Cognitive Labs

You might recall this story about the possible link between Alzheimer's Disease, ALS (or Lou Gehrig's Disease), Parkinson's Disease and 2.8 billion year old cyanobacteria or blue-green algae.

The connection seems to pivot around BMAA, a powerful neurotoxin that can impact the central nervous system (CNS) and contribute to the onset of these diseases.

A related group of researchers is coming to the perspective that a protein reservoir exists within your body, first absorbing BMAA and then slowly releasing it over years and even decades, causing chronic damage to the motor neuron system.

Scientists suggest that exposure to low levels of BMAA may be mediated by most people through metabolism or excretion. However, research also suggests that a few individuals accumulate, rather than excrete BMAA, and these individuals may be at great risk for developing ALS.

The best epidemiological data indicate that a gene/environment interaction probably lies at the roots of ALS/PDC in Guam and possibly sporadic ALS elsewhere. Some experts suspect that BMAA combined with certain metal ions can cause damage to the motor neuron system in vulnerable individuals.

A recent (2008) article profiles the bloom of cyanobacteria in lakes and ponds of upstate NY and Canada, which appears to cause die-offs of fish and fowl. One theory is that run-off of unnatural phosphorous-containing fertilizers is polluting soil, waters, and other aspects of the ecosystem and causing neurological damage. While a very extended hypothesis, the increase in these kinds of diseases since the Industrial Revolution and the rise of the chemical industry (began in Germany in the latter 19th century) suggests a possible link. Alois Alzheimer did not identify the Disease bearing his name until 1907, ALS was identified in 1861 and known as Charcot's Disease in Europe, and Parkinson's in 1817. Parkinson's is sometimes linked with neurotoxins derived from pesticides, again, another product of the chemical industry.

To complicate matters in the cyanobacteria question, other scientists have isolated a compound called nostocarboline by processing cyanobacteria intensively. This substance in early animal trials appears to function as a cholinesterase inhibitor, breaking down accumulation of cholinesterase and helping the build-up of acetylcholine, which is essential for the brain's instant messaging (IM) capability. So, on the one hand, cyanobacteria is toxic to the organism, on the other, its processed byproduct may be beneficial if delivered to a discrete target. In each of these cases, compounds can interact with genes as the frame of the organism, leading either to increased or decreased risk based on observed configuration.

Labels: ALS, alzheimers, CNS, cyanobacteria, parkinsons

// posted by neurofuture12:56 AM permanent link