[1]张国新 彭琴玉 郭笑迪等.胰岛淀粉样多肽在阿尔茨海默病发病机制中的作用研究进展[J].卒中与神经疾病杂志,2022,29(03):291-295.[doi:10.3969/j.issn.1007-0478.2022.03.019]
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胰岛淀粉样多肽在阿尔茨海默病发病机制中的作用研究进展()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第29卷
期数:
2022年03期
页码:
291-295
栏目:
综 述
出版日期:
2022-06-25

文章信息/Info

文章编号:
1007-0478(2022)03-0291-06
作者:
张国新 彭琴玉 郭笑迪等
430060 武汉大学人民医院神经内科[张国新 彭琴玉 郭笑迪 张振涛(通信作者)]
分类号:
R742
DOI:
10.3969/j.issn.1007-0478.2022.03.019
文献标志码:
A

参考文献/References:

[1] Aguirre-Acevedo DC, Lopera F, Henao E, et al. Cognitive decline in a colombian kindred with autosomal dominant alzheimer disease:a retrospective cohort study[J]. JAMA Neurol, 2016, 73(4): 431-438.
[2] Weinstein G, Maillard P, Himali JJ, et al. Glucose indices are associated with cognitive and structural brain measures in young adults[J]. Neurology, 2015, 84(23): 2329-2337.
[3] Luchsinger JA, Tang MX, Stern Y, et al. Diabetes mellitus and risk of Alzheimer’s disease and dementia with stroke in a multiethnic cohort[J]. Am J Epidemiol, 2001, 154(7): 635-641.
[4] Alagiakrishnan K, Zhao N, Mereu L, et al. Montreal cognitive assessment is superior to standardized Mini-Mental status exam in detecting mild cognitive impairment in the middle-aged and elderly patients with type 2 diabetes mellitus[J]. Biomed Res Int, 2013: 186106.
[5] Rasool M, Malik A, Waquar S, et al. Cellular and molecular mechanisms of Dementia: Decoding the causal Link of Diabetes Mellitus in Alzheimer’s disease[J]. CNS Neurol Disord Drug Targets, 2021.
[6] Lenore JL, Michael EM, Williamson JD, et al. Effects of intensive glucose lowering on brain structure and function in People with type 2 diabetes(ACCORD MIND): a randomised open-label substudy[J]. Lancet Neurol, 2011, 10(11): 969-977.
[7] Strachan MW, Price JF. Diabetes. cognitive decline and T2DM--a disconnect in the evidence?[J]. Nat Rev Endocrinol, 2014, 10(5): 258-260.
[8] Gj B, Gispen WH. The impact of diabetes on cognition: what can be learned from rodent models?[J]. Neurobiol Aging, 2005, 26( Suppl 1): 36-41.
[9] Roesti ES, Boyle CN, Zeman DT, et al. Vaccination against amyloidogenic aggregates in pancreatic islets prevents development of type 2 diabetes mellitus[J]. Vaccines(Basel), 2020, 8(1): 116.
[10] Oskarsson ME, Paulsson JF, Schultz SW, et al. In vivo seeding and cross-seeding of localized amyloidosis: a molecular Link between type 2 diabetes and Alzheimer disease[J]. Am J Pathol, 2015, 185(3): 834-846.
[11] R?er C, Kupreichyk T, Gremer L, et al. Cryo-EM structure of islet amyloid polypeptide fibrils reveals similarities with amyloid-β fibrils[J]. Nat Struct Mol Biol, 2020, 27(7): 660-667.
[12] Wijesekara, N, Ahrens R, Sabale M, et al. Amyloid-beta and islet amyloid pathologies Link Alzheimer’s disease and type 2 diabetes in a transgenic model[J]. FASEB J, 2017, 31(12): 5409-5418.
[13] Martinez-Valbuena I, Valenti-Azcarate R, Amat-Villegas I, et al. Amylin as a potential Link between type 2 diabetes and alzheimer disease[J]. Ann Neurol, 2019, 86(4): 539-551.
[14] Zhu H, Tao Q, Ang T, et al. Association of plasma amylin concentration with alzheimer disease and brain structure in older adults[J]. JAMA Netw Open, 2019, 2(8): e199826.
