"Our study demonstrates that arginine can suppress Aβ aggregation both in vitro and in vivo."
A naturally occurring amino acid has shown promise in reducing the buildup of toxic proteins linked to Alzheimer's disease, according to new research published in Neurochemistry International.
Scientists found that arginine blocked the formation of harmful Aβ42 aggregates in a lab setting in a concentration-dependent manner. When tested in living organisms, oral arginine treatment reduced amyloid buildup and associated damage in both a fruit fly model and a genetically engineered mouse model of Alzheimer's.
In the mouse model, arginine lowered amyloid plaque levels and reduced insoluble Aβ42 in the brain. Mice receiving the treatment also performed better on behavioral tests. Additionally, the amino acid reduced the activity of genes linked to pro-inflammatory cytokines, suggesting it may help calm damaging neuroinflammation.
The study was led by researchers from Kindai University, including Graduate Student Kanako Fujii, Professor Yoshitaka Nagai (Department of Neurology), and Associate Professor Toshihide Takeuchi (Life Science Research Institute). It was supported by MEXT, JSPS, JST, and the National Center of Neurology and Psychiatry.
"Arginine is clinically safe and inexpensive, making it a highly promising candidate for repositioning as a therapeutic option for AD."
Important cautionary notes apply: The doses and methods used in this research were designed for laboratory study and are not equivalent to over-the-counter arginine supplements. The researchers emphasized that additional preclinical and clinical studies are required to determine if the results can be reproduced in humans and to establish effective dosing strategies.
Professor Nagai added: "Our findings open up new possibilities for developing arginine-based strategies for neurodegenerative diseases caused by protein misfolding and aggregation."