WITHDRAWN: Investigating the ERG a-wave and Retinal Diseases with Rod Equivalent Circuit Model Based on the APD.

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Mimicking the retinal neuron functions by a photoresponsive single transistor with a double gate.

To realize a low-cost neuromorphic visual system, employing an artificial neuron capable of mimicking the retinal neuron functions is essential. A photoresponsive single transistor neuron composed of a vertical silicon nanowire is proposed. Similar to retinal neurons, various photoresponsive characteristics of the single transistor neuron can be modulated by light intensity as well as wavelength and have a high responsivity to green light like the human eye. The device is designed with a cylindrical surrounding double-gate structure, enclosed by an independently controlled outer gate and inner gate. The outer gate has the function of selectively inhibiting neuron activity, which can mimic lateral inhibition of amacrine cells to ganglion cells, and the inner gate can be utilized for the adjustment of the firing threshold voltage, which can be used to mimic the regulation of photoresponsivity by horizontal cells for adaptive visual perception. Furthermore, a myelination function that controls the speed of information transmission is obtained according to the inherent asymmetric source/drain structure of a vertical silicon nanowire. This work can enable photoresponsive neuronal function using only a single transistor, providing a promising hardware implementation for building miniaturized neuromorphic vision systems at low cost.

TMEM106B Knockdown Exhibits a Neuroprotective Effect in Parkinson's Disease via Decreasing Inflammation and Iron Deposition.

Parkinson's disease (PD) is closely related to iron accumulation and inflammation. Emerging evidence indicates that TMEM106B plays an essential role in PD. But whether TMEM106B could act on neuroinflammation and iron metabolism in PD has not yet been investigated. The aim of this study was to investigate the pathological mechanisms of inflammation and iron metabolism of TMEM106B in PD. 1-methyl-4-phenylpyridinium (MPP+)- and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced SH-SY5Y cells and mice were treated with LV-shTMEM106B and AAV-shTMEM106B to construct PD cellular and mouse models. Pole tests and open-field test (OFT) were performed to evaluate the locomotion of the mice. Immunohistochemistry and iron staining were used to detect TH expression and iron deposition in the SN. Iron staining was used to measure the levels of iron. Western blotting was used to detect the expression of inflammatory factors (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)), NOD-like receptor protein 3 (NLRP3) inflammasome, divalent metal transporter 1 (DMT1), and Ferroportin1 (FPN1)). Knockdown of TMEM106B improved motor ability and rescued dopaminergic (DA) neuron loss. TMEM106B knockdown attenuated the increases of TNF-α, IL-6, NLRP3 inflammasome, and DMT1 expression in the MPP+ and MPTP-induced PD models. Furthermore, TMEM106B knockdown also increases the expression of FPN1. This study provides the first evidence that knockdown of TMEM106B prevents dopaminergic neurodegeneration by modulating neuroinflammation and iron metabolism.

Short-term lifestyle education on obesity reduction in adolescents.

Backgrounds: Obesity is increasing in adolescents in China. However, the awareness of obesity and prevention on related risk factors were not well known. We aim to assess the effectiveness of short-term health education intervention on obesity in Chinese adolescents. Methods: In this study, 42 primary and secondary schools from Qingdao were randomly divided into the education and control groups. A total of 11,739 adolescents was included in the current study. The logistic regression was employed to assess odds ratio (OR) of education intervention on overweight and obesity prevalence adjusting for covariates. Results: The baseline prevalence of overweight and obesity was significantly higher in urban than in rural areas and in boys than in girls. After 1 year lifestyle intervention, the proportion of students with awareness of obesity was higher, meanwhile age-adjusted mean values of weight, body mass index, duration of watching TV and doing homework were lower in education group than control group. The corresponding figures were 43.6 [95% CI (confidence intervals); 43.3-43.9] kg versus 44.3 (95% CI; 44.0-44.6) kg, 18.6 (95% CI; 18.5-18.7) kg/m2 versus 18.9 (95% CI; 18.8-19.1) kg/m2, 1.3 (95% CI; 1.2-1.3) hours/d versus 1.4 (95% CI; 1.3-1.4) hours/d, and 1.5 (95% CI; 1.4-1.5) hours/d versus 1.8 (95% CI, 1.7-1.8) hours/d. The multivariable adjusted OR for combined prevalence of overweight and obesity was 0.85 (95% CI, 0.76-0.96) in education group as compared with control group. Conclusion: Short-term health education intervention results in significantly higher reductions in obesity parameters and improvement in awareness in Chinese adolescents.