[15] Raimundo AF, Ferreira S, Martins IC, et al. Islet amyloid polypeptide: a partner in crime with Aβ in the pathology of alzheimer’s disease[J]. Front Mol Neurosci, 2020, 13: 35.
[16] Ferreira S, Raimundo AF, Menezes R, et al. Islet amyloid polypeptide&amyloid beta peptide roles in Alzheimer’s disease:two triggers,one disease[J]. Neural Regen Res, 2021, 16(6): 1127-1130.
[17] Abedini A, Schmidt AM. Mechanisms of islet amyloidosis toxicity in type 2 diabetes[J]. FEBS Lett, 2013, 587(8): 1119-1127.
[18] Westermark P, Andersson A, Westermarkm GT,et al. Islet amyloid polypeptide, islet amyloid, and diabetes mellitus[J]. Physiol Rev, 2011, 91(3): 795-826.
[19] Jurgens CA, Toukatly MN, Fligner CL, et al. β-cell loss and β-cell apoptosis in human type 2 diabetes are related to islet amyloid deposition[J]. Am J Pathol, 2011, 178(6): 2632-2640.
[20] Park K, Verchere CB. Identification of a heparin binding domain in the N-terminal cleavage site of pro-islet amyloid polypeptide.Implications for islet amyloid formation[J]. J Biol Chem, 2001, 276(20): 16611-16616.
[21] Hull LR, Andrikopoulos S, Verchere CB, et al. Increased dietary fat promotes islet amyloid formation and beta-cell secretory dysfunction in a transgenic mouse model of islet amyloid[J]. Diabetes, 2003, 52(2): 372-379.
[22] Shigihara N, Fukunaka A, Hara A, et al. Human IAPP-induced pancreatic β cell toxicity and its regulation by autophagy[J]. J Clin Invest, 2014, 124(8): 3634-3644.
[23] Caberlotto L, Nguyen TP, Lauria M, et al. Cross-disease analysis of Alzheimer’s disease and type-2 Diabetes highlights the role of autophagy in the pathophysiology of two highly comorbid diseases[J]. Sci Rep, 2019, 9(1): 3965.
[24] Jackson K, Barisone GA, Diaz E, et al. Amylin deposition in the brain: A second amyloid in Alzheimer disease?[J]. Ann Neurol, 2013, 74(4): 517-526.
[25] Schultz N, Byman E, Netherlands Brain Bank, et al. Levels of retinal amyloid-β correlate with levels of retinal IAPP and hippocampal amyloid-β in neuropathologically evaluated individuals[J]. J Alzheimers Dis, 2020, 73(3): 1201-1209.
[26] Wakabayashi T, Yamaguchi K, Matsui K, et al. Differential effects of diet- and genetically-induced brain insulin resistance on amyloid pathology in a mouse model of Alzheimer’s disease[J]. Mol Neurodegener, 2019, 14(1): 15.
[27] Xi XX, Sun J, Chen HC, et al. High-Fat Diet increases amylin accumulation in the hippocampus and accelerates brain aging in hIAPP transgenic mice[J]. Front Aging Neurosci, 2019, 11: 225.
[28] Srodulski S, Sharma S, Bachstetter AB, et al. Neuroinflammation and neurologic deficits in diabetes linked to brain accumulation of amylin[J]. Mol Neurodegener, 2014, 9: 30.
[29] Andreetto E, Yan LM, Tatarek-Nossol M, et al. Identification of hot regions of the Abeta-IAPP interaction interface as high-affinity binding sites in both cross- and self-association[J]. Angew Chem Int Ed Engl, 2010, 49(17): 3081-3085.
[30] Hu R, Zhang M, Chen H, et al. Cross-Seeding interaction between β-Amyloid and human islet amyloid polypeptide[J]. ACS Chem Neurosci, 2015, 6(10): 1759-1768.
[31] Ly H, Verma N, Sharma S, et al. The association of circulating amylin with β-amyloid in familial Alzheimer’s disease[J]. Alzheimers Dement(N Y), 2021, 7(1): e12130.
[32] Chen HC, Cao JX, Cai YT, et al. Interaction of human IAPP and Abeta1-42 aggravated the AD-related pathology and impaired the cognition in mice[J]. Exp Neurol, 2020, 334: 113490.
