The lethal disease amyotrophic lateral sclerosis (ALS) features motor neuron destruction in the spinal cord and brain stem, while causing gradual body immobility. ALS arises mostly due to mutations in the superoxide dismutase 1 (SOD1) gene, which causes three distinct pathologic pathways including oxidative stress and disrupted proteostasis together with protein misfolding. The precise connection between mutant SOD1 and aging cells with disease development needs additional research for full comprehension. The chapter analyzes mutant SOD1 leads to neuronal degeneration while establishing how age-specific changes promote neurodegeneration. This chapter explains the differentiation of harmful cell processes from protective ones along with studying resilience mechanisms in cells. The discussion continues with existing therapeutic approaches for mutant SOD1 and senescence pathway intervention and mitochondrial dysfunction treatment to enhance ALS treatment success.