Cellular Senescence In Neurodegeneration is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Cellular senescence is a state of irreversible cell cycle arrest characterized by a pro-inflammatory secretory phenotype (SASP - Senescence-Associated Secretory Phenotype). In the brain, senescent neurons, astrocytes, and microglia accumulate with age and in neurodegenerative diseases, contributing to chronic neuroinflammation and neuronal dysfunction[1][2].
| Marker | Function |
|---|---|
| p16INK4a (CDKN2A) | Cyclin-dependent kinase inhibitor |
| p21CIP1 (CDKN1A) | Cell cycle arrest |
| p53 | Tumor suppressor, senescence driver |
| Drug | Target | Status |
|---|---|---|
| Navitoclax (ABT-263) | BCL-2 family | Preclinical |
| Dasatinib plus Quercetin | Multiple | Clinical trials |
| Fisetin | BCL-2, senescent pathways | Natural senolytic |
| ABT-993 | BCL-xl | Preclinical |
Rapamycin: mTOR inhibition reduces SASP
JAK inhibitors: Block inflammatory signaling
NF-kappaB inhibitors: Reduce SASP production
Cell-Types/Senescent-Cells-Neurodegeneration — This page
The study of Cellular Senescence In Neurodegeneration has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.