Aging is an independent risk factor for cardiovascular diseases such as hypertension and heart failure. Evidence from the literature suggests that sympathetic nervous system (SNS) dysregulation may play a causative role in age‐associated increased risk for cardiovascular diseases. The mechanisms underlying this phenomenon remains largely unknown. Senescent cells are known to accumulate in various tissues of the body with age and are implicated in the pathogenesis of several neurodegenerative diseases. Senescent cells are known to secrete cytokines, chemokines, and proteases through the acquisition of senescence‐associated secretory phenotype (SASP) and contribute to neuroinflammation in age‐related diseases. However, the presence of senescent cells in the brainstem, a region that contains several nuclei regulating sympathetic outflow and blood pressure has not been investigated. We hypothesized that senescent cells accumulate in the brainstem with age and promotes neuroinflammation, thereby contributing to age‐related SNS dysregulation. To test this, we isolated brainstem from young (2–4 months) and aged (24 months) male C57BL/6J mice (n=4–5/group) and performed gene expression analysis for cellular senescence markers and SASP using qPCR. Data were analyzed with students t‐test and expressed as mean ± S.E. Our results show significant increases in the mRNA expression of p16Ink4a (1.22 ± 0.4 vs 32.89 ± 8.78 fold, young vs aged, p<0.05) a well‐known senescence marker and pro‐inflammatory cytokines, and proteases like IL‐1β (1.03 ± 0.14 vs 2.13 ± 0.29 fold, p<0.05), MCP‐1 (1.02 ± 0.11 vs 4.33 ± 0.79 fold, p<0.05), IL‐1α (1.07 ± 0.2 vs 3.83 ± 0.73 fold, p<0.05, TNFα (1.06 ± 0.21 vs 4.48 ± 1.05 fold, p<0.05) and a trend for an increase in MMP3 in the aged brainstem, presenting evidence for senescence and SASP. We did not observe any age‐related changes in expression of metabotropic or ionotropic glutamate receptors, suggesting that the excitatory neurotransmitter machinery may not be altered in the brainstem with aging. Here we present, for the first time, evidence for cellular senescence in the brainstem of aged mice. Future studies will investigate the mechanistic role of senescence cells in the brainstem in age‐related SNS dysregulation.Support or Funding InformationRAC fund, CVHS, Oklahoma State UniversityThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.