Abstract
Population aging is occurring rapidly worldwide, challenging the global economy and healthcare services. Brain aging is a significant contributor to various age-related neurological and neuropsychological disorders, including Alzheimer’s disease and Parkinson’s disease. Several extrinsic factors, such as exposure to ionizing radiation, can accelerate senescence. Multiple human and animal studies have reported that exposure to ionizing radiation can have varied effects on organ aging and lead to the prolongation or shortening of life span depending on the radiation dose or dose rate. This paper reviews the effects of radiation on the aging of different types of brain cells, including neurons, microglia, astrocytes, and cerebral endothelial cells. Further, the relevant molecular mechanisms are discussed. Overall, this review highlights how radiation-induced senescence in different cell types may lead to brain aging, which could result in the development of various neurological and neuropsychological disorders. Therefore, treatment targeting radiation-induced oxidative stress and neuroinflammation may prevent radiation-induced brain aging and the neurological and neuropsychological disorders it may cause.
Highlights
Global population aging is currently occurring at an unprecedented rate
Current experimental studies on animal brains suggest that radiation induces aging in neural stem cells; mature and immature neurons; glial cells, including astrocytes, microglia, and oligodendrocytes; and endothelial cells of cerebral vessels
These effects result in brain aging, leading to cognitive impairment and the development of aging-related brain disorders in individuals who are exposed to radiation, such as survivors from the Chernobyl nuclear power plant accident or individuals receiving radiotherapy
Summary
Global population aging is currently occurring at an unprecedented rate. There has been a demographic shift toward an older population, and this may have far-reaching consequences. Several studies have shown that long-term exposure to low-dose IR in catheterization laboratories increases the risk of cardiovascular diseases, indicating that it causes enhanced vascular aging and early atherosclerosis [17]. Chronic low-dose IR exposure can accelerate the aging of blood vessels, including cerebral vessels This has been shown to correlate with age-related encephalopathy in individuals over 40 years of age, as well as with systemic atherosclerosis [31,32]. It has been reported that IR increases cellular senescence, and senescence-associated β-galactosidase (SA-β-Gal) and senescence specific genes (p16, p12, and Bcl-2) are highly expressed in irradiated bone marrow derived macrophages [39] These findings corroborate the in vivo evidence pointing to the potential senescence-inducing effects of radiation on the endothelial cells of cerebral blood vessels. Inflammation, immunosenescence, thyroid cancer, and childhood leukemia “Chernobyl AIDS,” CNS damage, premature aging, atherosclerosis, and senile encephalopathy
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