The Impact of Insulin signalling on a C. elegans Alzheimer’s Disease Model
Alzheimer's Disease (AD) represents a significant challenge in aging societies. Researchers found a strong correlation with diabetic patients more likely to develop AD. This study explores the interaction between AD and insulin signalling by employing a transgenic Caenorhabditis elegans model overexpressing human amyloid beta (Aβ) peptides, a hallmark of AD pathology. My findings reveal that C. elegans overexpressing Aβ exhibit phenotypes, including impaired neuronal morphology, decreased mobility, and reduced chemotactic responsiveness compared to wild-type counterparts. Remarkably, decreasing the insulin and insulin-like signalling (IIS) pathway via an insulin receptor daf-2(lf) mutation or expression of antagonistic insulins not only suppressed these adult phenotypes but also alleviated similar impairments observed in the earliest larval stage (L1), such as reduced starvation survival and motility. These results challenge the prevailing notion that AD's impact is predominantly a consequence of aging and instead suggest that early-life interventions in the IIS pathway could offer a strategic countermeasure against t Alzheimer’s Disease progression. My study highlights the potential of the IIS pathway as a therapeutic strategy against AD, opening avenues for research into regulating IIS at various life stages.
C. elegans, Insulin/Insulin-like Growth Factor signalling pathway, Alzheimer's Disease
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