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Research process of glucose transpoter 1 in Alzheimers disease |
LI Weiping1 ZHANG Lei2 SHEN Yanfang2 DU Jumei2 |
1.Shaanxi University of Traditional Chinese Medicine, Shaanxi Province, Xianyang 712046, China;
2.Department of Neurology, the Second Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Shaanxi Province, Xianyang 712046, China |
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Abstract Alzheimers disease (AD) is the most common type of dementia in the elderly. The incidence of Alzheimers disease is increasing year by year. At present, the pathogenesis of Alzheimers disease has not been fully elucidated and there is no effective preventive and therapeutic measures. Glucose transporter 1 (GLUT1) is a glucose transporter expressed mainly in the blood-brain barrier endothelial cells, which transports blood glucose to the brain tissue along the blood-brain barrier and provides energy for metabolism of brain cells. It is concluded that the expression of GLUT1 in the blood-brain barrier endothelial cells of AD patients is decreased, which may be related to the pathogenesis and pathological damage of AD. GLUT1 play a important role in the damage of blood-brain barrier integrity, amyloid β-peptide (Aβ) clearance and phosphorylation of tau. By reviewing relevant literatures in recent years, we hope to explore the GLUT1 in AD to provide a reference.
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[1] Hellstrom-Lindahl E,Viitaen M,MarutleA. Comparison of Aβ levels in the brain of familial and sporadic Alzheimer′s disease [J]. Neurochem Inter,2009,55(4):243-252.
[2] Mayeux R,Stern Y. Epidemiology of Alzheimer disease [J]. Cold Spring Harb Perspect Med,2012,2(8):-a006239.
[3] Prince M,Brycea R,Albanesea E,et al. The global prevalence of dementia:a systematic review and meta analysis [J]. Alzheimers Dement,2013,9(1):63-75.
[4] Thies W,Bleiler L,Alzheimer's Association. 2013 Alzheimer's disease facts and figures [J]. Alzheimers Dement,2013,9(2):208-245.
[5] Jia J,Wang F,Wei C,et al. The prevalence of dementia in urban and rural areas of China [J]. Alzheimers Dement,2014,10(1):1-9.
[6] 赵鹏,孙亚平,陈红.阿尔茨海默病发病机制探究[J].中风与神经疾病杂志,2016,33(1):86-89.
[7] Alzheimer′s Association. Alzheimer′s disease facts and figures [J]. Alzheimers Dement,2014,10(2):e47-e92.
[8] Zlokovic BV. The blood-brain barrier in health and chronic neurodegenerative disorders [J]. Neuron,2008,57(2):178-201.
[9] Winkler EA,Nishida Y,Sagare AP,et al. GLUT1 reductions exacerbate Alzheimer's disease vasculo-neuronal dysfunction and degeneration [J]. Nat Neurosci,2015,18(4):521-530.
[10] Olson AL,Pessin JE. Structure,function,and regulation of the mammalian facilitative glucose transporter gene family [J]. Annu Rev Nutr,1996,16:235-256.
[11] Allen A,Messier C. Plastic changes in the astrocyte GLUT1 glucose transporter and beta-tubulin microtubule protein following voluntary exercise in mice [J]. Behav Brain Res,2013,240:95-102.
[12] Deng D,Xu C,Sun P,et al. Crystal structure of the human glucose transporter GLUT1 [J]. Nature,2014,510(7503):121-125.
[13] Garg M,Thamotharan M,Becker DJ,et al. Adolescents with clinical type 1 diabetes display reduced red blood cell glucose transporter isoform 1(GLUT1)[J]. Pediatr Diabetes,2014,15(7):511-518.
[14] Sage JM,Carruthers A. Human erythrocytes transport dehydroascorbic acid and sugars using the same transporter complex [J]. Am J Physiol Cell Physiol,2014,306(10):C910-C917.
[15] Chen T,Ren Z,Ye LC,et al. Factor inhibiting HIF1α(FIH-1)functions as a tumor suppressor in human colorectal cancer by repressing HIF1α pathway [J]. Cancer Biol Ther,2015,16(2):244-252.
