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Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, is the most severe form of motor neuron degeneration. This study aims to: (1) compare genetic and non-genetic contributors to ALS development, (2) evaluate the pharmacological mechanisms of riluzole and its therapeutic potential across multiple conditions, and (3) explore treatment combinations for managing symptoms throughout ALS progression. The analysis was conducted using data from established electronic medical databases. The most frequently implicated genetic mutations in ALS include SOD1, SETX, FUS, VEGF, VAPB, ANG, TARDBP, FIG4, OPTN, ATXN2, VCP, UBQLN2, SIGMAR1, CHMP2B, PFN1, ERBB4, HNRNPA1, C9orf72, dynactin 1, H46R, and A4V. Additional risk factors include oxidative stress, glutamate-induced excitotoxicity, autoimmune responses, protein misfolding and aggregation, inflammation, and viral infections. Riluzole’s therapeutic actions are attributed to several mechanisms: (1) inhibition of repetitive neuronal firing, (2) blockade of persistent sodium currents in motor neurons, (3) enhancement of calcium-activated potassium currents, (4) reduction of presynaptic neurotransmitter release, and (5) attenuation of postsynaptic receptor responses. Combining riluzole with antioxidants such as vitamins E and C, coenzyme Q10, creatine, and selenium may enhance therapeutic efficacy in ALS. Symptomatic treatments include nonsteroidal anti-inflammatory drugs, opioids for pain relief, and agents like Baclofen and Dantrolene to manage spasticity. Memantine, Nimesulide, and Gabapentin show promise for further research. Due to its diverse mechanisms, riluzole is also being investigated for use in Parkinson’s disease, Huntington’s disease, Machado-Joseph disease, multiple sclerosis, spinal muscular atrophy, and various neuropsychiatric conditions, including anxiety, autism, depression, and schizophrenia.