[33] Brender JR, Ramamoorthy A. Membrane disruption and early events in the aggregation of the diabetes related peptide IAPP from a molecular perspective[J]. Acc Chem Res, 2012, 45(3): 454-462.
[34] Brender JR, Lee EL, Hartman K, et al. Biphasic effects of insulin on islet amyloid polypeptide membrane disruption[J]. Biophys J, 2011, 100(3): 685-692.
[35] Zhang M, Hu R, Ren B, et al. Molecular understanding of Aβ-hIAPP Cross-Seeding assemblies on lipid membranes[J]. ACS Chem Neurosci, 2017, 8(3): 524-537.
[36] Fu W, Ruangkittisakul A, Mactavish D, et al. Amyloid β(Aβ)peptide directly activates amylin-3 receptor subtype by triggering multiple intracellular signaling pathways[J]. J Biol Chem, 2012, 287(22): 18820-18830.
[37] Masters SL, Dunne A, Subramanian SL, et al. Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes[J]. Nat Immunol, 2010, 11(10): 897-904.
[38] Westwell-Roper CY, Verchere CB. Resident macrophages mediate islet amyloid polypeptide-induced islet IL-1beta production and beta-cell dysfunction[J]. Diabetes, 2014, 63(5): 1698-1711.
[39] Park YJ, Lee S, Kieffer TJ, et al. Deletion of Fas protects islet beta cells from cytotoxic effects of human islet amyloid polypeptide[J]. Diabetologia, 2012.
[40] Heneka MT, Sastre M, Dumitrescu-Ozimek L, et al. Focal glial activation coincides with increased BACE1 activation and precedes amyloid plaque deposition in APP[V717I] transgenic mice[J]. J Neuroinflammation, 2005, 2(1): 22.
[41] Tanaka S, Ide M, Shibutani T, et al. Lipopolysaccharide-induced microglial activation induces learning and memory deficits without neuronal cell death in rats[J]. J Neurosci Res, 2006, 83(4): 557-566.
[42] Paola D, Domenicotti C, Nitti M, et al. Oxidative stress induces increase in intracellular amyloid beta-protein production and selective activation of betaI and betaII PKCs in NT2 cells[J]. Biochem Biophys Res Commun, 2000, 268(2): 642-646.
[43] De Felice FG, Velasco PT, Lambert MP, et al. Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine[J]. J Biol Chem, 2007, 282(15): 11590-11601.
[44] Paula-Lima AC, Adasme T, SanMartín C, et al. Amyloid beta-peptide oligomers stimulate RyR-mediated Ca2+ release inducing mitochondrial fragmentation in hippocampal neurons and prevent RyR-mediated dendritic spine remodeling produced by BDNF[J]. Antioxid Redox Signal, 2011, 14(7): 1209-1223.
[45] Subramanian SL, Hull RL, Zraika S, et al. cJUN n-terminal kinase(JNK)activation mediates islet amyloid-induced beta cell apoptosis in cultured human islet amyloid polypeptide transgenic mouse islets[J]. Diabetologia, 2012, 55(1): 166-174.
[46] Bomfim TR, Forny-Germano L, Sathler LB, et al. An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer’s disease- associated Aβ oligomers[J]. J Clin Invest, 2012, 122(4): 1339-1353.
[47] Colombo A, Bastone A, Ploia C, et al. JNK regulates APP cleavage and degradation in a model of Alzheimer’s disease[J]. Neurobiol Dis, 2009, 33(3): 518-525.
[48] Feuk L, Prince JA, Breen G, et al. apolipoprotein-E dependent role for the FAS receptor in early onset alzheimer’s disease: finding of a positive association for a polymorphism in the TNFRSF6 gene[J]. Hum Genet, 2000, 107(4): 391-396.
[49] Rohn TT, Head E, Nesse WH, et al. Activation of caspase-8 in the Alzheimer’s disease brain[J]. Neurobiol Dis, 2001, 8(6): 1006-1016.
[50] Mack CM, Soares CJ, Wilson JK, et al. Davalintide(AC2307), a novel amylin-mimetic peptide: enhanced pharmacological properties over native amylin to reduce food intake and body weight[J]. Int J Obes(Lond), 2010, 34(2): 385-395.
