The neurotoxin BMAA is suspected to play a role in a.o. Alzheimer’s disease and Parkinson’s disease. Humans could be infected through contaminated water or food, such as fish and shellfish. However, whether BMAA was really present in aquatic systems, and at what levels, became the subject of a fierce scientific debate. And of the PhD thesis of Els Faassen. She promoted last Friday cum laude. Her promotor was Marten Scheffer. Co-promotor was Miquel Lurling.
In her study Els Faassen found BMAA to reduce survival, somatic growth, reproduction and population growth in Daphnia magna. Animals did not adapt to BMAA exposure: exposed animals born from exposed mothers had a lower brood viability and neonate weight than animals exposed to BMAA, but born from unexposed mothers. In addition, D. magna was shown to take up BMAA from the growth medium and to transfer it to its offspring. D. magna therefore might be an important vector for BMAA transfer along the pelagic food chain, but whether BMAA plays a role in preventing zooplankton from controlling cyanobacterial blooms needs further investigation.
Els Faassen: “Although BMAA research has much progressed between the start of my thesis’ work and its completion, some important questions still require an answer. Most urgently, it should be determined whether BMAA is indeed involved in the neurological diseases mentioned above, and if so, which doses trigger the onset of these diseases. Human exposure pathways should then be more systematically quantified, and it might be prudent to investigate if the occurrence of BMAA is restricted to aquatic systems, or whether sources from terrestrial systems contribute to BMAA exposure as well.”