Heartland The Role of Opioids in Accelerated Aging

Overview

Background: Opioid abuse is associated with cognitive impairments and can even accelerate the process of aging, specifically age -sensitive brain functional networks in patients. Furthermore, morphine administration has been shown to result in synaptodendri tic injury in rodent brains, leading to neurodegeneration and accelerated aging. Specifically, astrocytes have been shown by my lab to contribute to amyloidosis which could further contribute to both effects. However, the role of morphine in astrocyte - driven senescence leading to cognitive impairments remains an enigma. Hypothesis: Morphine induces a senescent phenotype, which would contribute to accelerated aging seen in long-term opioid users. Methods: I assessed morphine’s impact on the expression of senescence phenotype markers (p16, p21, cell cycle arrest, β-gal activity, neuroinflammatory cytokines) in vitro in human primary astrocytes (HPAs) and validated this in an in vivo model of morphine -administered mice, using various experimental techniques. Findings/Results: Morphine -exposed HPAs demonstrated significantly upregulated levels of these senescence phenotype markers as well as cell cycle arrest specifically in the Sphase of the cell cycle. In vivo results from the hippocampi of morphine-administered mice supported these findings. Conclusions: My findings demonstrate that morphine induces senescent phenotypes, which leads to widespread neuroinflammation and contributes to accelerated aging seen in opiate users.

Competition history

• JSHS 2024 Category not listed

Resources

• National JSHS abstract book ↗

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