The association between CD157/BST1 polymorphisms and the susceptibility of Parkinson’s disease: a meta-analysis

References

• Nakano N, Matsuda S, Ichimura M, et al. PI3K/AKT signaling mediated by G protein-coupled receptors is involved in neurodegenerative Parkinson‘s disease (Review). Int J Mol Med. 2017;39(2):253–260.28000847
   PubMed Web of Science ®Google Scholar
• Katunina EA, Bezdolny YN. [Epidemiology of Parkinson’s disease]. Zh Nevrol Psikhiatr Im S S Korsakova. 2013;113(12):81–88.
   Google Scholar
• Bonuccelli U, Del DP. New pharmacologic horizons in the treatment of Parkinson disease. Neurology. 2006;67(2):30–38. doi:10.1212/WNL.67.7_suppl_2.S30
   Web of Science ®Google Scholar
• Wakabayashi K, Tanji K, Odagiri S, Miki Y, Mori F, Takahashi H. The Lewy body in Parkinson‘s disease and related neurodegenerative disorders. Mol Neurobiol. 2013;47(2):495–508. doi:10.1007/s12035-012-8280-y22622968
   PubMed Web of Science ®Google Scholar
• Trinh J, Farrer M. Advances in the genetics of Parkinson disease. Nat Rev Neurol. 2013;9:445–454. doi:10.1038/nrneurol.2013.132
   Web of Science ®Google Scholar
• Kasai S, Yoshihara T, Lopatina O, et al. Selegiline ameliorates depression-like behavior in mice lacking the CD157/BST-1 gene, a risk factor for Parkinson’s disease. Front Behav Neurosci. 2017;11:75. doi:10.3389/fnbeh.2017.0024628515684
   PubMed Web of Science ®Google Scholar
• Fleming SM. Mechanisms of gene-environment interactions in Parkinson’s disease. Curr Envir Health Rpt. 2017;4(2):192–199. doi:10.1007/s40572-017-0143-2
   Google Scholar
• Spencer CC, Plagnol V, Strange A, et al. Dissection of the genetics of Parkinson‘s disease identifies an additional association 5ʹ of SNCA and multiple associated haplotypes at 17q21. Hum Mol Genet. 2011;20(2):345–353. doi:10.1093/hmg/ddq46921044948
   PubMed Web of Science ®Google Scholar
• Soto-Ortolaza AI, Heckman MG, Labbé C, et al. GWAS risk factors in Parkinson‘s disease: LRRK2 coding variation and genetic interaction with PARK16. Am J Neurodegener Dis. 2013;2(4):287–299.24319646
   PubMedGoogle Scholar
• Tan EK, Kwok HK, Tan LC, et al. Analysis of GWAS-linked loci in Parkinson disease reaffirms PARK16 as a susceptibility locus. Neurology. 2010;75(6):508–512. doi:10.1212/WNL.0b013e3181eccfcd20697102
   PubMed Web of Science ®Google Scholar
• Wan JY, Edwards KL, Hutter CM, et al. Association mapping of the PARK10 region for Parkinson‘s disease susceptibility genes. Parkinsonism Relat Disord. 2014;20(1):93–98. doi:10.1016/j.parkreldis.2013.10.00124156912
   PubMed Web of Science ®Google Scholar
• Sharma M, Maraganore DM, Ioannidis JP, et al. Role of sepiapterin reductase gene at the PARK3 locus in Parkinson‘s disease-neurobiology of aging. Neurobiol Aging. 2011;32(11):2108.e1-2108.e5. doi:10.1016/j.neurobiolaging.2011.05.024
   Web of Science ®Google Scholar
• Hamza TH, Zabetian CP, Tenesa A, et al. Common genetic variation in the HLA region is associated with late-onset sporadic Parkinson’s disease. Nat Genet. 2010;42(9):781–785. doi:10.1038/ng.64220711177
   PubMed Web of Science ®Google Scholar
• Maraganore DM, de Andrade AM, Lesnick TG, et al. High-resolution whole-genome association study of Parkinson disease. Am J Hum Genet. 2005;77(5):685–693. doi:10.1086/49690216252231
   PubMed Web of Science ®Google Scholar
• Zhu L-H, Luo X-G, Zhou Y-S, et al. Lack of association between three single nucleotide polymorphisms in the PARK9, PARK15, and BST1 genes and Parkinson‘s disease in the northern Han Chinese population. Chin Med J (Engl). 2012;125(4):588–592.22490479
   PubMed Web of Science ®Google Scholar
• Ahmed I, Tamouza R, Delord M, et al. Association between Parkinson‘s disease and the HLA-DRB1 locus. Mov Disord. 2012;27(9):1104–1110. doi:10.1002/mds.2503522807207
   PubMed Web of Science ®Google Scholar
• Li N-N, Tan E-K, Chang X-L, et al. Genetic association study between STK39 and CCDC62/HIP1R and Parkinson‘s disease. PLoS One. 2013;8(11):e79211. doi:10.1371/journal.pone.007921124312176
   PubMed Web of Science ®Google Scholar
• Liu X, Cheng R, Verbitsky M, et al. Genome-wide association study identifies candidate genes for Parkinson‘s disease in an Ashkenazi Jewish population. BMC Med Genet. 2011;12(1):104. doi:10.1186/1471-2350-12-10421812969
   PubMed Web of Science ®Google Scholar
• Ferrero E, Buono NL, Morone S, et al. Human canonical CD157/Bst1 is an alternatively spliced isoform masking a previously unidentified primate-specific exon included in a novel transcript. Sci Rep. 2017;7(1):15923. doi:10.1038/s41598-017-16184-w29162908
   PubMed Web of Science ®Google Scholar
