Aluminum Exposure Boosts Activity of Parkinson’s Genes: Zebrafish Study

Metal found to play role in activating neurodegeneration

Marisa Wexler, MS avatar

by Marisa Wexler, MS |

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aluminum and Parkinson's | Parkinson's News Today | Zebrafish model | illustration of scientist working in lab

Exposure to aluminum increased the activity of several genes related to Parkinson’s disease in zebrafish, a new study shows.

While these data do not necessarily demonstrate a link between aluminum exposure and Parkinson’s development, they shed further light on the neurotoxic properties of aluminum, researchers said.

The study, “Aluminium exposure leads to neurodegeneration and alters the expression of marker genes involved to parkinsonism in zebrafish brain,” was published in Chemosphere.

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Despite being a very common metal in the environment, aluminum does not play a normal role in human metabolism — in fact, heavy aluminum exposure can have toxic effects on body organs. The exact mechanisms of how aluminum affects the body are not well-understood.

In the study, researchers in Italy conducted a series of experiments where they exposed zebrafish — a model organism commonly used to investigate neurological disease — to an aluminum solution for 10, 15, or 20 days. Analyses of the fishes’ brains indicated that aluminum exposure in the brain was highest after 15 days of exposure.

“The aim of this work was to provide new insights into the neurotoxic effects of [aluminum] to understand its role in neurodegeneration,” the researchers wrote.

In fish not exposed to aluminum, brain tissue analyses showed “well-defined structures in all areas of the organ,” the researchers wrote. By contrast, in aluminum-exposed fish, there was “a marked cellular disorganization and a diffuse increase in edema [swelling],” with the most pronounced changes after 10 or 15 days of exposure. These changes “are probably caused by alteration of brains blood vessels” resulting from aluminum exposure.

Aluminum-treated fish also showed signs of brain degeneration, and other analyses suggested that aluminum reduced brain levels of myelin, a fatty covering around nerve cells that helps them send electrical signals. Alterations in the activity of glial cells, a broad class of nervous system cells that don’t send electrical signals, also were noted.

Prior research has suggested that aluminum exposure can promote oxidative stress, a type of cellular damage that has been linked to the development and progression of Parkinson’s. Here, the scientists analyzed gene expression levels — essentially, the extent to which genes are “turned on or off” — for 10 Parkinson’s-related genes in the fishes’ brains.

Results showed that aluminum exposure increased the expression for all 10 genes, though there was some variability in timing and expression changes among the individual genes.

“In the light of the results of the previous study regarding the oxidative state of the brain of [aluminum]-exposed zebrafish, the main marker genes of parkinsonism were evaluated, and it was found that the expression of all the genes considered was altered by [aluminum]-treatment,” the scientists concluded.

The team added that “gene expression data do not provide a complete picture of the link between [aluminum]-exposure and the onset of [Parkinson’s], which needs further investigation; however, they support and confirm the ability of [aluminum] to have a neurotoxic action and a role in activating neurodegeneration.”

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