A recent study from Kindai University has revealed that the common amino acid arginine can significantly reduce damage associated with Alzheimer’s disease (AD). Published on November 21, 2025, in the journal Neurochemistry International, the research indicates that arginine may block harmful amyloid β (Aβ) aggregation, a key factor in the progression of Alzheimer’s.
Alzheimer’s disease is a progressive neurodegenerative disorder that leads to the deterioration of nerve cells, resulting in memory loss and cognitive decline. Current treatment options, while available, often provide modest benefits and can be costly. The emergence of antibody-based drugs targeting Aβ has been met with limited success and potential side effects, highlighting the urgent need for safer and more affordable alternatives.
Researchers at Kindai University, including Graduate Student Kanako Fujii and Professor Yoshitaka Nagai, conducted experiments using animal models to examine the effects of oral arginine. Their findings demonstrated that the amino acid not only reduced plaque levels but also alleviated inflammation and improved behavioral outcomes in both flies and mice.
Research Findings and Implications
Initial laboratory tests showed that arginine effectively slows the formation of Aβ42 aggregates in a concentration-dependent manner. In both the fly and mouse models of AD, treatment with arginine resulted in a notable decrease in Aβ accumulation and its associated toxic 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 already known to be clinically safe and inexpensive.”
In the mouse model specifically, oral administration of arginine led to reduced amyloid plaque formation and lower levels of insoluble Aβ42 in the brain. Additionally, mice treated with arginine exhibited improved performance in behavioral assessments and showed a decrease in the expression of pro-inflammatory cytokine genes, which are linked to neuroinflammation—a significant contributor to Alzheimer’s progression.
The researchers suggest that arginine’s benefits may extend beyond simply preventing aggregation. They believe it may also provide broader neuroprotective and anti-inflammatory effects. Professor Nagai remarked, “Our findings open up new possibilities for developing arginine-based strategies for neurodegenerative diseases caused by protein misfolding and aggregation.”
Potential for Drug Repositioning
This research underscores the potential advantages of drug repositioning, which involves repurposing existing compounds for new therapeutic uses. Since arginine is already approved for clinical applications in Japan and shows good permeability in the brain, it may bypass some of the hurdles encountered in traditional drug development processes.
The team emphasized the necessity for further preclinical and clinical studies to confirm that these promising effects will translate to humans, as well as to establish appropriate dosing strategies. Despite these needs, the results provide strong proof of concept that simple nutritional or pharmacological supplementation could help reduce amyloid pathology and improve neurological health.
The implications of this research could have a global impact. As the understanding of Aβ aggregation deepens, the study presents a practical approach that could be implemented on a larger scale. It suggests a cost-effective, readily available strategy that may one day support those affected by Alzheimer’s disease worldwide.
Funding for this research was provided by the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) and several other Japanese scientific organizations, emphasizing the collaborative effort to address this pressing health issue.
