عنوان
پدید آورنده
موضوع
رده
کتابخانه
محل استقرار
IR
۲۲۶۷پ
فارسی
IR
بررسی ارتباط پلی مورفیسم های ژن های GSTM1, GSTT1,GSTP1(rs1695)با بیماری آلزایمر اسپورادیک در جمعیت ایرانی
[پایان‌نامه]
Association study between GSTM1, GSTT1, GSTP1(rs1695) gene polymorphisms and late-onset (sporadic) Alzheimers disease in Iranian population
علوم بهزیستی و توانبخشی University of Social Welfare and Rehabilitation))
، ۱۳۹۵
ر،۱۰۶ص.
چاپی
کارشناسی ارشد
ژنتیک انسانی Genetics Human
علوم بهزیستی و توانبخشی University of Social Welfare and Rehabilitation))
,ه ,هA, Karhunen P. GlutathioneSTransferase GST M1 Null Genotype and the Risk of Alcoholic Liver Disease. Alcoholism: Clinical and Experimental Research. 1996;20(8):1340-5. 81.Duncan H, Swanx C, Green J, Jones P, Brannigan K, Alldersea J, et al. Susceptibility to ulcerative colitis and Crohn's disease: interactions between glutathione S-transferase GSTM1 and GSTT1 genotypes. Clinica chimica acta. 1995;240(1):53-61. 82.Fraser PA, Ding W-Z, Mohseni M, Treadwell EL, Dooley MA, St Clair EW, et al. Glutathione S-transferase M null homozygosity and risk of systemic lupus erythematosus associated with sun exposure: a possible gene-environment interaction for autoimmunity. The Journal of rheumatology. 2003;30(2):276-82. 83.Agrawal S, Tripathi G, Khan F, Sharma R, Pandirikkal Baburaj V. Relationship between GSTs gene polymorphism and susceptibility to end stage renal disease among North Indians. Renal failure. 2007;29(8):947-53. 84.Datta SK, Kumar V, Pathak R, Tripathi AK, Ahmed RS, Kalra OP, et al. Association of glutathione S-transferase M1 and T1 gene polymorphism with oxidative stress in diabetic and nondiabetic chronic kidney disease. Renal failure. 2010;32(10):1189-95. 85.Zhong S, Wyllie A, Barnes D, Wolf C, Spurr N. Relationship between the GSTM1 genetic polymorphism and susceptibility to bladder, breast and colon cancer. Carcinogenesis. 1993;14(9):1821-4. 86.AZIZIAN M, YAGHMAEI B, KHOSRAVI A. BREAST CANCER AND GLUTATHIONE S-TRANSFERASE GENETIC POLYMORPHISM. 2009. 87.Spalletta G, Bernardini S, Bellincampi L, Federici G, Trequattrini A, Ciappi F, et al. Glutathione S-transferase P1 and T1 gene polymorphisms predict longitudinal course and age at onset of Alzheimer disease. The American Journal of GeriaPaola. Glutathione S-transferase P1 and T1 gene polymorphisms predict longitudinal course and age at onset of Alzheimer disease. The American Journal of Geriatric Psychiatry. 2007; 15(10): 879-887 100. Bernardini, Sergio Bellincampi, Lorenza Ballerini, Sabrina Federici, Giorgio Iori, Roberta Trequattrini, Alberto Ciappi, Fabrizio Baldinetti, Francesca Bossr, AA. The glutathione S-transferases: influence of polymorphism on cancer susceptibility. IARC scientific publications. 1998; 148: 231-249 108. Wang, Dan Zhai, Jun-Xia Zhang, Li-Mei Liu, Dian-Wu. Null genotype of GSTT1 contributes to increased Parkinsons disease risk in Caucasians: evidence from a meta-analysis. Molecular biology reports. 2014; 41(11): 7423-7430 109. Cho, Ssang-Goo Lee, Yong Hee Park, Hee-Sae Ryoo, Kanghyun Kang, Keon Wook Park, Jihyun Eom, Soo Jung Kim, Myung Jin Chang, Tong-Shin Choi, Soo-Yeon. Glutathione S-transferase mu modulates the stress-activated signals by suppressing apoptosis signal-regulating kinase 1. Journal of Biological Chemistry. 2001; 276(16): 12749-12755 110. Dorion, Sonia Lambert, Herman Landry, Jacques. Activation of the p38 signaling pathway by heat shock involves the dissociation of glutathione S-transferase Mu from Ask1. 2002; 277(34): 30792-30797 111. McIlwain, CC Townsend, DM Tew, KD. Glutathione S-transferase polymorphisms: cancer incidence and therapy. Oncogene. 2006; 25(11): 1639-1648
