Similarly, in a rat model carrying the ALS-related SOD1G93A mutation, microglia exhibit typical senescent features: enhanced SA-β-Gal activity, increased expression of p16INK4a and p53, accompanied by release of SASP factors such as matrix metalloproteinase-1 (MMP-1) and nitrotyrosine, confirming the central role of glial senescence in motor neuron injury [140]. Here, CDKN2A is linked to amyotrophic lateral sclerosis.