Elucidating the Biochemical Role of Novel Enzyme Targets in Neurodegenerative Disorders

Abstract

Abstract Introduction: Neurodegenerative disorders, characterized by progressive neuronal loss, remain a significant clinical challenge due to their multifactorial etiology. While numerous enzymes have been implicated in their pathogenesis, there remains a knowledge gap regarding the precise biochemical roles of several novel enzyme targets. Methods: This study encompassed a multi-pronged approach, involving patient-derived samples from Alzheimer's and Parkinson's cases (n=156), an ALS mouse model (n=50), and a CRISPR-Cas9 edited Huntington's Disease zebrafish model (n=100). Enzyme activity assays, localization microscopy, and interaction pathway analyses were conducted. Results: Elevated Aminotransferases activity was observed in 78% of Alzheimer's samples compared to controls (p<0.05). The ALS mouse model revealed a 30% reduction in motor neuron counts in tandem with altered enzyme activity (p<0.01). The Huntington's zebrafish model successfully displayed genetic markers post-CRISPR editing, indicating a 95% editing efficiency. Furthermore, novel interactions between the enzymes and established neurodegenerative pathways were identified. Conclusion: Mine findings highlight the pivotal role of novel enzyme targets in neurodegenerative disorders, offering potential avenues for early detection and therapeutic interventions. The intricate interplay of these enzymes with known disease pathways underscores the need for an integrated approach to understand disease mechanisms holistically.