Association between NEK1 gene polymorphisms and the potential risk of sporadic Parkinson's disease in the Chinese Northern Han population: A case-control study.

OBJECTIVE: Parkinson's disease (PD) has been identified as a genetically influenced disease linked to various genetic loci. Previous studies have suggested that neurodegenerative illnesses, including PD, Alzheimer's disease, and Amyotrophic lateral sclerosis (ALS), may share certain genetic loci. Recently, the NEK1 gene was identified as overlapping between PD and ALS. We therefore wanted to explore the potential association between the NEK1 gene single nucleotide polymorphisms (SNPs) and the clinical features and pathophysiology of sporadic PD in a northern Chinese population. METHODS: A total of 510 sporadic PD patients and 510 age- and sex-matched healthy controls (HCs) were included in this study. Two SNPs (rs4563461 and rs66509122) of the NEK1 gene were genotyped using polymerase chain reaction (PCR). And we analyzed the association between NEK1 gene polymorphisms and clinical manifestations. RESULTS: Allele T (C vs. T, P = 0.018) and genotype TT (CC vs. TT: P = 0.021) of rs66509122 among PD group and HCs were significantly different. In addition, we discovered that the rs66509122 genotype TT was associated with depression in early-onset PD (EOPD) (P = 0.031) and diabetes in female PD (P = 0.032). Unfortunately, no distinct correlation of rs4563461 polymorphisms with sporadic PD susceptibility was found in either the overall group (C vs. T, P = 0.086) or other subgroups. However, the T allele of rs4563461 was significantly correlated with sleep disorders in the PD group, especially in the late-onset PD (LOPD) group and male PD group. CONCLUSION: This study found that the NEK1 rs66509122 polymorphism was associated with a lower risk of sporadic PD, while T allele of rs66509122 may be a protective factor for PD. The NEK1 rs4563461 and rs66509122 polymorphisms both showed correlations with some non-motor symptoms in sporadic PD patients. Further research with a larger sample and varied ethnic groups is needed to investigate the role of NEK1 gene polymorphisms in the pathophysiology of PD.

Detection of calcitonin gene-related peptide based on increased antigen-driven interaction with antibody variable regions.

Introduction: Calcitonin gene-related peptide (CGRP) is involved in trigeminal neuralgia and migraine, and measuring the CGRP concentration in the serum is crucial for the early prediction of these conditions. Current methods for CGRP detection are primarily radioimmunoassay, which needs radioactive substances and enzyme-linked immunosorbent assays (ELISAs) which need long detection time and some have a narrow detection range. Methods: The genes of anti-CGRP antibody variable regions were cloned into pDong1 vector to obtain pDong1/Fab-CGRP, with which phage-Fab was prepared, and the concentration of CGRP was detected by competitive ELISA. The pDong1/Fab-CGRP was modified to obtain pDong1/OS-CGRP, with which the co-expression solution containing phage-displayed heavy chain variable fragments (phage-VH) and light chain was obtained. CGRP was detected by OS-ELISA based on phage-VH, antibody light chain, and anti-light chain antibody. The VL gene was cloned into the pMAL vector to obtain pMAL-VL (CGRP), with which maltose binding protein fused with VL (MBP-VL) was prepared. CGRP was detected by OS-ELISA employing MBP-VL and phage-VH. Results: OS-ELISAs that measure the CGRP concentration by quantifying the interaction between variable regions were investigated. OS-ELISA using phage-VH and secreted light chains in the same culture system exhibited a limit of detection (LOD) of 0.05 nM, offering higher sensitivity than competitive assay with an LOD of 0.75 nM, whereas using phage-VH and separately prepared MBP-VL exhibited an LOD of 0.15 nM and a broader detection range of 0.15-500 nM than competitive ELISA, whose detection range was 0.75-10 nM. Discussion: The combination of the two OS assays achieved high sensitivity and a broad detection range for CGRP, which may have significance in clinical applications.

CD33 polymorphisms and Parkinson's disease Parkinson's disease in northern Chinese Han population: A case-control study.

