title: Do vervets and macaques respond differently to BMAA?
abstract: Vervets with chronic dietary exposure to BMAA develop neurofibrillary tangles (NFT) and sparse β-amyloid plaque-like deposits in the brain. Macaques dosed via oral gavage with BMAA developed marked neurological signs in the absence of cell death. These differences may result from increased vulnerability of macaques to BMAA, the higher effective dose they received via oral gavage, and the possibility of stable adducts due to the bicarbonate used to neutralize their BMAA dose. Confirmation of chromatolysis and cell death in macaque brains was visualized using toluidine staining. In contrast, immunological staining with AT8 and β-amyloid (1-42) antibodies and thioflavine-S stain in vervet brains suggests early stage labeling of neurites and NFT and plaque-like formation in the absence of neuronal loss. The lack of neurologic deficits reported in vervets is in keeping with early preclinical pathology observed with these immunohistochemical methods. BMAA toxicity in vervet brains causes the early events that occur in the genesis of neurofibrillary pathology. Taken together, these different studies of vervets and macaques demonstrate BMAA toxicity in the brain due to chronic exposures. The use of more sensitive immunohistochemical methods in the vervet study most likely explains the differences in neuropathology reported for vervets and macaques.
authors.affiliation: Brain Chemistry Labs, Institute for Ethnomedicine, Jackson Hole, WY, USA. Electronic address: paul@ethnomedicine.org.
authors.forename: Paul Alan
authors.initials: PA
authors.lastname: Cox
authors.affiliation: Department of Neurology, University of Miami, Miller School of Medicine, Miami, FL, USA.
authors.forename: David A
authors.initials: DA
authors.lastname: Davis
authors.affiliation: Department of Neurology, University of Miami, Miller School of Medicine, Miami, FL, USA.
authors.forename: Deborah C
authors.initials: DC
authors.lastname: Mash
authors.affiliation: Brain Chemistry Labs, Institute for Ethnomedicine, Jackson Hole, WY, USA.
authors.forename: James S
authors.initials: JS
authors.lastname: Metcalf
authors.affiliation: Brain Chemistry Labs, Institute for Ethnomedicine, Jackson Hole, WY, USA.
authors.forename: Sandra Anne
authors.initials: SA
authors.lastname: Banack
mesh_terms: D000544:Alzheimer Disease / Q000139:chemically induced* / Q000473:pathology*; D000599:Amino Acids, Diamino / Q000633:toxicity*; D000818:Animals; D000087522:Cyanobacteria Toxins; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity*; D008252:Macaca fascicularis; D016874:Neurofibrillary Tangles / Q000473:pathology*
chemical_list: D000599:Amino Acids, Diamino; D000087522:Cyanobacteria Toxins; D018690:Excitatory Amino Acid Agonists; C001824:beta-N-methylamino-L-alanine
keywords: BMAA; Beta-amyloid; Hyperphosphorylation; Macaques; Neurofibrillary tangles; Neuropathology; Thioflavin; Vervets