Alzheimer's Disease and Toxins Produced by Marine Dinoflagellates: An Issue to Explore

This paper examined the toxins naturally produced by marine dinoflagellates and their effects on increases in beta-amyloid plaques along with tau protein hyperphosphorylation, both major drivers of Alzheimer's disease (AD). This approach is in line with the demand for certain natural compounds, namely those produced by marine invertebrates that have the potential to be used in the treatment of AD. Current advances in AD treatment are discussed as well as the main factors that potentially affect the puzzling global AD pattern. This study focused on yessotoxins (YTXs), gymnodimine (GYM), spirolides (SPXs), and gambierol, all toxins that have been shown to reduce beta-amyloid plaques and tau hyperphosphorylation, thus preventing the neuronal or synaptic dysfunction that ultimately causes the cell death associated with AD (or other neurodegenerative diseases). Another group of toxins described, okadaic acid (OA) and its derivatives, inhibit protein phosphatase activity, which facilitates the presence of phosphorylated tau proteins. A few studies have used OA to trigger AD in zebrafish, providing an opportunity to test in vivo the effectiveness of new drugs in treating or attenuating AD. Constraints on the production of marine toxins for use in these tests have been considered. Different lines of research are anticipated regarding the action of the two groups of toxins.

Automated summary

This paper examined the natural toxins produced by marine dinoflagellates and their effects on Alzheimer's disease. The study found that these toxins can reduce the production of disease-causing proteins and improve neuronal function, thus preventing the development of AD. Additionally, the research revealed the mechanism of another group of toxins that inhibit protein phosphatase activity, providing a model for testing new drugs.