[51] Zhang XX, Pan YH, Huang YM, et al. Neuroendocrine hormone amylin in diabetes[J]. World J Diabetes, 2016, 7(9): 189-197.
[52] Costes S, Huang CJ, Gurlo T, et al. β-cell dysfunctional ERAD/ubiquitin/proteasome system in type 2 diabetes mediated by islet amyloid polypeptide-induced UCH-L1 deficiency[J]. Diabetes, 2011, 60(1): 227-238.
[53] Adler BL, Yarchoan M, Hwang HM, et al. Neuroprotective effects of the amylin analogue pramlintide on Alzheimer’s disease pathogenesis and cognition[J]. Neurobiol Aging, 2014, 35(4): 793-801.
[54] Pithadia A, Brender JR, Fierke CA, et al. Inhibition of IAPP aggregation and toxicity by natural products and derivatives[J]. J Diabetes Res, 2016, 2016: 2046327.
[55] Park YJ, Ao Z, Kieffer TJ, et al. The glucagon-like peptide-1 receptor agonist exenatide restores impaired pro-islet amyloid polypeptide processing in cultured human islets: implications in type 2 diabetes and islet transplantation[J]. Diabetologia, 2013, 56(3): 508-519.
[56] Fan R, Li X, Gu X, et al. Exendin-4 protects pancreatic beta cells from human islet amyloid polypeptide-induced cell damage: potential involvement of AKT and mitochondria biogenesis[J]. Diabetes Obes Metab, 2010, 12(9): 815-824.
[57] He L, Wong CK, Cheung KK, et al. Anti-inflammatory effects of exendin-4, a glucagon-like peptide-1 analog, on human peripheral lymphocytes in patients with type 2 diabetes[J]. J Diabetes Investig, 2013, 4(4): 382-392.
[58] Kim MK, Cho JH, Lee JJ, et al. Differential protective effects of exenatide, an agonist of GLP-1 receptor and Piragliatin, a glucokinase activator in beta cell response to streptozotocin-induced and endoplasmic reticulum stresses[J]. PLoS One, 2013, 8(9): e73340.
[59] Jantrapirom S, Nimlamool W, Chattipakorn N, et al. Liraglutide suppresses Tau hyperphosphorylation, amyloid beta accumulation through regulating neuronal insulin signaling and BACE-1 activity[J]. Int J Mol Sci, 2020, 21(5): 1725.
[60] McClean LP, Parthsarathy V, Faivre E, et al. The diabetes drug liraglutide prevents degenerative processes in a mouse model of Alzheimer’s disease[J]. J Neurosci, 2011, 31(17): 6587-6594.
[61] Larsen CM, Faulenbach M, Vaag A, et al. Sustained effects of interleukin-1 receptor antagonist treatment in type 2 diabetes[J]. Diabetes Care, 2009, 32(9): 1663-1668.
[62] Van Asseldonk EJ, Stienstra R, Koenen TB, et al. Treatment with Anakinra improves disposition index but not insulin sensitivity in nondiabetic subjects with the metabolic syndrome: a randomized, double-blind, placebo-controlled study[J]. J Clin Endocrinol Metab, 2011, 96(7): 2119-2126.
[63] Tarkowski E, Liljeroth AM, Nilsson A, et al. Decreased levels of intrathecal interleukin 1 receptor antagonist in Alzheimer’s disease[J]. Dement Geriatr Cogn Disord, 2001, 12(5): 314-317.
[64] Craft JM, Watterson DM, Hirsch E, et al. Interleukin 1 receptor antagonist knockout mice show enhanced microglial activation and neuronal damage induced by intracerebroventricular infusion of human beta-amyloid[J]. J Neuroinflammation, 2005, 2: 15.
[65] Thornton P, Pinteaux E, Gibson RM, et al. Interleukin-1-induced neurotoxicity is mediated by glia and requires caspase activation and free radical release[J]. J Neurochem, 2006, 98(1): 258-266.
[66] Depino AM, Alonso M, Ferrari C, et al. Learning modulation by endogenous hippocampal IL-1: blockade of endogenous IL-1 facilitates memory formation[J]. Hippocampus, 2004, 14(4): 526-535.
[67] Isoda K, Young JL, Zirlik A, et al. Metformin inhibits proinflammatory responses and nuclear factor-kappaB in human vascular wall cells[J]. Arterioscler Thromb Vasc Biol, 2006, 26(3): 611-617.
