The scientists conducted the vervet study at the Behavioural Science Foundation, a specialized research facility on the Caribbean island of St. Kitts. After being exposed to a cyanobacterial neurotoxin called BMAA, the vervets developed aggregations of misfolded proteins similar to those seen in human ALS patients, and activated microglia, a type of immune cells, in their spinal cord and brain, similar to those that occur in the early stages of ALS. In contrast, vervets that also received the amino acid L-serine had significantly reduced ALS pathology.
Dr. David Davis at the Department of Neurology, University of Miami Miller School of Medicine who served as first author on the paper, said that the differences were profound. "Without L-serine co-administration, the BMAA-exposed vervets developed motor neuron degeneration, pro-inflammatory microglia and dense inclusions of TDP-43 and other misfolded proteins known to be associated with ALS," Dr. Davis explained. "In animals dosed with L-serine, the progression of these ALS-like changes was considerably reduced."
ALS is a devastating disease that hits people in the prime of life, causing increasing paralysis and often results in death within two to three years after diagnosis. At present, only two drugs are available that slow the disease modestly. This study offers the possibility that L-serine may slow the progression of the disease even more.
Potential Implications for L-Serine as a Treatment
Neurobiologist Dr. Deborah Mash of Nova Southeastern University, who was also an author on the study, said that the results "holds promise for identifying a cause of sporadic ALS, which accounts for 90 percent of all ALS cases."