COULD degenerative brain diseases such as Alzheimer鈥檚 be triggered by toxins from cyanobacteria that end up in our food and water? That is the startling question raised by the latest study of a devastating neurodegenerative disease that afflicts the islanders of Guam in the western Pacific.
The latest theory is that the islanders鈥� taste for flying foxes is to blame for the disease, which in some ways resembles Alzheimer鈥檚. The animals鈥� flesh is thought to contain a high concentration of the neurotoxin beta-methylamino-L-alanine (BMAA), found in the fruit of the cycad trees on which they feed. BMAA is made by a cyanobacterium in the trees鈥� roots (New 杏吧原创, 10 January, p 50).
But this theory does not explain everything. Many islanders develop the disease decades after leaving Guam. Yet BMAA is a water-soluble chemical, and the body should soon get rid of it. So how could BMAA cause long-term brain damage?
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Now a team led by Paul Cox, director of the National Tropical Botanic Garden in Hawaii, may have the answer. BMAA is similar in structure to an amino acid, and Cox鈥檚 team has found that it can be incorporated into proteins in place of natural amino acids. What鈥檚 more, levels of BMAA within proteins are typically a hundred times as high as the free form in the flesh of flying foxes and in the brains of people with the disease (Proceedings of the National Academy of Sciences of the USA, DOI: 10.1073/pnas.0404926101).
The Cox team speculate that as these proteins naturally break down over time, BMAA is slowly released, exposing people鈥檚 brains to low levels of the neurotoxin for years. The abnormal proteins containing BMAA could also damage the brain in a variety of ways: by, for instance, binding together to form the microscopic 鈥渢angles鈥� seen in the brains of people with the Guam disease or Alzheimer鈥檚.
The work also raises intriguing questions. For comparison, brain tissue from Canada was tested for BMAA. To the researchers鈥� surprise, they found proteins containing BMAA in the brains of eight people who had died from Alzheimer鈥檚 disease. No BMAA was found in the brains of 13 Canadians who had died from other causes.
So could BMAA be involved in Alzheimer鈥檚? Or is the presence of the protein in Alzheimer鈥檚 patients a sign that they have been exposed to other as-yet-unknown cyanobacterial toxins? Cox says these are open questions for now, but the idea is plausible. Several species of cyanobacteria produce toxins similar to BMAA.