The addition of dietary L-serine, a naturally occurring amino acid necessary for formation of proteins and nerve cells, delayed signs of amyotrophic lateral sclerosis (ALS) in an animal study.

The research also represents a significant advance in animal modeling of ALS, a debilitating neurodegenerative disease, said David A. Davis, Ph.D., lead author and research assistant professor of neurology and associate director of the Brain Endowment Bank at the University of Miami Miller School of Medicine.

The new research protocol using vervets appears more analogous to how ALS develops in humans, Dr. Davis said, compared to historic models using rodents. When he and colleagues gave the vervets a toxin produced by blue-green algae known as ?-N-methylamino-L-alanine or BMAA, they developed pathology that closely resembles how ALS affects the spinal cords in humans.

When a group of these animals were fed L-serine together with BMAA for 140 days, the strategy was protective — the vervets showed significantly reduced signs of protein inclusions in spinal cord neurons and a decrease in pro-inflammatory microglia. The results were published on Thursday, February 20 at 5 a.m. EST in the Journal of Neuropathology & Experimental Neurology.

«The big message is that dietary exposure to this cyanobacterial toxin triggers ALS-type pathology, and if you include L-serine in the diet, it could slow the progression of these pathological changes,» Dr. Davis said.

«I was surprised at how close the model mirrored ALS in humans,» he added. Beyond looking at changes in the brain, «When we looked at the spinal cord, that was really surprising.» The investigators observed changes specific to ALS seen in patients, including presence of intracellular occlusion such as TDP-43 and other protein aggregates.

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