds for new therapeutic purposes. Because arginine is already approved for clinical use in Japan and exhibits good brain permeability, it may overcome common early hurdles seen in traditional drug development. The research team acknowledged that further preclinical and clinical studies are crucial to confirm if these promising effects will translate to human patients and to establish appropriate dosing strategies.
This research opens new avenues for addressing Alzheimer’s disease, highlighting a cost-effective approach that could be implemented globally. The findings offer hope for developing therapies that can significantly impact the lives of individuals affected by AD.
The study received support from various organizations, including the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) and the Japan Society for the Promotion of Science (JSPS). As the scientific community continues to explore innovative solutions to combat neurodegenerative diseases, arginine’s role may soon be pivotal in transforming the landscape of Alzheimer’s treatment.
