ABSTRACT
This chapter presents the TSE-EBPT potential of CP in the clinical management of various NDDs. Chu et al. summarized key features of the major cargo recognition pathways for selective CP/ATG, highlighting their potential impact in the pathogenesis or amelioration of NDDs. The onset of progressive NDDs is primarily linked to mutations in mitochondrial and lysosomal regulators. Recent genetic and biochemical evidence has improved our understanding of the mechanisms that lead to ALS and FTD, two devastating NDDs with overlapping symptoms and causes. Changes in axonal transport and nucleocytoplasmic transport suggested that further insight into intracellular trafficking defects will elucidate our understanding of the ALS pathogenesis and will provide novel avenues for theranostic interventions. Thioacetamide-induced HE revealed mitochondrial changes in the ACC and SN of rats. A novel role of autism-linked Wdfy3 gene in the brain MTG was proposed. Neurodegeneration is characterized by mitochondrial malfunction and protein aggregates due to intracellular redox imbalance.
