AI Article Synopsis
- - Alzheimer's disease (AD) is a progressive neurological disorder and the leading cause of dementia, with apolipoprotein E (APOE) identified as the strongest genetic risk factor for its late onset.
- - ApoE influences AD development by affecting the deposition of amyloid-β (Aβ) and also plays a significant role in regulating the innate immune response, particularly through the activation of microglia and astrocytes.
- - This review highlights recent findings regarding ApoE's impact on AD pathogenesis and the immune response, while also identifying areas where further research is needed.
Article Abstract
Alzheimer's disease (AD) is a progressive neurological disorder and the most common cause of dementia. Genetic analyses identified apolipoprotein E (APOE) as the strongest genetic risk for late-onset AD. Studies have shown that ApoE modulates AD pathogenesis in part by influencing amyloid-β (Aβ) deposition. However, ApoE also appears to regulate elements of AD via regulation of innate immune response, especially through microglial and astrocyte activation. In model systems, it also regulates changes in T-cells. This review focuses on the key findings that have advanced our understanding of the role of ApoE in the pathogenesis of AD and the current view of innate immune response regulated by ApoE in AD, while discussing open questions and areas for future research.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11578782 | PMC |
| http://dx.doi.org/10.1111/imr.13414 | DOI Listing |
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