Exploring the causal relationship between telomere regulation, aging and neurological disorders

Telomere biology is important for aging and is the cause of the pathogenesis of many neurological disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), stroke, and brain tumors. Telomere shortening is considered to play a role in neurodegeneration, immune senescence, and cerebrovascular dysfunction. Shorter leukocyte telomere length (LTL) is associated with increased risk and severity of stroke, poorer cognitive outcomes in AD, and increased neuroinflammation in MS, highlighting a possible biomarker for disease progression. Glioblastoma and medulloblastoma are characterized as adult and childhoodd neoplasms,respectively; however they aree similarinn terms of telomere regulatio,nwhicht allows malignant growth. However, disease pathophysiology has been associated with telomere dynamics, oxidative stress, and neuroinflammation, but the causal association between telomere attrition and neurological disorders is still unclear. In studies of Mendelian randomization, neurodegenerative diseases have been associated with telomere length regulation in addition to telomere attrition. Approaches to target telomeres include telomerase activators for neuroprotection, telomerase inhibitors, and ALT-directed therapies for brain tumors. These telomere-derived biomarkers should be further refined, and their mechanistic links to the acceleration of neurodegeneration should be determined. Telomere-modifying therapies should be balanced to optimize benefits with minimal oncogenic risks. This review explores the causal relationship between telomere biology, aging, and neurological disorders, indicating novel therapeutic strategies and future directions in telomere research.