Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disorder. This chronic, progressive disease is characterized by loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) and the presence of cytoplasmic inclusions called Lewy bodies (LBs) in surviving neurons. PD is attributed to a combination of environment and genetic factors, but the precise underlying molecular mechanisms remain elusive. Oxidative stress is generally recognized as one of the main causes of PD, and excessive reactive oxygen species (ROS) can lead to DA neuron vulnerability and eventual death. Several studies have demonstrated that small non-coding RNAs termed microRNAs (miRNAs) can regulate oxidative stress in vitro and in vivo models of PD. Relevant miRNAs involved in oxidative stress can prevent ROS-mediated damage to DA neurons, suggesting that specific miRNAs may be putative targets for novel therapeutic targets in PD.
Highlights
Parkinson’s disease (PD) is the most common degenerative movement disorder affecting 1–2% of individuals older than 65 (de Lau and Breteler, 2006)
It is well accepted that oxidative stress contributes to PD, and there is interest in understanding how oxidative stress is exacerbated by the emerging regulators, microRNAs via contributing to the pathological processes which are responsible for oxidative stress like mitochondrial dysfunction (Subramaniam and Chesselet, 2013), α-synuclein aggregation (Hsu et al, 2000), neuroinflammation (Tansey et al, 2007), and dysregulation of the endogenous antioxidant system (Buendia et al, 2016). microRNAs are highly conserved noncoding RNAs, ∼18–25 nucleotides in length that can regulate protein expression either by translational inhibition or targeted mRNA cleavage (Bartel, 2009; Guo et al, 2010). miRNA transcripts are produced in the nucleus and processed into hairpin RNA by the Drosha microprocessor complex
Numerous studies have provided evidence that miRNAs play a role in PD pathogenesis by regulating oxidative stress, the field is still in its infancy
Summary
PD is the most common degenerative movement disorder affecting 1–2% of individuals older than 65 (de Lau and Breteler, 2006). Another study has proposed that reduced miR34b/c levels along with decreased expression of DJ-1 could contribute to abnormal mitochondrial defects in the brain of PD patients, which is confirmed in miR-34b/c-depleted cells. In the course of PD, the two processes form a vicious circle and accelerate progression of the disease It has been suggested the decreased level of miR-7 and miR-214 possibly contributes to increased α-Syn accumulation in the MPTP-induced model of PD (Junn et al, 2009; Wang et al, 2015). One study has revealed that the decreased level of miR-34b/c in specific brain areas of PD patients, including the amygdala, frontal cortex, substantia nigra, and cerebellum, might contribute to PD pathogenesis for losing its function of inhibiting αSyn expression (Kabaria et al, 2015b). Other studies have demonstrated that miR-320a and miR-16-1 could promote aberrant α-Syn accumulation by targeting hsc in PD (Li et al, 2014; Zhang and Cheng, 2014)
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