OBJECTIVE: Parkinson's disease (PD) represents the multisystem illness involving immunological and neuroinflammatory dysfunction. The present work focused on evaluating link of CD33 single nucleotide polymorphisms (SNPs) with PD vulnerability of the northern Chinese Han people, considering CD33's role as a critical immunoregulatory receptor in neuroinflammatory responses. METHODS: The present case-control study included 475 PD cases together with 475 normal controls. A further division of PD patients into two categories was made: 74 patients with early-onset PD (EOPD; onset age ≤ 50 years) and 401 patients with late-onset PD (LOPD; onset age > 50 years). DNA extraction was conducted, followed by genotyping for 2SNPs of CD33 polymorphisms with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: Alleles (G vs. A, P = 0.028) and AA genotypes (P = 0.042) of rs12985029 were significantly different between the groups. Distinctions were observed between the two groups in the recessive, co-dominant, and additive models (nominal P = 0.030, nominal P = 0.045, and P = 0.032). AA genotype frequency among male PD was higher compared to corresponding male controls (P = 0.034), and in the male group allele A was a factor causing the disease (P = 0.026). The rs12985029 genotypes and allele frequency were different in EOPD compared with LOPD (P = 0.002, P = 0.002, respectively), and in LOPD group relative to healthy control group (P = 0.020 and P = 0.004, separately). Regarding the rs3826656 polymorphism, the frequency of GA genotype was higher in the control group than in the case group (nominal P = 0.036). Overdominance and co-dominant models were different between these groups (P = 0.026, nominal P = 0.030). Subgroup analysis revealed genotype frequency differences between rs3826656 LOPD group and control group (P = 0.018). Furthermore, relationship between rs3826656 and rs12985029 (D' = 0.162, r2 = 0.021) did not reach a complete level of linkage disequilibrium (LD) of northern Chinese Han people. CONCLUSION: This study establishes an association between CD33 rs12985029 and rs3826656 polymorphisms and PD risk among the selected northern Chinese Han people. The GA genotype, rs3826656, may act as a protective factor against PD, while the A allele, rs12985029,could be genetic risk factor related to PD. Future research should include larger sample sizes and other human populations to further investigate how CD33 polymorphisms contribute to PD.

Association of AQP4 single nucleotide polymorphisms (rs335929 and rs2075575) with Parkinson's disease: A case-control study.

OBJECTIVE: The glymphatic system plays an important role in brain waste removal and is functionally and structurally dependent on astrocyte aquaporin-4 (AQP4). Genetic variation in the AQP4 gene has therefore been hypothesized to be associated with genetic susceptibility to neurodegenerative diseases. This study aimed to investigate whether two specific single nucleotide polymorphisms (SNP) in the AQP4 gene, rs335929, and rs2075575, are associated with the risk and clinical features of PD. METHODS: A total of 950 participants, including 475 patients with sporadic PD and 475 independent healthy controls, were included in this case-control study. Two SNPs (rs335929 and rs2075575) of the AQP4 gene were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Sanger sequencing was used to determine whether the genotyping results were accurate. A chi-square (χ2) test was used to compare the frequencies of alleles and genotypes between patients and controls. Logistic regression was used to calculate dominance ratios (OR) and 95% confidence intervals (CI). RESULTS: The difference between rs2075575 in the dominant model (GG vs GA + AA: P = 0.019) and the overdominant model (GG + AA vs GA: P = 0.013) was statistically significant. Subgroup analysis showed that the frequency of the rs2075575 A allele was significantly higher in female PD patients than in matched female controls (P = 0.017). rs2075575 A allele was significantly more frequent in LOPD patients than in matched elderly controls (P = 0.033). rs335929 polymorphism was not significantly correlated with PD susceptibility in either the overall or subgroup analysis. Haplotype analysis between the two SNPs did not show an association with PD susceptibility. In addition, we found that the rs2075575 G allele was significantly associated with Rapid Eye Movement Behaviour Disorder (RBD) (P = 0.044), and the rs335929 A allele with memory impairment (P = 0.028) in PD. CONCLUSION: The AQP4 gene rs2075575 polymorphism may be associated with PD susceptibility, but not the rs335929 polymorphism. rs2075575 is associated with RBD and rs335929 is associated with memory cognition. Regulation of the glymphatic system by interfering with the genetics of AQP4 and thus influencing the pathology of PD may be a direction worth investigating. Studies in larger sample sizes and across ethnicities are essential for further understanding the potential association between AQP genes and PD pathogenesis.

The associations of cerebrospinal fluid biomarkers with cognition, and rapid eye movement sleep behavior disorder in early Parkinson's disease.

