This review discusses the links between the autophagy pathway, aging, and age-associated neurodegeneration in Alzheimer’s, Parkinson’s, motor neuron, and Huntington’s diseases. The authors highlight the functions of autophagy in neurons and glia and how aging and neurodegenerative diseases affect autophagy.

The interaction between cellular senescence and cancer is complex and multifaceted, senescence can both promote and inhibit tumor progression through various mechanisms. M6A methylation modification regulates the aging process of cells and tissues by modulating senescence-related genes. In this review, we comprehensively discuss the characteristics of cellular senescence, the signaling pathways regulating senescence, the biomarkers of senescence, and the mechanisms of anti-senescence drugs. Notably, this review also delves into the complex interactions between senescence and cancer, emphasizing the dual role of the senescent microenvironment in tumor initiation, progression, and treatment. Finally, we thoroughly explore the function and mechanism of m6A methylation modification in cellular senescence, revealing its critical role in regulating gene expression and maintaining cellular homeostasis. In conclusion, this review provides a comprehensive perspective on the molecular mechanisms and biological significance of cellular senescence and offers new insights for the development of anti-senescence strategies.

Cellular senescence is a complex and multifaceted biological process characterized by a stable arrest of the cell cycle in response to various stressors, such as DNA damage, oxidative stress, and oncogene activation (1). Although senescent cells no longer proliferate, they remain metabolically active and exhibit distinct phenotypic changes, including the secretion of pro-inflammatory factors, collectively termed the senescence-associated secretory phenotype (SASP) (2, 3). Senescence plays dual roles in physiological and pathological contexts: it is essential for processes like tissue remodeling, wound healing, and tumor suppression, yet its accumulation contributes to aging, chronic inflammation, and the progression of age-related diseases, including cancer and neurodegenerative disorders (4). Understanding the mechanisms underlying cellular senescence is crucial for developing therapeutic strategies to harness its beneficial aspects while mitigating its detrimental effects.

Summary: Scientists have discovered that neural stem cells (NSCs) receive constant feedback from their daughter cells, influencing whether they remain dormant or activate to form new neurons and glia. This parent-child relationship helps regulate brain regeneration and repair.

The study also reveals that calcium signaling plays a key role in how NSCs decode multiple signals from their environment. If NSCs produce only a few daughter cells, they activate; if they produce many, they stay dormant.

These findings challenge previous assumptions that NSCs function independently and open new avenues for treating neurodevelopmental disorders. Future research will explore how these processes change in aging and disease.