What is it about?

The majority of Alzheimer's cases are characterized as late-onset in which the greatest risk factors for the disease are environmental (e.g., aging and lifestyle choices) in addition to the inheritance of apolipoprotein E4 (APOE4). A carrier of the APOE4 allele increases the risk of developing AD by four- to twelve-fold. However, the mechanisms of how ApoE4 contributes to increased risk of disease have remained elusive. In this study, we tested whether APOE4 could lead to toxicity or other potential negative consequences in an in vivo model consisting of zebrafish.

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Why is it important?

Our results demonstrate that treatment of zebrafish embryos with APOE4 led to an increase in toxicity and other morphological abnormalities. In addition, there was a decrease in motor function as well as enhanced Alzheimer's-like pathology. Taken together, these results support the hypothesis that a key step in the mechanism of action is a toxic gain of function by APOE4. Therefore, the neutralization of this protein may serve as an important therapeutic strategy in the treatment of AD.


My aim in writing this article was to try to engage readers and make them interested in the topic of Alzheimer's disease, by presenting it as something that is not only relevant but also potentially exciting and thought-provoking. Concerning the normal role of the APOE4 protein, our article contains examples or insights that challenge conventional wisdom and offer a fresh perspective on an important genetic risk factor for Alzheimer's disease.

Troy Rohn

Read the Original

This page is a summary of: An amino-terminal fragment of apolipoprotein E4 leads to behavioral deficits, increased PHF-1 immunoreactivity, and mortality in zebrafish, PLoS ONE, December 2022, PLOS, DOI: 10.1371/journal.pone.0271707.
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