"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," said Professor Yoshitaka Nagai from the Department of Neurology at Kindai University Faculty of Medicine, Japan, in a press release.
Amyloid-beta plaques in the brain are a hallmark of Alzheimer's disease. While drugs that target the plaques exist, they have limited efficacy and potentially trigger other immune-related side effects while coming at a high cost. There is an urgent need for new approaches to inhibiting amyloid-beta aggregation that are both safe and cost-effective.
In the current study, researchers investigated the effects of arginine, a naturally occurring amino acid sold as a dietary supplement, on models of Alzheimer's disease. To begin, they tested the amino acid in vitro, ultimately finding that it slows the formation of amyloid-beta aggregates in a concentration-dependent manner.
Following this, the researchers tested the amino acid on two widely used models of Alzheimer's disease: fruit flies and mice. Arginine significantly reduced the buildup of amyloid beta in both models and reduced harmful effects linked to amyloid beta exposure.
In the mouse model in particular, oral arginine reduced amyloid plaque formation and reduced insoluble amyloid-beta levels in the brain. Mice also performed better in behavioral assessments and displayed decreased expression of pro-inflammatory cytokine genes linked to neuroinflammation. The findings suggest that arginine may have broad neuroprotective and anti-inflammatory effects.
"Our findings open up new possibilities for developing arginine-based strategies for neurodegenerative diseases caused by protein misfolding and aggregation. Given its excellent safety profile and low cost, arginine could be rapidly translated to clinical trials for Alzheimer's and potentially other related disorders," said Nagai.
Sources: Science Daily, Neurochemistry International
