Abstract: Neurodegenerative disorders represent a pervasive global health challenge, yet therapeutic options remain conspicuously limited. These disorders are inherently dynamic processes within the central nervous system, unfolding across distinct sub-stages: initial structural neuronal alterations (sub-stage 1), functional impairment (sub-stage 2), and culminating in neuronal death (sub-stage 3). Previous studies have revealed shared pathological features between amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD) (van Rheenen et al., 2021; Mantle and Hargreaves, 2022) including common genetic risk factors identified through genome-wide association studies (van Rheenen et al., 2021). Both disorders manifest similar neurodegenerative mechanisms, such as oligomer formation, aberrant protein accumulation, and protein misfolding-specifically, superoxide dismutase 1 in ALS and α-synuclein in PD. Mitochondrial dysfunction further serves as a common denominator in the pathogenesis of ALS and PD (Mantle and Hargreaves, 2022).