Research from Kindai University has unveiled that the amino acid arginine can significantly mitigate damage caused by Alzheimer’s disease (AD). This discovery, published on November 21, 2025, indicates that arginine can block the aggregation of harmful amyloid β (Aβ) protein and lessen its toxic effects in animal models, paving the way for potentially accessible therapies for this debilitating condition.
Alzheimer’s disease is a progressive neurological disorder that leads to cognitive decline and is a leading cause of dementia globally. Existing treatments primarily focus on managing symptoms, as there is no known cure. Recent antibody-based therapies targeting Aβ have shown limited effectiveness and can be costly, highlighting the urgent need for safer, low-cost alternatives.
The study, detailed in the journal Neurochemistry International, involved researchers, including graduate student Kanako Fujii and Professor Yoshitaka Nagai from the Department of Neurology at Kindai University, along with Associate Professor Toshihide Takeuchi. Their findings suggest that oral arginine acts as a safe chemical chaperone, significantly reducing Aβ aggregation in various models of AD.
Laboratory Findings on Arginine’s Efficacy
Initial laboratory experiments demonstrated that arginine effectively slows the formation of Aβ42 aggregates in a concentration-dependent manner. Subsequent trials using two established animal models of Alzheimer’s revealed that arginine treatment resulted in a marked decrease in Aβ buildup and alleviated the harmful effects associated with Aβ exposure. Professor Nagai emphasized, “Our study demonstrates that arginine can suppress Aβ aggregation both in vitro and in vivo.”
In the mouse model, oral arginine not only reduced amyloid plaque formation but also improved behavioral performance in cognitive assessments. Additionally, the treatment led to a decrease in the expression of pro-inflammatory cytokine genes linked to neuroinflammation, which is a significant factor in the progression of Alzheimer’s disease. These findings suggest that arginine offers broader benefits beyond just Aβ reduction, providing neuroprotective and anti-inflammatory effects.
Potential for Drug Repurposing
This research highlights the advantages of drug repositioning, where existing compounds are used for new therapeutic purposes. Arginine is already approved for clinical use in Japan and demonstrates good brain permeability, which may facilitate its transition to clinical trials. The researchers caution, however, that further preclinical and clinical studies are essential to confirm these benefits in humans and to establish appropriate dosing strategies.
The implications of this research extend beyond academic interest, as the findings present a cost-effective and accessible strategy for addressing Alzheimer’s disease. The study received support from various Japanese organizations, including the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) and the Japan Society for the Promotion of Science (JSPS).
In conclusion, the work from Kindai University not only enhances the understanding of Aβ aggregation mechanisms but also proposes a practical approach that could potentially benefit individuals affected by Alzheimer’s disease globally. The promise of arginine as a simple, safe supplement opens new avenues in the search for effective Alzheimer’s therapies.
