A recent study from researchers at Kindai University reveals that the amino acid arginine may significantly mitigate the damaging effects of Alzheimer’s disease. Published on November 21, 2025, in the journal Neurochemistry International, the research indicates that arginine can block the aggregation of amyloid beta (Aβ), a key factor in the progression of Alzheimer’s.
Alzheimer’s disease is a progressive neurological disorder that leads to the degeneration of nerve cells in the brain, contributing to dementia in millions worldwide. Current treatments are limited, often yielding modest results and carrying risks of side effects. This underscores the pressing need for safer, more cost-effective therapeutic options.
The research team, led by Graduate Student Kanako Fujii and Professor Yoshitaka Nagai, along with Associate Professor Toshihide Takeuchi, conducted experiments using animal models. They discovered that administering oral arginine led to a marked reduction in Aβ plaque levels, inflammation, and associated behavioral issues.
Laboratory Evidence of Arginine’s Efficacy
Initial in vitro tests showed that arginine slowed the formation of Aβ42 aggregates in a concentration-dependent manner. Building on these findings, the researchers evaluated arginine’s effects in two widely recognized Alzheimer’s models: flies and mice. Both models demonstrated a significant decrease in Aβ accumulation and the toxic effects typically associated with Aβ exposure.
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, making it a highly promising candidate for repositioning as a therapeutic option for Alzheimer’s.”
In the mouse model, those treated with arginine showed not only reduced amyloid plaque formation but also improved performance in behavioral assessments. Additionally, the treatment resulted in lower levels of pro-inflammatory cytokine genes, which are linked to neuroinflammation—a critical contributor to Alzheimer’s progression.
Potential for Drug Repurposing
The implications of this research extend beyond simply reducing amyloid buildup. The findings suggest that arginine may offer broader neuroprotective and anti-inflammatory benefits. Professor Nagai elaborated, “Our findings open up new possibilities for developing arginine-based strategies for neurodegenerative diseases caused by protein misfolding and aggregation.”
Arginine, which is already approved for clinical use in Japan and boasts good brain permeability, exemplifies the advantages of drug repositioning. This method involves repurposing established compounds for new therapeutic uses, potentially allowing for quicker pathways to clinical application.
While the study presents compelling evidence, the researchers emphasize that further preclinical and clinical trials are necessary to confirm whether these positive effects can be replicated in humans and to establish appropriate dosing strategies.
The research was funded by the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) and the Japan Society for the Promotion of Science (JSPS), among other organizations.
The findings not only deepen the scientific understanding of Aβ aggregation but also offer a practical, scalable approach to addressing Alzheimer’s disease. With its low cost and accessibility, arginine supplementation could potentially support individuals affected by Alzheimer’s globally, highlighting a significant step forward in the quest for effective treatments.
