Dietary exposure to an environmental toxin triggers neurofibrillary tangles and amyloid deposits in the brain

Paul Alan Cox, David A. Davis, Deborah C Mash, James S. Metcalf, Sandra Anne Banack

Research output: Contribution to journalArticle

109 Scopus citations

Abstract

Neurofibrillary tangles (NFT) and β-amyloid plaques are the neurological hallmarks of both Alzheimer’s disease and an unusual paralytic illness suffered by Chamorro villagers on the Pacific island of Guam. Many Chamorros with the disease suffer dementia, and in some villages one-quarter of the adults perished from the disease. Like Alzheimer’s, the causal factors of Guamanian amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC) are poorly understood. In replicated experiments, we found that chronic dietary exposure to a cyanobacterial toxin present in the traditional Chamorro diet, β-N-methylamino-L-alanine (BMAA), triggers the formation of both NFT and β-amyloid deposits similar in structure and density to those found in brain tissues of Chamorros who died with ALS/PDC. Vervets (Chlorocebus sabaeus) fed for 140 days with BMAA-dosed fruit developed NFT and sparse β-amyloid deposits in the brain. Co-administration of the dietary amino acid L-serinewith L-BMAA significantly reduced the density of NFT. These findings indicate that while chronic exposure to the environmental toxin BMAAcan trigger neurodegeneration in vulnerable individuals, increasing the amount of L-serine in the diet can reduce the risk.

Original languageEnglish (US)
Article number20152397
JournalProceedings of the Royal Society B: Biological Sciences
Volume283
Issue number1823
DOIs
StatePublished - Jan 20 2016

Keywords

  • Alzheimer’s
  • Amyotrophic lateral sclerosis
  • BMAA
  • Cyanobacteria
  • L-serine
  • Tau

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Environmental Science(all)
  • Immunology and Microbiology(all)
  • Medicine(all)

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