Background: In Parkinson's disease (PD), levels of cerebrospinal fluid (CSF) biomarkers and progression of non-motor symptoms are associated, but the specifics are not yet clear. Objective: The aim of this study was to investigate the associations of non-motor symptoms with CSF biomarkers in PD. Materials and methods: We assessed 487 individuals from the Parkinson's Progression Markers Initiative (PPMI), consisting of 155 healthy controls (HCs) and 332 individuals with PD. Patients with PD were grouped according to non-motor symptoms and compared CSF α-synuclein (α-syn), amyloid-beta 1-42 (Aß1-42), and total tau (t-tau) levels. Multiple linear regressions were used in baseline analysis and linear mixed-effects models in longitudinal analysis. Analyses of mediating effects between cognition and CSF biomarkers were also performed. Results: At baseline, PD patients with cognitive impairment (PDCI) exhibited significantly lower CSF α-syn (ß = -0.1244; P = 0.0469), Aß (ß = -0.1302; P = 0.0447), and t-tau (ß = -0.1260; P = 0.0131) levels than PD patients without cognitive impairment (PDCU). Moreover, a faster decline of α-syn (ß = -0.2152; P = 0.0374) and Aß (ß = -0.3114; P = 0.0023) and a faster rise of t-tau (ß = -0.1534; P = 0.0274) have been found in longitudinal analysis. The Aß positive group showed an earlier decline in cognitive performance (ß = -0.5341; P = 0.0180) compared with the negative Aß group in both analyses. In addition, we found that PD patients with probable rapid eye movement sleep behavior disorder (pRBD) showed decreased CSF α-syn (ß = -0.1343; P = 0.0033) levels. Finally, mediation analysis demonstrated that olfactory function partially mediated the relationship between cognition and CSF biomarkers levels. Conclusion: Our study shows that CSF biomarkers are associated with cognition at baseline and longitudinally. Cognitive impairment is more severe in patients with a heavier Aß burden. CSF α-syn decreased in PD patients with pRBD. This study suggests that early recognition of the increased risk of non-motor symptoms is important for disease surveillance and may be associated with the pathological progression of CSF markers.

Role of CD36 rs1761667 AA genotype in the expression of inflammatory cytokines and Parkinson's disease progression: A case-control study in a northern Han Chinese population.

OBJECTIVE: This study aimed to investigate the effect of CD36 rs1761667 gene polymorphisms on the expression of CD36 and inflammatory cytokines and the progression of Parkinson's disease (PD). METHODS: A total of 138 patients with PD (60 men and 78 women) and 132 healthy controls (48 men and 84 women) from a northern Han Chinese population were enrolled in this case-control study. Polymerase chain reaction-restriction fragment length polymorphism was used to detect the CD36 rs1761667 genotype. An enzyme-linked immunosorbent assay was used to determine the expression of CD36, interleukin (IL)-6, IL-1ß, and tumor necrosis factor (TNF)-α in the plasma. RESULTS: The frequency of the rs1761667 AA genotype was significantly higher in patients with PD than that in healthy controls, suggesting AA genotype to be a risk factor for PD. When compared with those in healthy controls, CD36 levels were significantly lower in patients with PD, whereas IL-6, IL-1ß, and TNF-α levels were significantly higher in patients with PD. Furthermore, GA and AA carriers with PD showed lower levels of CD36, and GG, GA, and AA carriers showed higher levels of IL-6, IL-1ß, and TNF-α than those in healthy controls. In the PD patient group, AA and GA carriers had lower expression levels of CD36 than GG carriers did, and CD36 levels were lower in AA carriers than in GA carriers. Conversely, AA carriers had elevated expression levels of IL-6 compared with that of GG and GA carriers. Logistic regression analysis revealed that IL-6, IL-1ß, and TNF-α levels were risk factors for PD in a northern Han Chinese population. CONCLUSION: The CD36 rs1761667 AA genotype may increase susceptibility to PD and the expression of inflammatory cytokines.

Incidence and mortality rates of lung cancer in Qingdao, China (2013-2017).

