“…Since PD patients share many aspects of cellular senescence including inflammation (Yan et al, ), oxidative stress (Dias, Junn, & Mouradian, ), and mitochondrial dysfunction (Jiang, Jiang, Zuo, & Gu, ) and astrocytes have been shown to senesce in response to various stressors, it has been proposed that astrocyte senescence in response to environmental toxins could be a contributor to PD (Chinta et al, ). Indeed, astrocytes treated with TCDD underwent premature senescence with growth arrest accompanied by cytoskeletal remodeling and increases in p16, p21, and SA‐β gal (Nie et al, ). Since this phenotype included an increase in ROS levels, it was thought that TCDD might be inducing astrocyte senescence via oxidative stress.…”