N6-methyladenosine (m6A) RNA methylation is a prevalent post-transcriptional modification in eukaryotic mRNA and non-coding RNAs. It plays a crucial role in regulating gene expression through reversible epigenetic modifications, impacting RNA metabolism at multiple levels. These modifications influence mRNA maturation, translation, and stabilization by binding to RNA-binding proteins (RBPs). While the topic of m6A in neurodegeneration has procured conflicting theories, a possible genetic association to motor neuron diseases, such as amyotrophic lateral sclerosis (ALS), has brought forth the importance of understudied biomolecules involved in RNA metabolism and cytoplasmic transport. ALS is a progressive neurodegenerative disease due to gradual motor neuron (MN) degeneration. Interestingly, studies have found aberrant RNA methylation in postmortem human ALS in upper and lower MNs. The discovery tied to RNA degradation makes m6A an exciting novel pathway implicated in ALS and other related neurodegenerative disorders. However, the mechanisms by which m6A-related mutations cause human disease or alter protein complexes remain unclear. For example, altered RNA Binding Proteins (RBPs) in neurodegenerative models may implicate critical m6A RNA metabolism functions in neurons, suggesting its mutations could impact neuronal function in disease contexts. As a result, this present study aims to 1) define the extent of m6A pathology in neurodegenerative conditions using post-mortem tissue and 2) characterize how individual m6A members are altered in different disease contexts. Overall, we hypothesize that in neurodegeneration, the m6A homeostasis is dysregulated. These studies will begin to help define the role of m6A homeostasis in neurodegenerative diseases.