Deep Brain Stimulation and Gene Expression Alterations in Parkinson’s Disease
نویسندگان
چکیده
*Corresponding author: A. Mohammadi, Ph.D; Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran E-mail: ar.mohammadi@ bmsu.ac.ir Parkinson disease (PD) is a neurobiological disorder caused by the death of dopaminergic neurons in the substantia nigra pars compacta (SNc). PD is typically characterized by features including rigidity, tremor, stiffness, and bradykinesia, as well as walking problems. Although, brain imaging and electroencephalography (EEG) is used in the primary evaluation of neurological disorders [1, 2], but it’s unfortunate that PD symptoms appear when approximately 60% of dopaminergic neurons have been destroyed [3]. The discovery of mutations in the genes for parkin (PARK2), DJ-1 (PARK7), PTEN-induced putative kinase 1 (PINK1), α-synuclein (SNCA), Ubiquitin Carboxyl-Terminal Esterase L1 (UCHL1), and Leucine-rich repeat kinase 2 (LRRK2) has made a unique glance into the mechanisms responsible for the etiology of PD [4]. Deep brain stimulation (DBS) is a neuroengineering procedure introduced in 1987 as a surgical handling for movement disorders specially the enervating symptoms of PD [5, 6]. Although, DBS has now been extensively considered as a lucrative method to patients whose medications have intensive signs cannot be sufficiently controlled with drugs, but it can improve movement disorders and the patient’s quality of life. Traditionally, the subthalamic nucleus (STN), globus pallidus interna (GPi) and ventral intermediate nucleus of the thalamus (VIM) are three targets for DBS in PD. Whereas STN stimulation improves tremor, motor scores and some other dysfunctions, but there is also the potential for neurobiological and psychiatric side-effects, including gene expression alteration, hallucinations, depression, hyper-sexuality, apathy and cognitive dysfunction. Despite its noteworthy therapeutic potency, the exact mechanisms underlying the therapeutic effects of DBS haven’t been determined [7]. There are at least four hypotheses to explain the mechanisms of DBS including Synaptic depression [8], Synaptic inhibition [9], Depolarization blockade [10], and Stimulation-induced disruption of pathological network activity [11]. Regardless of the unclear mechanism of DBS, changes in crucial genes involved in Parkinson’s Editorial
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