The development of multiple sclerosis (MS) heavily depends on cellular senescence, which results in permanent cell cycle arrest that subsequently leads to tissue damage alongside chronic inflammation. Senescent cells inside the central nervous system (CNS) use pro-inflammatory substances to damage CNS cells while also causing cellular breakdown, which becomes two main elements in MS development. The development and severity of illness within experimental autoimmune encephalomyelitis (EAE) animal models can be attributed to senescence. Physical tests conducted on MS patients have revealed the presence of senescence markers, which might serve as indicators for monitoring disease activity. A potential method to combat illness progression consists of employing senolytics alongside other modulators, but scientists must find solutions regarding specificity and safety concerns and determine optimal times for intervention. The assessment of unintentional tissue damage from treatments requires thorough investigation since these treatments could potentially affect normal tissues. Long-term studies must develop reliable biomarkers that detect cellular aging in individuals so they can get personalized medical care which enables better management of MS with targeted treatment plans. Eventually, senescence-targeted therapies will develop into new therapeutic approaches for delaying multiple sclerosis disease progression while improving treatment results.