Old Drug, New Hope: Arginine Reduces Alzheimer’s Plaques and Restores Cognition in Mice

A research team in Japan reports that oral administration of the amino acid arginine significantly reduced amyloid‑beta plaque burden and improved behavior and cognition in mice with Alzheimer’s‑like pathology. The findings, presented in the journal Neurochemistry International, raise the possibility that an already‑available, inexpensive compound could be repurposed for further study in Alzheimer’s disease.

“Our study demonstrates that arginine can suppress amyloid‑beta aggregation both in vitro and in vivo,” said Yoshitaka Nagai, a neuroscientist at Kindai University and a coauthor of the paper. “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 disease.”

What the study did

The researchers gave mice with established amyloid‑beta deposits modest doses of arginine mixed into drinking water and food. They documented reduced plaque accumulation and signs that existing aggregates were dispersed. The investigators also measured functional outcomes: mice treated with arginine performed better in standard behavioral assays that probe exploration, anxiety and spatial memory, including maze tests that assess avoidance of exposed spaces and spontaneous navigation.

Why this matters—and the limitations

Amyloid‑beta proteins are widely implicated in Alzheimer’s disease because they can clump into sticky plaques, a common pathological hallmark. However, their precise role in causing dementia remains unresolved, and not all patients show prominent plaque pathology. While the mouse results are encouraging, animal studies often fail to predict human outcomes for complex brain diseases.

The authors and outside experts emphasize that human clinical trials are required to determine whether arginine’s plaque‑reducing and behavioral effects translate to patients. Arginine’s established safety profile and low cost make it an attractive candidate for rapid clinical evaluation, but safety and efficacy in older adults with Alzheimer’s must be demonstrated.

Related preclinical approaches

This work joins other laboratory efforts to clear plaques and restore cognition: for example, investigators have reported rapid plaque removal and cognitive gains in mice using nanoparticles injected into the brain, while other teams have tested synthetic peptides that reverse early disease signs. Still, the field continues to debate whether targeting amyloid‑beta alone will yield meaningful therapies for the diverse clinical presentations of Alzheimer’s disease.

Bottom line: In mice, oral arginine reduced amyloid‑beta aggregates and improved behavioral measures. The result is promising but preliminary—carefully designed human trials are needed before any clinical claims can be made.