Abstract
Neurodegenerative diseases (NDs) include more than 600 disease entities that are characterized by loss of specific neurons located in anatomically related functional areas which progressively lead to motor and cognitive deficits. The pathogenesis of NDs involves mitochondrial dysfunction/oxidative stress, programmed cell death or abnormal protein aggregation, trafficking, and/or degradation. In most cases, the end stage neuropathology is characterized by a highly specific distribution of abnormal protein aggregates in disease specific patterns in the affected neuronal populations. These proteins include β-amyloid and TAU in Alzheimer's disease (AD), α-synuclein in Parkinson's disease (PD), and huntingtin (Htt) polyglutamine (poly-Q) elongation in Huntington's disease (HD) (Maiese, 2015). NDs result in disability and death for more than 30 million individuals worldwide and the number of individuals afflicted is expected to increase with the increased life span of the global population. Although clinical treatments for NDs have progressed over the years with some promising results, the availability of treatments that can limit or prevent NDs remains limited (Maiese, 2015).
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