Examining the relationship between mitochondrial dysfunction and Parkinson's disease pathology: a review on potential risk factors and treatments for parkinsonism
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The most prevalent histological risk factor for Parkinson’s disease is the development of alpha-synuclein clumps, known as Lewy Bodies, in the substantia nigra portion of the midbrain. However, the etiology of the disease remains unknown. Neurons are heavily dependent on aerobic respiration for ATP due to their high energy demands. In neurons, mitochondria are transported throughout axons and dendrites for facilitating subcellular functions, and are critically important for membrane excitability and neurotransmission. Past evidence indicates that mitochondrial dysfunction plays a significant role in the progression of degenerative pathologies in the brain. In this review, genetic factors and biochemical mechanisms representative of healthy mitochondrial structure and function are examined to determine the role of mitochondrial dysfunction in the onset and progression of Parkinson’s disease. Treatments and therapies targeting mitochondrial dysfunction for the purposes of improving Parkinson’s disease pathologies are also explored. Published data examined in this review has shown that mitochondrial dysfunction plays a significant role in the development and progression of Parkinson’s disease. Through interactions with alpha-synuclein protein aggregates and through facilitation of general dopaminergic neurodegeneration, mitochondrial dysfunction provides a pathway for the progression of Parkinsonian pathologies. In addition, genes involved with mitochondrial biogenesis, as well as genes involved in the onset of Parkinson’s disease show overlap and interactions indicative of an association between defective mitochondria and parkinsonism. With a focus on improving mitochondrial function and reducing Parkinson’s disease pathology, a number of potential drug treatments and therapies have proven to be of interest. While there is currently no cure for Parkinson’s disease, evidence consolidated in this review supports the need for investigation into Parkinson’s disease treatments that target mitochondrial dysfunction and oxidative stress. Subsequent research studies and treatments should focus on genes that play a regulatory role in mitochondrial biogenesis, with the goal of determining more transcriptional pathways that overlap between mitochondrial dysfunction and parkinsonism. Drug compound screens for improving mitochondrial biogenesis and reducing alpha-synuclein aggregation should be explored as well.