[68] Chen Y, Zhou K, Wang R, et al. Antidiabetic drug metformin(GlucophageR)increases biogenesis of Alzheimer’s amyloid peptides via up-regulating BACE1 transcription[J]. Proc Natl Acad Sci USA, 2009, 106(10): 3907-3912.
[69] Zhou R, Tardivel A, Thorens B, et al. Thioredoxin-interacting protein links oxidative stress to inflammasome activation[J]. Nat Immunol, 2010, 11(2): 136-140.
[70] Gillies PS, Dunn CJ. Pioglitazone[J]. Reactions Weekly, 2002, 894(1): 10-10.
[71] Gumieniczek AH, Zabek A. Protective effects of a PPARgamma agonist pioglitazone on anti-oxidative system in testis of diabetic rabbits[J]. Pharmazie, 2008, 63(5): 377-378.
[72] Diaz-Delfin JM, Caelles C. Hypoglycemic action of thiazolidinediones/peroxisome proliferator-activated receptor gamma by inhibition of the c-Jun NH2-terminal kinase pathway[J]. Diabetes, 2007, 56(7): 1865-1871.
[73] Lourenco MV, Ledo JH. Targeting alzheimer’s pathology through PPARγ signaling: modulation of microglial function[J]. J Neurosci, 2013, 33(12): 5083-5084.
[74] De Felice FG, Vieira MN, Bomfim TR, et al. Protection of synapses against Alzheimer’s-linked toxins: insulin signaling prevents the pathogenic binding of Abeta oligomers[J]. Proc Natl Acad Sci U S A, 2009, 106(6): 1971-1976.
[75] Xu J, Zhao C, Huang X, et al. Regulation of artemisinin and its derivatives on the assembly behavior and cytotoxicity of amyloid polypeptides hIAPP and Aβ[J]. ACS Chem Neurosci, 2019, 10(11): 4522-4534.
[76] Zhu H, Wang X, Wallack M, et al. Intraperitoneal injection of the pancreatic peptide amylin potently reduces behavioral impairment and brain amyloid pathology in murine models of Alzheimer’s disease[J]. Mol Psychiatry, 2015, 20(2): 252-262.
[77] Fu W, Patel A, Kimura R, et al. Amylin receptor: a potential therapeutic target for alzheimer’s disease[J]. Trends Mol Med, 2017, 23(8): 709-720.
[78] Patrick S, Corrigan R, Grizzanti J, et al. Neuroprotective effects of the amylin analog, pramlintide, on alzheimer’s disease are associated with oxidative stress regulation mechanisms[J]. J Alzheimers Dis, 2019, 69(1): 157-168.
[79] Corradi A, Zanardi A, Giacomini C, et al. Synapsin-I-and synapsin-II-null mice display an increased age-dependent cognitive impairment[J]. J Cell Sci, 2008, 121(Pt 18): 3042-3051.
[80] Jessberger S, Aigner S, Clemenson GJ, et al. Cdk5 regulates accurate maturation of newborn granule cells in the adult hippocampus[J]. PLoS Biol, 2008, 6(11): e272.
[81] Fu W, Patel A, Jhamandas JH, et al. Amylin receptor: a common pathophysiological target in Alzheimer’s disease and diabetes mellitus[J]. Front Aging Neurosci, 2013, 5: 42.
[82] Kimura R, Mactavish D, Yang J, et al. Beta amyloid-induced depression of hippocampal long-term potentiation is mediated through the amylin receptor[J]. J Neurosci, 2012, 32(48): 17401-17406.
[83] Fu W, Vukojevic V, Patel A, et al. Role of microglial amylin receptors in mediating beta amyloid(Aβ)-induced inflammation[J]. J Neuroinflammation, 2017, 14(1): 199.
[84] Soudy R, Patel A, Fu W, et al. Cyclic AC253,a novel amylin receptor antagonist,improves cognitive deficits in a mouse model of Alzheimer’s disease[J]. Alzheimers Dement(N Y), 2017, 3(1): 44-56.

备注/Memo

备注/Memo:
基金项目:国家重点研发计划(2019YFE0115900)、国家自然科学基金(81822016)
更新日期/Last Update: 1900-01-01