参考文献/References:
[1] 王英全,梁景宏,贾瑞霞,等.2020-2050年中国阿尔茨海默病患病情况预测研究[J].阿尔茨海默病及相关病,2019,2(1):289-298.
[2] Alzheimer’s Disease International. World Alzheimer Report 2018[R], 2018. London, https://www.alz.co.uk/research/world-report-2018.
[3] Martini-Stoica H, Xu Y, Ballabio A, et al. The Autophagy-Lysosomal pathway in neurodegeneration: a TFEB perspective[J]. Trends Neurosci, 2016, 39(4): 221-234.
[4] Hodjat M, Rezvanfar MA, Abdollahi M. A systematic review on the role of environmental toxicants in stem cells aging[J]. Food Chem Toxicol, 2015, 86(11): 298-308.
[5] Hou Y, Dan X, Babbar M, et al. Ageing as a risk factor for neurodegenerative disease[J]. Nat Rev Neurol, 2019, 15(10): 565-581.
[6] Kuang H, Tan CY, Tian HZ, et al. Exploring the bi-directional relationship between autophagy and Alzheimer’s disease[J]. CNS Neurosci Ther, 2020, 26(2): 155-166.
[7] Tammineni P, Cai Q. Defective retrograde transport impairs autophagic clearance in Alzheimer disease neurons[J]. Autophagy, 2017, 13(5): 982-984.
[8] Moloudizargari M, Asghari MH, Ghobadi E, et al. Autophagy, its mechanisms and regulation: Implications in neurodegenerative diseases[J]. Ageing Res Rev, 2017, 40(9): 64-74.
[9] Cai Y, Arikkath J, Yang L, et al. Interplay of endoplasmic reticulum stress and autophagy in neurodegenerative disorders[J]. Autophagy, 2016, 12(2): 225-244.
[10] Shaerzadeh F, Motamedi F, Minai-Tehrani D, et al. Monitoring of neuronal loss in the hippocampus of Aβ-injected rat: autophagy, mitophagy, and mitochondrial biogenesis stand against apoptosis[J]. Neuromolecular Med, 2014, 16(1): 175-190.
[11] Calsolaro V, Edison P. Neuroinflammation in alzheimer’s disease: current evidence and future directions[J]. Alzheimers Dement, 2016, 12(6): 719-732.
[12] Morales I, Guzmán-Martínez L, Cerda-Troncoso C, et al. Neuroinflammation in the pathogenesis of Alzheimer’s disease. A rational framework for the search of novel therapeutic approaches[J]. Front Cell Neurosci, 2014, 8: 112. DOI: 10.3389/fncel.2014.00112.
[13] Heneka MT, Carson MJ, El Khoury J, et al. Neuroinflammation in alzheimer’s disease[J]. Lancet Neurol, 2015, 14(4): 388-405.
[14] Pereira CF, Santos AE, Moreira P, et al. Is alzheimer’s disease an inflammasomopathy?[J]. Ageing Res Rev, 2019, 56: 100966. DOI: 10.1016/j.arr.2019.100966.
[15] Dansokho C, Heneka MT. Neuroinflammatory responses in Alzheimer’s disease[J]. J Neural Transm, 2018, 125(5): 771-779.
[16] Schilling T, Eder C. Amyloid-β-induced reactive Oxygen species production and priming are differentially regulated by ion channels in microglia[J]. J Cell Physiol, 2011, 226(12): 3295-3302.
[17] Micha? EB, Napolioni V, Greicius MD. A quarter century of APOE and alzheimer’s disease: progress to date and the path forward[J]. Neuron, 2019, 101(5): 820-838.
[18] Verkhratsky A, Nedergaard M. Physiology of astroglia[J]. Physiol Rev, 2018, 98(1): 239-389.
[19] Ferrer I. Diversity of astroglial responses across human neurodegenerative disorders and brain aging[J]. Brain Pathol, 2017, 27(5): 645-674.
[20] Arranz AM, De Strooper B. The role of astroglia in Alzheimer’s disease: pathophysiology and clinical implications[J]. Lancet Neurol, 2019, 18(4): 406-414.
[21] Hsu ET, Gangolli M, Su S, et al. Astrocytic degeneration in chronic traumatic encephalopathy[J]. Acta Neuropathol, 2018, 136(6): 955-972.