AIMS: To analyze lung cancer incidence and mortality rates from 2013 to 2017 in Qingdao, Shandong Province, China. METHODS: The lung cancer new cases and death data during 2013-2017 were collected from the Qingdao Cancer Surveillance System. The crude incidence and mortality rates were calculated by residential area and gender. The annual percentage change (APC) was determined to evaluate the incidence and mortality rate trends. RESULTS: Between 2013 and 2017, 31 653 new lung cancer cases and 24 965 deaths from lung cancer were retrieved. The age-standardized incidence rates by Chinese standard population (ASIRC) were 42.1 per 100 000. The crude incidence rates for men and women increased from 85.2 and 46.3 per 100 000 in 2013 to 124.0 and 67.4 per 100 000 in 2017, respectively. The APCs were 7.8% for men (P < .001) and 7.5% (P = .027) for women. The crude mortality rates increased from 56.3 per 100 000 in 2013 to 68.0 per 100 000 in 2017. The age-standardized mortality rates by ASIRC were 32.3 per 100 000. The APCs of mortality rates were higher in men than in women and were higher in rural than in urban areas. Age-specific incidence and mortality rates were lower in individuals aged <40 years, increased sharply in those aged >40 years, and were the highest in 80-year-old individuals. CONCLUSION: These data show different patterns of incidence and mortality rate according to gender and resident area during 2013-2017. Early screening and targeted prevention should be implemented to control the increased trend of lung cancer.

Biallelic XPR1 mutation associated with primary familial brain calcification presenting as paroxysmal kinesigenic dyskinesia with infantile convulsions.

BACKGROUND: Mutations in the XPR1 gene are associated with primary familial brain calcifications (PFBC). All reported mutations are missense and inherited as an autosomal dominant trait. PFBC patients exhibited movement disorders, neuropsychiatric symptoms, and other associated symptoms with diverse severity, even within the same family. MATERIALS AND METHODS: We identified and enrolled a patient with PFBC. Clinical data were comprehensively collected, including the age of onset, seizure types and frequency, trigger factors of paroxysmal dyskinesia, response to drugs, and general and neurological examination results. Whole-exome sequencing (WES) was performed to detect pathogenic variants. We further systematically reviewed the phenotypic and genetic features of patients with XPR1 mutations. RESULTS: The patient showed bilateral calcification involving basal ganglia and cerebellar dentate. Clinically, he presented as paroxysmal kinesigenic dyskinesia with infantile convulsions (PKD/IC) with favorable outcome. We identified a compound heterozygous XPR1 mutation (c.786_789delTAGA/p.D262Efs*6, c.1342C>T/p.R448W), which were inherited from unaffected parents respectively. Further literature review shows a wide range of clinical manifestations of patients with XPR1 mutations, with movement disorders being the most common. CONCLUSIONS: This is the first report of biallelic mutations in XPR1. The findings suggest for the first time a possible link between PKD/IC and XPR1 mutations.

Overexpression of circARF3 mitigates TNF-α-induced inflammatory damage by up-regulating miR-125b.

Encephalitis is the highest disability illness. We studied the function and mechanisms of circular RNA circARF3 (circARF3) in neurocyte cell inflammatory damage. CCK-8 assay and flow cytometry were, respectively, employed for examining the influences of tumor necrosis factor α (TNF-α), circARF3 and microRNA (miR)-125b on cell viability and apoptosis. The expression of circARF3 and miR-125b were changed by employing cell transfection and the results were determined by using qRT-PCR. Besides, the expression of Bcl-2, Bax, Cleaved-caspase-3, interleukin (IL)-1ß, IL-6, IL-8 and cell pathways-related proteins were examined by using Western blot. The productions of IL-6, IL-8 and IL-1ß were also tested by ELISA. The level of reactive oxygen species (ROS) was examined by ROS assay. We found that TNF-α caused inflammatory damage showing as suppressed cell viability, enhanced cell apoptosis, and increased cytokines production and ROS generation. Besides, TNF-α inducement also markedly reduced circARF3 expression. circARF3 overexpression mitigated TNF-α-induced cell inflammatory damage. Moreover, miR-125b was targeted and positively regulated by circARF3. Furthermore, miR-125b inhibition could reverse the influences of circARF3 overexpression. Besides, circARF3 restrained the JNK and NF-κB pathways by up-regulation of miR-125b. In conclusion, overexpression of circARF3 mitigated cell inflammatory damage via inactivation of JNK and NF-κB pathways and thereby up-regulation of miR-125b.

Association of rs356219 and rs3822086 polymorphisms with the risk of Parkinson's disease: A meta-analysis.

