The brain is uniquely vulnerable to cellular stress, making it crucial to understand the mechanisms that regulate stress response. N6-methyladenosine (m6A), the most prevalent internal modification on eukaryotic mRNA, plays an essential role in various stress responses. This work investigates the impact of m6A mRNA methylation in the adult Drosophila brain with acute heat stress and chronic stress of aging and disease. Using m6A-immunoprecipitation sequencing, we find that Mettl3-dependent m6A is enriched in transcripts of neuronal processes and signaling pathways that increase upon stress. Mettl3 knockdown conferred resilience to stress and increased levels of m6A modified heat stress chaperones, indicating that m6A modification in Drosophila dampens the brain’s biological response to stress. Additionally, the tRNA methyltransferase TRMT10A has been implicated in m6A modulation. We investigate the role of the homolog of TRMT10A, CG14618/dTrmt10A, and its impact on m6A regulation in the Drosophila brain and stress response. Using m6A-IP RNA sequencing on head tissue, we find that upregulation of dTrmt10A results in a global decrease in m6A levels in the brain and increases resilience to acute heat stress. Collectively, our data confirm dTrmt10A acts as an additional regulator of m6A and in the acute stress response. Furthermore, we examine the regulation of m6A in the brain upon chronic stresses of aging and degenerative disease. We find that m6A levels dynamically increase with age and disease, marking neurogenesis and signaling pathway transcripts that become transcriptionally downregulated with age. Additionally, m6A regulation in neuron vs glial cells confers different outcomes on animal longevity and translation regulation.