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High-grade gliomas cannot be fully understood without considering the biology of aging. In this study, we demonstrate that a set of genes previously established as predictors of tumor subtype and patient survival in gliomas can also be independently characterized as biomarkers associated with aging. Moreover, their expression changes during aging parallel with those seen in malignant transformation: genes which upregulation worsen prognosis are also upregulated with age. These findings support the hypothesis that glioma progression and aging share partially overlapping molecular mechanisms. We also demonstrate that while accelerated epigenetic and mitotic senescence - gauged by mathematical models (biological clocks) that track aging through specific changes in the DNA methylation of a set of CpG sites - appears inherent to various molecular variants of gliomas, its nature and prognostic significance vary depending on the specific subtype and the epigenetic clock model employed. Moreover, accelerated aging does not represent a universal hallmark of aggressiveness but rather a phenomenon specific to individual glioma subtype. In this paper, we provide a detailed discussion of the role of cellular senescence in glioma pathogenesis, with a particular focus on its key contribution to tumor growth control and therapeutic response. Additionally, we highlight the yet unresolved question of whether age-associated inflammation (inflammaging) acts as an independent driver of glioma progression or whether the tumor itself accelerates aging, and suggest the potential of profiling patients cellular aging in developing personalized treatment strategies.