Updated: ALS, Alzheimer's and climate change, who knows? who knew?

Alzheimer's and ALS brains contain BMAA toxin.
The BMAA toxin is among a class of chemicals that bind to glutamate receptors.
There are many of those,  and some are are essential to cell function while others are toxic.
BMAA is a "mixed glutamate receptor agonist."
In nature, BMAA toxin is made by cyanobacteria.
Cyanobacteria are part of the food chains for fish and mollusks.
Cyanobacteria multiply in warm water.
The warm water could be the warming ocean, or in the intestines of an individual.

That's the basic version.

Actually, it's more complicated, and more interesting. In recent reports on the brain chemistry, it turns out there is another chemotoxin, methylazoxymethanol (MAM) or cycasin, also implicated in some neurodegenerative disease. Research on MAM reveals a pattern that could explicate more about Alzheimer's, ALS,  Parkinson's, and also several cancers.   

I continue to eat wild-caught fish from very cold water, such as Canadian herring, Icelandic cod, Alaskan salmon.
These fish tissues seem unlikely to have high BMAA loads, but I don't actually know that for sure, do I?

I don't have a family history of Alzheimer's, so following Pablo et al's premise,  the presence of the toxin in my diet might not by itself trigger the onset of disease.

Note the frequent updates are due to continuing exploration of recent literature on the subject. Of note is Brenner's proposition that the toxin-producing bacteria can be among the micro-flora of an individual's intestines. That is neither fish-diet nor a genetic component.  If correct, that opens up research into what could change gut flora composition in the high-risk parts of our population.

Meanwhile the burst of recently published research includes some of the 'how' on a biochemical level -  BMAA acts as a glutamate agonist, interfering with neural firing.

Some cites with links:
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Acta Neurol Scand. 2009 Oct;120(4):216-25. Epub 2009 Feb 26.
Cyanobacterial neurotoxin BMAA in ALS and Alzheimer's disease.

Pablo J, Banack SA, Cox PA, Johnson TE, Papapetropoulos S, Bradley WG, Buck A, Mash DC.
CONCLUSIONS:

The occurrence of BMAA in North American ALS and AD patients suggests the possibility of a gene/environment interaction, with BMAA triggering neurodegeneration in vulnerable individuals.

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Are Toxins in Seafood Causing ALS, Alzheimer's, and Parkinson's?

"Constituting the foundation of the aquatic food chain, cyanobacteria are a favorite meal of fish and mollusks, which are in turn eaten by us."

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Foods That May Help Prevent Alzheimer's Disease

First, they found that foods rich in vitamin E were associated with a reduced risk of developing Alzheimer's disease. Those foods include oil-based salad dressings, fortified cereals, green leafy vegetables, cantaloupe, seeds and nuts.

They also found that people who eat fish at least once a week were 60 percent less likely to develop Alzheimer's disease than those who rarely or never ate fish. The key ingredient, the Rush team believes, is the n-3 polyunsaturated fatty acids in fish.

From these data, the team made an association between high intakes of saturated and trans-unsaturated fats and Alzheimer's disease. That means it's better to limit fatty meats, full-fat dairy products like butter and milk and vegetable shortening, which is often found in crackers and cookies.

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Med Hypotheses. 2012 Nov 9. pii: S0306-9877(12)00461-6. doi: 10.1016/j.mehy.2012.10.010. [Epub ahead of print]

Blue-green algae or cyanobacteria in the intestinal micro-flora may produce neurotoxins such as Beta-N-Methylamino-l-Alanine (BMAA) which may be related to development of amyotrophic lateral sclerosis, Alzheimer's disease and Parkinson-Dementia-Complex in humans and Equine Motor Neuron Disease in Horses.

Brenner SR.

Source

Dept. of Neurology and Psychiatry, Saint Louis University School of Medicine, Montelone Hall, 1438 South Grand Blvd., St. Louis, MO 63104, USA. Electronic address: SBren20979@aol.com.


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Comp Biochem Physiol C Toxicol Pharmacol. 2012 Nov;156(3-4):171-7. doi: 10.1016/j.cbpc.2012.07.004. Epub 2012 Jul 25.

The physiological effect of ingested β-N-methylamino-L-alanine on a glutamatergic synapse in an in vivo preparation.

Goto JJ, Koenig JH, Ikeda K.

Source

Department of Chemistry, California State University, Fresno, 2555 East San Ramon Ave., MS SB 70, Fresno, CA 93740, USA. jgoto@csufresno.edu

Abstract

The neurotoxin, BMAA (β-N-methylamino-L-alanine), may be a risk factor for amyotrophic lateral sclerosis (ALS), Parkinson's (PD) and Alzheimer's (AD) disease. In vivo experiments have demonstrated that BMAA can cause a number of motor dysfunctions if ingested or injected, and in vitro experiments show that this toxin binds to glutamate receptors with deleterious results. Also, BMAA exists in the human food chain worldwide, and has been detected in the brains of ALS and AD patients. This paper offers the first demonstration by intracellular recording of the effect of ingested BMAA on the postsynaptic response of an identified glutamatergic cell in a living, undissected organism (Drosophila melanogaster), and correlates these observations with the specific motor dysfunctions that result from ingestion. The results suggest that BMAA acts as a glutamate agonist, causing NMDA receptor channels to remain open for prolonged periods of time, thereby damaging the cell by excitotoxicity. The effect on the postsynaptic response became apparent days before the function of the postsynaptic cell (wing beat) became affected. Severely depolarized cells were able to fully recover with the removal of BMAA from the food source, suggesting that blocking BMAA binding in the brain might be a good treatment strategy.
Copyright © 2012 Elsevier Inc. All rights reserved.

PMID:

22841708

[PubMed - in process]

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Joan Savage 2012 Updated December 11