Numerous case-control studies have investigated the relationship between rs356219 and rs3822086 polymorphisms and Parkinson's disease (PD) susceptibility. However, these publications have obtained contradictory results. In this study, we conducted a meta-analysis to evaluate the possible association between the two polymorphisms and PD. Literature searches were conducted on PubMed, Web of Science, EMBASE, CNKI and the Wanfang database on studies published until March 2019. Authentic data were calculated utilizing STATA 12.0 statistics software on the data provided in each study. The genetic association between SNCA polymorphisms and the risk of PD was evaluated using the pooled odds ratios (OR) and 95% confidence interval (CI). The results indicate that there is a significant association between rs356219 polymorphism and PD susceptibility for all genetic models (allelic: OR = 1.377, 95% CI: 1.275-1.487, p = 0.000; homozygous: OR = 1.958, 95% CI: 1.666-2.301, p = 0.000; heterozygous: OR = 1.261, 95% CI: 1.158-1.373, p = 0.000; dominant: OR = 1.431, 95% CI: 1.320-1.550, p = 0.000; recessive: OR = 1.632, 95% CI: 1.431-1.861, p = 0.000), which is consistent with the results of the subgroup analyses on Asians and Caucasians. In addition, rs3822086 polymorphism was found to be related to PD in the allelic (OR = 1.249, 95% CI: 1.099-1.419, p = 0.001), homozygous (OR = 1.479, 95% CI: 1.142-1.915, p = 0.003), heterozygous (OR = 1.292, 95% CI: 1.033-1.615, p = 0.025) and dominant (OR = 1.331, 95% CI: 1.030-1.719, p = 0.029) models. Therefore, our results suggest that the presence of SNCA rs356219 and rs3822086 variants may increase the risk of PD.

Relationship between mitochondrial DNA A10398G polymorphism and Parkinson's disease: a meta-analysis.

Many studies have researched the mitochondrial DNA (mtDNA) A10398G in Parkinson's disease (PD) to determine the association between mtDNA A10398G and PD, but the results of their research were not consistent. Therefore, we performed a meta-analysis to demonstrate the connection between mtDNA A10398G and the susceptibility of PD. We searched PubMed, Web of Science, Springer Link, EMBASE and EBSCO databases up to identify relevant studies. Through strict inclusion and exclusion criteria, at last, 9 studies (total 3381 cases and 2810 controls) were included in our meta-analysis. We used the STATA 12.0 statistics software to calculate the pooled odds ratios (ORs) and 95% confidence intervals (CIs) to evaluate the genetic association between mtDNA A10398G and the risk of PD. We performed subgroup analysis to clarify the possible roles of the mtDNA A10398G polymorphism in the aetiology of PD in different ethnicities. Our meta-analysis indicates that although there was no significant association between mtDNA A10398G and PD in the Asian population (G vs. A: OR = 1.090, 95% CI = 0.939-1.284, P = 0.242), in the Caucasian population the G allele of mtDNA A10398G mutations may be a potential protective factor of PD (G vs. A: OR = 0.699, 95% CI = 0.546-0.895, P = 0.005). Further well-designed studies with larger samples are needed to validate these results.

Association between SNCA rs2736990 polymorphism and Parkinson's disease: a meta-analysis.

Emerging evidence suggests that the SNP rs2736990 of SNCA is a susceptibility factor for idiopathic Parkinson's disease (PD) in different populations, but the studies which examined the association have provided inconsistent results. Therefore, we performed a meta-analysis of some case-control studies to obtain a more exact estimation of there associations. All the relevant studies were extracted from PubMed, Embase, EBSCO, Chineses national knowledge infrastructure, Google Scholar and Wanfang databases (up to February 2017). A total of six studies with 2525 PD cases and 2165 controls were eventually enrolled in the present meta-analysis based on the strict inclusion and exclusion criteria. The pooled analysis showed that there is a significant association between rs2736990 polymorphism and PD susceptibility in all genetic models (T vs. C: OR=0.772, 95%CI: 0.709-0.840, P=0.001; TT vs. CC: OR=0.586, 95%CI: 0.490-0.701, P=0.001; TC vs. CC: OR=0.814, 95%CI: 0.716-0.925, P=0.002; TT+TC vs. CC: OR=0.752, 95%CI: 0.666-0.848, P=0.001; TT vs. TC+CC: OR=0.658, 95%CI: 0.561-0.772, P=0.001). Our meta-analysis provides evidence that the T allele, TT and TC genotype of rs2736990(C/T) polymorphism may decrease the risk of PD.