[16] Allen A,Messier C. Plastic changes in the astrocyte GLUT1 glucose transporter and beta-tubulin microtubule protein following voluntary exercise in mice [J]. Behav Brain Res,2013,240:95-102.
[17] Choeiri C,Staines W,Miki T,et al. Glucose transporter plastic during memory processing [J]. Neuroscience,2005,130(3):591-600.
[18] Zeller K,Rahner-Welsc S,Kuschinsky W. Distrubution of Glut1 glucose transporters in different brain structures compared to glucose utilization and capillary density of adult rat brains [J]. J Cereb Blood Flow Metab,1997,17(2):204-209.
[19] Allen A,Messier C. Plastic changes in the astrocyte GLUT1 glucose transporter and beta-tubulin microtubule protein following voluntary exercise in mice [J]. Brain Res,2013,240(1):95-102.
[20] Pearson TS,Akman C,Hinton VJ,et al. Phenotypic spectrum of glucose transportertype1 dificiency syndrome(Glut1DS) [J]. Neurosci Rep,2013,13(4):342.
[21] Ossenkoppele R. Differential effect of APOE genotype on amyloid load and glucose metabolism in AD dementia [J]. Neurology,2013,80(4):359-365.
[22] Protas HD. Posterior cingulated glucose metabolism,hippocampal glucose metabolism,and hippocampal volume in cognitively normal,late-middle-aged persons at 3 levels of genetic risk for Alzheimer disease [J]. JAMA Neurol,2013,70:320-325.
[23] 许兵.血脑屏障的研究进展[J].生理学报,2016,68(3):306-322.
[24] Paul J,Strickland S,Melchor JP. Fibrin deposition accelerates neurovascular damage and neuroinflammation in mouse models of Alzheimers disease [J]. Exp Med,2007, 204(8):1999-2008.
[25] Ito S,Ohtsuki S,Kamiie J,et al. Cerebral clearance of human amyloid-beta peptide(1-40)across the blood-brain barrier is reduced by self-aggregation and formation of low-density lipoprotein-related protein-1 ligand complexes [J]. J Neurochem,2007,103(6):2482-2490.
[26] 赵昊譞,宋军营,宫洪涛,等.阿尔茨海默病血脑屏障研究进展[J].中国老年学杂志,2016,36(14):3595-3697.
[27] Zlokovic BV,Yamada S,Holtzman D,et al. Clearance of amyloid beta-peptide from brain:transport or metabolism [J]. Nat Med,2000,6(7):718-719.
[28] Selkoe DJ. Clearing the brain′s amyloid cobwebs [J]. Neuron,2001,32(2):177-180.
[29] Tanzi RE,Moir RD,Wagner SL. Clearance of Alzheimer′s Abetapeptide:the many roads to perdition [J]. Neuron,2004,43(5):605-608.
[30] Uchida Y. A study protocol for quantitative targeted absolute proteomics(QTAP)by LCMS/MS:application for inter-strain differences in protein expression levels of transporters,receptors,claudin-5,and marker proteins at the blood-brain barrier in ddY,FVB,and C57BL/6Jmice [J]. Fluids Barriers CNS,2013,10(1):21.
[31] 赵鹏.阿尔茨海默病发病机制探究[J].中风与神经疾病杂志,2016,33(1):86-89.
[32] Liu Y,Liu F,Grundke-Iqbal I,et al. Brain glucose transporters,O-GlcNAcylation and phosphorylationof tau in diabetes and Alzheimer′s disease [J]. J Neurochem,2009, 111(1):242-249.
[33] Liu Y,Liu F,Iqbal K,et al. Decreased glucose transporters correlate to abnormal hyperphosphorylation of tau in Alzheimer disease [J]. FEBS Lett,2008,582(2):359-364.
[34] Deng Y,Li B. Dysregulation of insulin signaling,glucosetransporters,O-GlcNAcylation,and phosphorylation of tau and neurofilaments in the brain:implication for Alzheimer′s disease [J]. Am J Pathol,2009,175(5):2089-2098. |
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