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.
Photo by Astrid Schaffner on Unsplash
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.
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.
You can read the full text:
The following have contributed to this page