Researchers Examine Data On Well-Known Toxins Suspected Of Causing Neurodegeneration

Researchers Examine Data On Well-Known Toxins Suspected Of Causing Neurodegeneration

Understanding the origins of human neurodegenerative disorders is a global scientific goal that necessitates regular assessments of existing information. In doing so, biologists from the University of Guam’s Plant Physiology Laboratory and neuroscientists from The University of British Columbia’s Experimental Medicine Program provided an update on the alleged environmental toxins suspected of being implicated in animal neurodegeneration.

Researchers Examine Data On Well-Known Toxins Suspected Of Causing Neurodegeneration

Due to an unexpected surge of neurodegenerative cases among the indigenous CHamoru population, the world’s magnifying glass was focused on the island of Guam in the 1950s. The exact illness that momentarily afflicted Guam is known as amyotrophic lateral sclerosis-parkinsonism dementia (ALS-PDC), and it is also known locally as lytico-bodig in CHamoru.

Researchers Examine Data On Well-Known Toxins Suspected Of Causing Neurodegeneration

The attention on this small number of instances led to decades of research into the poisons discovered in the seeds of Guam’s native cycad tree. These seeds were part of the local diet at the time, and greater dependence on this type of food starch during World War II was a probable explanation for the rise in neurodegenerative cases immediately after the war.

Since the 1950s, there has been an ebb and flow of consecutive disappointments, as the discovery of a single causative cycad toxin has remained elusive.

However, these setbacks have been offset by triumphs. It is now known that multiple variables likely combine to form a synchronized perfect storm, resulting in an unprecedented rise of localized neurological cases, such as what occurred momentarily on Guam. Exposure to large concentrations of the environmental toxin by the most sensitive gender with the most susceptible genes at the most vulnerable age, followed by a latency period before the neuronal damage manifests itself, maybe among these co-factors.

The UOG-UBC partnership has lasted more than two decades, and throughout that period, various members of the team have published more than 100 scientific publications on various areas of cycad biology. 14 of these papers dealt with the toxicity of Guam cycad seeds.

When he began working with UOG, he had the advantage of building on decades of study from Guam, according to co-author and UBC neurologist Christopher Shaw. They took advantage of the fact that no plant scientist had been personally engaged in any of the previously published studies to get funding to examine different problems involving cycad seed poisons.

One of the many perplexing elements of this research is the distinction between acute toxins, which produce rapid toxic responses after ingesting cycad seed, and slow-acting toxins, which cause neurodegeneration.

The distinctions between these two types of poisons are frequently misunderstood, and scientists are continually reminding the public that many years must elapse after exposure to a slow plant toxin before harmful health effects occur, according to Benjamin Deloso, a cycad biologist at UOG.

Another advantage of the marathon search for the causative cycad toxin is that a massive amount of literature has emerged that reveals that biomolecules are not involved. This is how science works, according to Shaw. The intense empirical examination of each potential toxin was justified, and the creation of superseding hypotheses that were rigorously tested was refined.

Cassava roots, for example, have sugar-based molecules that liberate cyanide after mammalian consumption, but cycad seeds contain no free cyanide and the discovered sugar-based cycad compounds in cycads are incapable of releasing lethal amounts of cyanide after mammalian ingestion. The careful investigation proved that the allegations of cyanide being a possible cycad toxin and that consuming cycad seed may result in cyanide poisoning were false.

According to the research team, scientists are not immune to making erroneous statements regarding cycads. This is common when scientists rely on grey literature or online encyclopedia-style websites that have not been verified by cycad specialists.

The authors believe that their new article will reduce the dissemination of erroneous information regarding cycad poisoning, as false comments harm the international community’s efforts to enhance cycad conservation.

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