[22] Lian H, Yang L, Cole A, et al. NFκB-activated astroglial release of complement C3 compromises neuronal morphology and function associated with Alzheimer’s disease[J]. Neuron, 2015, 85(1): 101-115.
[23] Sensi SL, Granzotto A, Siotto M, et al. Copper and Zinc dysregulation in alzheimer’s disease[J]. Trends Pharmacol Sci, 2018, 39(12): 1049-1063.
[24] Wang, P, Wang, et al.Metal ions influx is a double edged sword for the pathogenesis of Alzheimer’sdisease[Z],2016.
[25] Crouch PJ, Tew DJ, Du T, et al. Restored degradation of the Alzheimer’s amyloid-beta peptide by targeting amyloid formation[J]. J Neurochem, 2009, 108(5): 1198-1207.
[26] Damante CA, Osz K, Nagy Z, et al. Metal loading capacity of Abeta N-terminus: a combined potentiometric and spectroscopic study of Zinc(Ⅱ)complexes with Abeta(1-16), its short or mutated peptide fragments and its polyethylene glycol-ylated analogue[J]. Inorg Chem, 2009, 48(21): 10405-10415.
[27] Boom A, Authelet M, Dedecker R, et al. Bimodal modulation of tau protein phosphorylation and conformation by extracellular Zn2+ in human-tau transfected cells[J]. Biochim Biophys Acta, 2009, 1793(6): 1058-1067.
[28] Mo ZY, Zhu YZ, Zhu HL, et al. Low micromolar Zinc accelerates the fibrillization of human Tau via bridging of Cys-291 and Cys-322[J]. Journal of Biological Chemistry, 2009, 284(50): 34648-34657.
[29] Alzheimer.s association Calcium hypothesis workgroup[Z],2017:1-6.
[30] Stutzmann G. The pathogenesis of Alzheimers disease is it a lifelong "calciumopathy"?[J]. Neuroscientist, 2007, 13(5): 546-559.
[31] Li TR, Wang XN, Sheng C, et al. Extracellular vesicles as an emerging tool for the early detection of Alzheimer’s disease[J]. Mech Ageing Dev, 2019, 184: 111175. DOI: 10.1016/j.mad.2019.111175.
[32] Xiao T, Zhang W, Jiao B, et al. The role of exosomes in the pathogenesis of Alzheimer’ disease[J]. Transl Neurodegener, 2017, 6(1): 3.
[33] Angelopoulou E, Paudel YN, Mohd FS, et al.Flotillin:a promising biomarker for alzheimer’s disease; J[Z],2020:20.
[34] Chen JJ, Zhao B, Zhao J, et al. Potential roles of exosomal MicroRNAs as diagnostic biomarkers and therapeutic application in alzheimer’s disease[J]. Neural Plast, 2017: 7027380. DOI: 10.1155/2017/7027380.
[35] Lee S, Mankhong S, Kang JH. Extracellular vesicle as a source of alzheimer’s biomarkers: opportunities and challenges[J]. Int J Mol Sci, 2019, 20(7): 1728.
[36] 韩琳琳,郭斌.外泌体在阿尔茨海默病发病机制中的研究进展[J].国际神经病学神经外科学杂志,2017,44(3):336-339.
[37] Sanderson, Ralph D, Bandari, et al.Vlodavsky[Z],2017.
[38] Tamboli IY, Barth E, Christian L, et al. Statins promote the degradation of extracellular amyloid {beta}-peptide by microglia via stimulation of exosome-associated insulin-degrading enzyme(IDE)secretion[J]. J Biol Chem, 2010, 285(48): 37405-37414.
[39] Malm, T, Loppi, et al.Exosomes in alzheimer’s disease,neurochemistry international(2016),doi:10[Z],2016.
[40] Asai H, Ikezu S, Tsunoda S, et al. Depletion of microglia and inhibition of exosome synthesis halt tau propagation[J]. Nat Neurosci, 2015, 18(11): 1584-1593.
[41] Delpech JC, Herron S, Botros MB, et al. Neuroimmune crosstalk through extracellular vesicles in health and disease[J]. Trends Neurosci, 2019, 42(5): 361-372.