Development of treatments for neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis faces medical challenges due to an increasingly aging population. However, some pharmaceutical companies have stopped developing drugs to treat neurodegenerative diseases, and no new treatments for neurodegenerative diseases have been created in the last decade. The relationship between the pathogenesis of neurodegenerative diseases and risk factors has not been fully elucidated. It is known that transient receptor potential (TRP) channels cause neuronal apoptosis in cases of oxidative stress and Ca²⁺ homeostasis in neurodegenerative diseases. TRP channels sensitive to reactive oxygen species (ROS) may be the main risk factors as polymodal sensors due to the onset of secondary pathological damage after the initial toxic effect, typical features of neurodegenerative diseases, and late stages. Recent evidence shows that there is a relationship between neuronal loss and disruption of Ca²⁺ balance in neurological diseases. It has been reported that excessive Ca²⁺ influx in the intracellular fluid in neurons increases mitochondrial dysfunction and activation of apoptotic pathways in neurons. It has been reported that excessive Ca²⁺ influx and oxidative stress caused by TRPM2 channel activation play a role in neuron toxicity and death. Therefore, the TRPM2 channel may be useful in preventing oxidative stress-induced cellular damage in neurodegenerative disorders. Additionally, it has been shown that by using TRPM2 channel antagonists, Ca²⁺ influx into the intracellular environment can be prevented and thus cell homeostasis can be maintained. As a new hope for neurological diseases, drugs developed using TRPM2 channel antagonists will shed light on the solution of the problem. In this review, we examined the role of the TRPM2 channel in neurodegenerative diseases based on recent studies.