.Abstract Objective: Evidence suggests that oxidative stress plays a role in several stages of the neurodegenarative disease like Alzheimer's disease. Free radicals and similar molecules are classified as reactive oxygen species (ROS) can cause oxidative modifications in the cell. Oxidative stress is a condition that cell antioxidant defense can not cope with ROS products. Central nervous system (CNS) is particularly vulnerable to oxidative stress, by oxidative metabolism due to factors (high oxygen levels, low levels of antioxidants and related enzymes). Polymorphisms in genes that are involved in the metabolism and metabolic detoxification such as ROS and also change the capacity of the antioxidant system, can make a difference in DNA damage level.so, oxidative stress condition, can lead to Alzheimer's disease. In this study we have focused our attention on the cytosolic GST gene family that comprises multiple isoenzymes. In particular, we have investigated polymorphisms of cytosolic GST genes including nullity of GSTT1 and GSTM1, GSTP1(rs1695) associated with functional changes in catalytic activity and/or enzyme expression in order to evaluate the AD risk for these genetic variants in Iranian population. Methods and materials: The patient group consisted of 280 cases for GSTP1 gene and 215 cases for GSTT1 and GSTM1 investigations whose Alzheimer disease had been approved by psychologists based on clinical test (DSM-IV) and the control group included 168 healthy individuals for GSTP1 gene and 158 healthy individuals for GSTT1 and GSTM1 investigations, satisfying the condition of not having any psychological disorders. Individuals genotype have been determined by PCR-RFLP method.statistical analysis were done using OpenEpi 2.3.1 and SPSS 16 and logestic regression. Results: Significant association observed between heterozygote genotype (AG) rs1695 A/G of GSTP1 gene and the risk of Alzheimer disease (P: 0.005, OR: 0.57(0.38_0.84)).this genotype is doing as protective factor.also this result observed in gender assess within women group. (P: 0.02) Further, Differences in genotype distributions between AD patients and controls were found for the GSTT1 null genotype (P: 0.038, OR: 1.65(1.03_2.66)) and GSTM1 null genotype (P<0.001, OR: 3.6(2.2_6)). also this result observed in gender assess within men group. (P<0.001) We found a Significant interaction between heterozygote genotype (AG) rs1695 A/G of GSTP1 gene (protective factor) and absent 4 allele in our study group(P: 0.001).in addition, there was a Significant interaction between GSTM1 null deletion polymorphism and present 4 allele in our research. (P: 0.000) Discussion: Considering our result, we suggest heterozygote genotype (AG) rs1695 A/G of GSTP1 gene, GSTT1 null genotype and GSTM1 null genotype can acting as a risk factor for AD in Iranian population.regarding to high OR for GSTM1 null genotype, we need more comprehensive and functional research in terms of more clear information of relationship between stress oxidative correlated genes and Alzheimer disease خ‌یرات و ءاضما ی‌گداوناخ م‌ان و م‌ان . م‌راد ی‌م م‌لاعا ق‌یقحت ن‌یا رد م‌رامیب ت‌کرش اب ار دوخ ت‌قفاوم ، ق‌یقحت طیارش و ف‌ادها زا ع‌لاطا اب و ه‌دومن ه‌علاطم ار ق‌وف ب‌لاطم ه‌یلک . . . . . . . . . . . . . . . . . . . . . .م‌ناخ/ی‌اقآ رامیب م‌یق ب‌ناجنیا دش دهاوخ ل‌اسرا ت‌نوکس ل‌حم زکرم ه‌ب ،ک‌یتنژ و ی‌لوکلوم ی‌اهشیامزآ ج‌یاتن .