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.
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http://dx.doi.org/10.3390/cells10123570 | DOI Listing |
Zool Res
January 2025
Research & Development Institute of Northwestern Polytechnical University in Shenzhen, Shenzhen, Guangdong 518057, China.
DNA2, a multifunctional enzyme with structure-specific nuclease, 5 -to-3 helicase, and DNA-dependent ATPase activities, plays a pivotal role in the cellular response to DNA damage. However, its involvement in cerebral ischemia/reperfusion (I/R) injury remains to be elucidated. This study investigated the involvement of DNA2 in cerebral I/R injury using conditional knockout (cKO) mice ( -Cre) subjected to middle cerebral artery occlusion (MCAO), an established model of cerebral I/R.
View Article and Find Full Text PDFFront Neurol
January 2025
Department of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
White matter hyperintensities (WMHs) are commonly detected on T2-weighted magnetic resonance imaging (MRI) scans, occurring in both typical aging and Alzheimer's disease (AD). Despite their frequent appearance and their association with cognitive decline in AD, the molecular factors contributing to WMHs remain unclear. In this study, we investigated the transcriptomic profiles of two commonly affected brain regions with coincident AD pathology-frontal subcortical white matter (frontal-WM) and occipital subcortical white matter (occipital-WM)-and compared with age-matched cognitively intact controls.
View Article and Find Full Text PDFBrain Commun
January 2025
Queensland Aphasia Research Centre, University of Queensland, Brisbane 4029, Australia.
The integrity of the frontal segment of the corpus callosum, forceps minor, is particularly susceptible to age-related degradation and has been associated with cognitive outcomes in both healthy and pathological ageing. The predictive relevance of forceps minor integrity in relation to cognitive outcomes following a stroke remains unexplored. Our goal was to evaluate whether the heterogeneity of forceps minor integrity, assessed early after stroke onset (2-6 weeks), contributes to explaining variance in longitudinal outcomes in post-stroke aphasia.
View Article and Find Full Text PDFBrain Commun
January 2025
Translational Neuroimaging Laboratory, McGill University Research Centre for Studies in Aging, Montreal, QC, Canada H4H 1R2.
Blood-based biomarkers have been revolutionizing the detection, diagnosis and screening of Alzheimer's disease. Specifically, phosphorylated-tau variants (p-tau, p-tau and p-tau) are promising biomarkers for identifying Alzheimer's disease pathology. Antibody-based assays such as single molecule arrays immunoassays are powerful tools to investigate pathological changes indicated by blood-based biomarkers and have been studied extensively in the Alzheimer's disease research field.
View Article and Find Full Text PDFBrain Commun
January 2025
Institute for Stroke and Dementia Research, University Hospital, Ludwig Maximilian University of Munich, Munich 81377, Germany.
Traumatic brain injury is widely viewed as a risk factor for dementia, but the biological mechanisms underlying this association are still unclear. In previous studies, traumatic brain injury has been associated with the hallmark pathologies of Alzheimer's disease, i.e.
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