• Satake W, Nakabayashi Y, Mizuta I, et al. Genome-wide association study identifies common variants at four loci as genetic risk factors for Parkinson‘s disease. Nat Genet. 2009;41(12):1303–1307. doi:10.1038/ng.48519915576
   PubMed Web of Science ®Google Scholar
• Saad M, Lesage S, Saintpierre A, et al. Genome-wide association study confirms BST1 and suggests a locus on 12q24 as the risk loci for Parkinson‘s disease in the European population. Hum Mol Genet. 2011;20(3):615–627. doi:10.1093/hmg/ddq49721084426
   PubMed Web of Science ®Google Scholar
• Chang X-L, Mao X-Y, Li H-H, et al. Association of GWAS loci with PD in China. Am J Med Genet B Neuropsychiatr Genet. 2011;156(3):334–339. doi:10.1002/ajmg.b.v156.3
   Web of Science ®Google Scholar
• Chang KH, Wu YR, Chen YC, et al. STK39, But Not BST1, HLA-DQB1, and SPPL2B Polymorphism, Is Associated With Han-Chinese Parkinson‘s Disease in Taiwan. Medicine. 2015;94(41):e1690. doi:10.1097/MD.000000000000087426469904
   PubMed Web of Science ®Google Scholar
• Sharma M, Ioannidis JPA, Aasly JO, et al. Large-scale replication and heterogeneity in Parkinson disease genetic loci. Neurology. 2012;79(7):659–667. doi:10.1212/WNL.0b013e318264e35322786590
   PubMed Web of Science ®Google Scholar
• Simón-Sánchez J, van Hilten JJ, van de Warrenburg B, et al. Genome-wide association study confirms extant PD risk loci among the Dutch. Eur J Hum Genet. 2011;19(6):655–661. doi:10.1038/ejhg.2010.25421248740
   PubMed Web of Science ®Google Scholar
• Cui C, Liu WG, Hua P, et al. Association of BST1 gene polymorphism with Parkinson‘s disease risk in Chinese population. Chin J Clin Neurosci 2018;16(1):1–8.
   Google Scholar
• Chen M-L, Lin C-H, Lee M-J, Wu R-M. BST1 rs11724635 interacts with environmental factors to increase the risk of Parkinson‘s disease in a Taiwanese population. Parkinsonism Relat Disord. 2014;20(3):280–283. doi:10.1016/j.parkreldis.2013.11.00924342025
   PubMed Web of Science ®Google Scholar
• Miyake Y, Tanaka K, Fukushima W, et al. Lack of association between BST1 polymorphisms and sporadic Parkinson‘s disease in a Japanese population. J Neurol Sci. 2012;323(1–2):162–166. doi:10.1016/j.jns.2012.09.00823026536
   PubMed Web of Science ®Google Scholar
• Harms M. The EQUATOR network and the PRISMA statement for the reporting of systematic reviews and meta-analyses. Physiotherapy. 2009;95(4):237–240. doi:10.1016/j.physio.2009.10.00119892087
   PubMed Web of Science ®Google Scholar
• Han Y, Xia Z, Guo S, Yu X, Li Z, Sung S-Y. Laparoscopically assisted anorectal pull-through versus posterior sagittal anorectoplasty for high and intermediate anorectal malformations: a systematic review and meta-analysis. PLoS One. 2017;12:e0170421. doi:10.1371/journal.pone.017042128099464
   PubMed Web of Science ®Google Scholar
• Tian JY. Polymorphism Analysis of PARK16, PARK17, PARK18, BST1 and Polygenic Determinants Analysis of Parkinson‘S Disease. Changsha: Central South University; 2012.
   Google Scholar
• Xie D. The Study of Relationship between polymorPhism in BSTI Gene Rs4698412 and Sporadic Parkinson‘S Disease. Hengyang: University of South China; 2011.
   Google Scholar
• Ishihara K, Hirano T. BST-1/CD157 regulates the humoral immune responses in vivo. Chem Immunol. 2004;75(4):235–255.
   Google Scholar
• Yokoyama S, Mahmuda NA, Munesue T, et al. Association study between the CD157/BST1 gene and autism spectrum disorders in a Japanese population. Brain Sci. 2015;5(2):188–200. doi:10.3390/brainsci502018826010484
   PubMedGoogle Scholar
• Sassi C. Genetics of Parkinson disease. Neurorx. 2004;1(2):235–242. doi:10.1602/neurorx.1.2.23515717024
   PubMedGoogle Scholar
• Chung SJ, Jung Y, Hong M, et al. Alzheimer‘s disease and Parkinson‘s disease genome-wide association study top hits and risk of Parkinson‘s disease in Korean population. Neurobiol Aging. 2013;34(11):2695.e. doi:10.1016/j.neurobiolaging.2012.06.026
   Web of Science ®Google Scholar
• Higashida H, Liang M, Yoshihara T, et al. An immunohistochemical, enzymatic, and behavioral study of CD157/BST-1 as a neuroregulator. BMC Neurosci. 2017;18:35. doi:10.1186/s12868-017-0350-728340569
   PubMed Web of Science ®Google Scholar
• Baralle D, Baralle M. Splicing in action: assessing disease causing sequence changes. J Med Genet. 2005;42:737–748. doi:10.1136/jmg.2004.02953816199547
   PubMed Web of Science ®Google Scholar
• Buratti E, Baralle M, Baralle FE. Defective splicing, disease and therapy: searching for master checkpoints in exon definition. Nucleic Acids Res. 2006;34:3494–3510. doi:10.1093/nar/gkl49816855287
   PubMed Web of Science ®Google Scholar