As many as five in every 100,000 deaths in people that are 20 years or older are affected by amyotrophic lateral sclerosis, commonly known as ALS (ALS News Today). There are multiple gene mutations, changes in the DNA sequence of a gene, that can cause the development of ALS. The SOD1 gene mutation is one of the most common, leading to the protein aggregation process, in which mutated or misfolded proteins accumulate and clump together, ultimately leading to neuron degeneration. There are not a lot of clinical trials of gene therapies for ALS genes, even though the first genetic analysis of the disease was back in 1993, and ALS patients have to deal with large financial costs to treat the disease (Siddique and Ajroud-Driss, 2011). By learning more about the key mechanisms by which ALS is caused, patients’ health can be improved and the costs needed for the treatments can be minimized. Through a content analysis inquiry, the data collected will be analyzed by summarizing the key findings and main ideas of research journals on different aspects of ALS with SOD1 protein aggregations and mechanisms. The studies in the meta-analysis are selected if they discuss background information on SOD1, the toxicity of mutant and misfolded SOD1 in ALS, the disease's signaling pathways, data to expand on research uncertainties, specificity of mutant and misfolded SOD1, mechanisms of aggregation propagation, purpose of protein aggregation, or therapeutic implications.