 A study performed in 2015 with vervets ("Chlorocebus sabaeus") in St. Kitts, which are homozygous for the apoE4 gene (a condition which in humans is a risk factor for Alzheimer's disease), found that vervets that were administered BMAA orally, developed hallmark histopathology features of Alzheimer's Disease including amyloid beta plaques and neurofibrillary tangle accumulation.Vervets in the trial fed smaller doses of BMAA were found to have correlative decreases in these pathology features.Additionally, vervets that were co-administered BMAA with serine were found to have 70% less beta-amyloid plaques and neurofibrillary tangles than those administered BMAA alone, suggesting that serine may be protective against the neurotoxic effects of BMAA.