Scientists Discover Simple Supplement That Could Help Slow Alzheimer’s

A new study finds that taking arginine orally may lower amyloid buildup and neuroinflammation, suggesting a safe, low-cost treatment strategy for Alzheimer’s disease.

Alzheimer’s disease (AD) is a progressive condition that gradually damages the brain and is one of the primary causes of dementia around the world. There is still no cure. Although new antibody-based treatments designed to target amyloid β (Aβ) have emerged in recent years, their benefits remain modest.

These medications can also be expensive and may trigger immune-related side effects, which reinforces the need for safer, more affordable options that can reliably slow the advance of AD.

A recent study published in Neurochemistry International reveals that scientists from Kindai University and partner organizations have found that giving arginine by mouth can successfully reduce Aβ buildup and its harmful impacts in animal models of Alzheimer’s disease.

Arginine is a naturally present amino acid that functions as a safe chemical chaperone. The scientists stressed that while arginine can be purchased as an over-the-counter dietary supplement, the specific dosage and delivery method used in their research was tailored for scientific investigation and differs from what is available in commercial products.

The project was conducted by Graduate Student Kanako Fujii and Professor Yoshitaka Nagai from the Department of Neurology, Kindai University Faculty of Medicine, Osaka, along with Associate Professor Toshihide Takeuchi from the Life Science Research Institute, Kindai University, Osaka.

In Vitro Evidence of Aggregation Inhibition

Using in vitro assays, the researchers showed that arginine reduces the formation of Aβ42 aggregates, with stronger inhibition observed at higher concentrations. After confirming this effect in the lab, the team tested orally administered arginine in two well-known AD models:

• A Drosophila model, expressing Aβ42 with the Arctic mutation (E22G)
• An App^NL-G-F knock-in mouse model, carrying three familial AD mutations

In both models, arginine administration significantly reduced Aβ accumulation and alleviated Aβ-induced toxicity.

“Our study demonstrates that arginine can suppress Aβ aggregation both in vitro and in vivo,” explains Prof. Nagai. “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 AD.”

In the mouse model, oral arginine significantly decreased amyloid plaque deposition and lowered insoluble Aβ42 levels in the brain. Moreover, arginine-treated mice showed improved behavioral performance and reduced expression of pro-inflammatory cytokine genes associated with neuroinflammation, one of the key pathological features of AD. These results suggest that arginine’s protective effects extend beyond aggregation inhibition to include broader neuroprotective and anti-inflammatory actions.

Potential for Broader Therapeutic Applications

“Our findings open up new possibilities for developing arginine-based strategies for neurodegenerative diseases caused by protein misfolding and aggregation,” notes Prof. Nagai. “Given its excellent safety profile and low cost, arginine could be rapidly translated to clinical trials for Alzheimer’s and potentially other related disorders.”

This research underscores the potential of drug repositioning—repurposing existing, safe compounds for new therapeutic uses—as an efficient pathway toward accessible Alzheimer’s treatments. Because arginine is already used clinically in Japan and has demonstrated high safety and brain permeability, it may overcome several early barriers faced by conventional drug development.

The researchers note that further preclinical and clinical studies are needed to determine whether these therapeutic effects can be replicated in humans and to establish optimal dosing regimens. Nonetheless, the present findings provide compelling proof of concept that simple nutritional or pharmacological supplementation could mitigate amyloid pathology and improve neurological outcomes.

This study not only deepens our understanding of Aβ aggregation dynamics but also highlights a readily implementable and cost-effective strategy that could ultimately benefit the growing global population affected by AD.

Reference: “Oral administration of arginine suppresses Aβ pathology in animal models of Alzheimer’s disease” by Kanako Fujii, Toshihide Takeuchi, Yuzo Fujino, Noriko Tanaka, Nao Fujino, Akiko Takeda, Eiko N. Minakawa and Yoshitaka Nagai, 30 October 2025, Neurochemistry International.
DOI: 10.1016/j.neuint.2025.106082

This work was supported by the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) (Grant No. 20H05927), Japan Society for the Promotion of Science (JSPS) (Grant Nos. 24H00630, 21H02840, 22H02792, and 25K02432), Japan Science and Technology Agency (JST) Super-Highway Program (SHW2023-03), and National Center of Neurology and Psychiatry.

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