دوب دهاوخ م‌ان ن‌ودب اهنآ زا ه‌دافتسا و ه‌دنام ه‌نامرحم لاماک امش رامیب زا ه‌دش ب‌سک ت‌اعلاطا .دشاب ی‌م ه‌نابلطواد ه‌علاطم ن‌یا رد ت‌کرش .دشابیم) ت‌بون ک‌ی طقف( ،ج‌لاعم ک‌شژپ رظن ت‌حت ی‌دیرو ن‌وخ رتیل ی‌لیم5 رثکادح ن‌داد و ل‌اوس دنچ ه‌ب خ‌ساپ ،رامیب ه‌دنورپ ه‌ب ه‌عجارم دنمزاین ش‌هوژپ ن‌یا رد ی‌راکمه .دیدرگ دنهاوخ ه‌علاطم دراو ،ن‌دوب طیارش دجاو ت‌روصرد و ه‌تفرگ رارق ی‌سررب دروم دورو ی‌اهرایعم ی‌خرب رظن زا ادتبا رد دارفا ه‌یلک .دزادرپب رمیازلآ ی‌رامیب رد ن‌ژ دنچ ش‌قن ی‌سررب ه‌ب دراد دصق ه‌ک دومن دهاوخ ت‌کرش ی‌ا ه‌علاطم رد امش رامیب رامیب م‌یق ه‌مان ت‌یاضر م‌رف خ‌یرات و ءاضما ی‌گداوناخ م‌ان و م‌ان . م‌راد ی‌م م‌لاعا ق‌یقحت ن‌یا رد ت‌کرش اب ار دوخ ت‌قفاوم ، ق‌یقحت طیارش و ف‌ادها زا ع‌لاطا اب و ه‌دومن ه‌علاطم ار ق‌وف ب‌لاطم ه‌یلک . . . . . . . . . . . . . . . . . . . . . .م‌ناخ/ی‌اقآ ب‌ناجنیا دش دهاوخ ل‌اسرا ت‌نوکس ل‌حم زکرم ه‌ب ،ک‌یتنژ و ی‌لوکلوم ی‌اهشیامزآ ج‌یاتن .دوب دهاوخ م‌ان ن‌ودب اهنآ زا ه‌دافتسا و ه‌دنام ه‌نامرحم لاماک امش زا ه‌دش ب‌سک ت‌اعلاطا .دشاب ی‌م ه‌نابلطواد ه‌علاطم ن‌یا رد ت‌کرش .دشابیم) ت‌بون ک‌ی طقف( ،ج‌لاعم ک‌شژپ رظن ت‌حت ی‌دیرو ن‌وخ رتیل ی‌لیم5 رثکادح ن‌داد و ل‌اوس دنچ ه‌ب خ‌ساپ ،رامیب ه‌دنورپ ه‌ب ه‌عجارم دنمزاین ش‌هوژپ ن‌یا رد ی‌راکمه .دیدرگ دنهاوخ ه‌علاطم دراو ،ن‌دوب طیارش دجاو ت‌روصرد و ه‌تفرگ رارق ی‌سررب دروم دورو ی‌اهرایعم ی‌خرب رظن زا ادتبا رد دارفا ه‌یلک .دزادرپب رمیازلآ ی‌رامیب رد ن‌ژ دنچ ش‌قن ی‌سررب ه‌ب دراد دصق ه‌ک دومن دیهاوخ ت‌کرش ی‌ا ه‌علاطم رد امش رامیب ه‌مان ت‌یاضر م‌رف )2(68 ;2002 .y5yShS enil llec amotsalboruen namuh no edisopote fo tceffe eht gnitaidem ni 11P TSG fo eloR .G ,iciredeF C ,esetroC A ,erotsaP M ,illanaR S ,inirellaB L ,ipmacnilleB S ,inidranreB .601 461-751 :)1(77 ;1002 .yrtsimehcoruen fo lanruoJ .noitavitca esanik lanimretN nuJc seriuqer sisotpopa lanoruen decudnidiolymA .A dyolL ,eneerG L leahciM ,iksnalehS J samohT ,sronnoC C annA ,yenoraM gnehihZ ,uX A aivlyS ,ihccabaR M loraC ,yorT .501 0657-1557 ;)91(12 ;1002 .ecneicsorueN fo lanruoJ ehT .dnagil saF fo noitcudni eht dna yawhtap esanik lanimret-N nuJ-c eht sevlovni taht msinahcem a aiv sisotpopa lanoruen secudni diolymA- .E leahciM ,grebneerG imufusaY ,ikasarihS J regoR ,sivaD drahciR ,llevalF ihcimoriH ,onakaT aremaT ,tterraB eninaJ ,geiZ okikuY ,hotoG ikuyihsoY ,amihsiroM .401 541-731 :)2(71 ;1002 .ecneicsorueN raluceloM fo lanruoJ .esaesid sremiehzlA ni sisenegohtap dna noitalumucca diolyma fo smsinahcem ralullecartnI .selrahC ,ebalG .301 63-922 : )2(72 ;9002 .lotamuehR pxE nilC .sitirhtra diotamuehr fo ytivitca esaesid dna sesarefsnart-S enoihtatulg fo smsihpromylop citeneG .V ,nazloD alB ,namzoR M ,cismoT nauD ,ragoL cenahoB P ,rabarG .201 075-565 :)9(55 ;0102 .sciteneg namuh fo lanruoJ .ytilitrefni elam cihtapoidi htiw )1PTSG ,1TTSG ,1MTSG( smsihpromylop eneg esarefsnart-S-enoihtatulg fo noitaicossa ehT .avihS ,dajenirafaS reyyaN ,ieifahS azeR dammahoM ,dajenirafaS .101 159-449 :)6(15 ;5002 .yrtsimehc lacinilC .elella 4 E nietorpopilopa htiw pihsnoitaler dna yduts noitaicossa :esaesid remiehzlA tesno-etal rof ytilibitpecsus sesaercni tnairav cilella C *1P esarefsnart-S enoihtatulG .olraC ,enorigatlaC aloaP:
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Association study between GSTM1, GSTT1, GSTP1(rs1695) gene polymorphisms and late-onset (sporadic) Alzheimers disease in Iranian population
بیماری آلزایمر دیررس
Alzheimer’s disease
بیماری آلزایمر دیررس
جعفریان، زهرا
Jafarian,Zahra
خرم خورشید، حمیدرضا
ایران
دانشگاه علوم توان بخشی و سلامت اجتماعی
20210626
محل نگهداری: دانشگاه علوم بهزیستی و توانبخشی
نمایه‌سازی قبلی
چاپی-الکترونیکی
TF
92029
1
a
Y
