[1] Bonardi C, de Pulford F, Jennings D, et al. A detailed analysis of the early context extinction deficits seen in APPswe/PS1dE9 female mice and their relevance to preclinical Alzheimer's disease[J]. Behav Brain Res, 2011,222(1):89-97. [2] Citron M.Strategies for disease modification in Alzheimer's disease[J]. Nature Reviews Neuroscience, 2004, 5(9):677-685. [3] 闵嵘, 盛树力, 赵志炜, 等. App17肽对app转基因小鼠aβ相关蛋白表达的影响[J]. 中国老年学杂志, 2008, 28(12):1045-1048. [4] 吴云. Tau蛋白与阿尔茨海默病关系研究进展[J]. 中国健康月刊: B, 2011, 30(1):44-46. [5] 苏怡汀, 李乐华. 阿尔茨海默病的神经生物学发病机制及相关治疗研究进展[J]. 医学临床研究, 2011,28(5):947-951. [6] 秦红兵, 杨朝晔, 范忆江, 等. D-半乳糖诱导衰老小鼠模型的建立与评价[J]. 中国组织工程研究与临床康复, 2009, 13(7):1275-1278. [7] 宋彩梅, 王红梅, 刘新民, 等. 肾虚型老年痴呆动物模型的建立[J]. 现代中西医结合杂志, 2011,20(22):2744-2748. [8] 林海英, 吴春云, 于建云, 等. 学习记忆功能障碍与基底前脑胆碱能神经元改变的关系[J]. 泸州医学院学报, 2005, 28(5):385-387. [9] 梁逸超, 崔玲玲, 王维. 铝与阿尔茨海默病的研究进展[J]. 医学综述, 2009, 15(16):2455-2458. [10] 杨芳, 王双, 孙志伟. 阿尔茨海默病的免疫治疗策略及研究进展[J]. 生物技术通讯, 2009, 20(4):584-586. [11] Walker JM, Fowler SW, Miller DK, et al.Spatial learning and memory impairment and increased locomotion in a transgenic amyloid precursor protein mouse model of Alzheimer's disease[J]. Behav Brain Res, 2011,222(1):169-175. [12] Bekris LM, Yu CE, Bird TD, et al.Genetics of Alzheimer disease[J]. J Geriatr Psychiatry Neurol, 2010, 23(4):213-227. [13] Han X.The pathogenic implication of abnormal interaction between apolipoprotein E isoforms, amyloid-beta peptides, and sulfatides in Alzheimer's disease[J]. Molecular Neurobiology, 2010, 41(2):97-106. [14] Hsia AY, Masliah E, McConlogue L, et al. Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models[J]. Proc Natl Acad Sci U S A, 1999, 96(6):3228-3233. [15] Minati L, Edginton T, Bruzzone MG, et al.Current concepts in Alzheimer's disease: a multidisciplinary review[J]. Am J Alzheimers Dis Other Demen, 2009, 24(2):95-121. [16] Franberg J, Svensson AI, Winblad B, et al.Minor contribution of presenilin 2 for gamma-secretase activity in mouse embryonic fibroblasts and adult mouse brain[J]. Biochem Biophys Res Commun, 2011, 404(1):564-568. [17] Fitzjohn SM, Kuenzi F, Morton RA, et al.A study of long-term potentiation in transgenic mice over-expressing mutant forms of both amyloid precursor protein and presenilin-1[J]. Mol Brain, 2010, 3(1):21. [18] Holcomb L, Gordon MN, McGowan E, et al. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes[J]. Nat Med, 1998, 4(1):97-100. [19] Hussain I.APP transgenic mouse models and their use in drug discovery to evaluate amyloid- lowering therapeutics[J]. CNS Neurol Disord Drug Targets, 2010, 9(4):395-402. [20] Noble W, Hanger DP, Gallo JM.Transgenic mouse models of tauopathy in drug discovery[J]. CNS Neurol Disord Drug Targets, 2010, 9(4):403-428. [21] Rovelet-Lecrux A, Hannequin D, Guillin O, et al.Frontotemporal dementia phenotype associated with MAPT gene duplication[J]. Journal of Alzheimer's Disease, 2010, 21(3):897-902. [22] Nixon RA,Yuan A.Cytoskeleton of the Nervous System[M]. New York :Springer,2011.73-82. [23] Santa Cruz KS PJ, Lewis J, Mariash A, et al. Cell loss and gliosis in a transgenic mouse with regulatable P301L tau overexpression[C]. In: Society for Neuroscience meeting. New Orleans, LA, 2003. [24] Higuchi M, Maeda J, Ji B, et al.In-vivo visualization of key molecular processes involved in Alzheimer's disease pathogenesis: Insights from neuroimaging research in humans and rodent models[J]. Biochim Biophys Acta, 2010, 1802(4):373-388. [25] Allen B, Ingram E, Takao M, et al.Abundant tau filaments and nonapoptotic neurodegeneration in transgenic mice expressing human P301S tau protein[J]. J Neurosci, 2002, 22(21):9340-9351. [26] Miyasaka T, Sato S, Tatebayashi Y, et al.Microtubule destruction induces tau liberation and its subsequent phosphorylation[J]. FEBS Lett, 2010, 584(14):3227-3232. [27] Hutton M, Lewis J, Dickson D, et al.Analysis of tauopathies with transgenic mice[J]. Trends Mol Med, 2001, 7(10):467-470. [28] Lewis J, McGowan E, Rockwood J, et al. Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein[J]. Nat Genet, 2000, 25(4):402-405. [29] Lewis J, Dickson DW, Lin WL, et al.Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP[J]. Science, 2001,293(5534):1487-1491. [30] Gang B, Yue C, Han N, et al.Limited hippocampal neurogenesis in SAMP8 mouse model of Alzheimer's disease[J]. Brain Res, 2011, 1389:183-193. [31] Zhu L, Yu J, Shi Q, et al.Strain- and age-related alteration of proteins in the brain of SAMP8 and SAMR1 mice[J]. J Alzheimers Dis, 2011,23(4):641-654. [32] Ma Q, Qiang J, Gu P, et al.Age-related autophagy alterations in the brain of senescence accelerated mouse prone 8 (SAMP8) mice[J]. Exp Gerontol, 2011, 46(7):533-541. [33] Cui YJ, Huang MW, He YB, et al.Genetic ablation of apolipoprotein A-IV accelerates Alzheimer's disease pathogenesis in a mouse model[J]. American Journal of Pathology, 2011, 178(3):1298-1308. [34] Harris JA, Devidze N, Verret L, et al.Transsynaptic progression of amyloid-beta-induced neuronal dysfunction within the entorhinal-hippocampal network[J]. Neuron, 2010, 68(3):428-441. [35] Cisse M, Halabisky B, Harris J, et al.Reversing EphB2 depletion rescues cognitive functions in Alzheimer model[J]. Nature, 2011, 469(7328):47-52. [36] Butler D, Hwang J, Estick C, et al.Protective effects of positive lysosomal modulation in alzheimer's disease transgenic mouse models[J/OL]. PLoS One, 2011, 6(6):e20501. [37] Medeiros R, Kitazawa M, Caccamo A, et al.Loss of muscarinic M1 receptor exacerbates alzheimer's disease-like pathology and cognitive decline[J]. The American journal of pathology, 2011, 179(2):980-991. [38] Pereson S, Wils H, Kleinberger G, et al.Progranulin expression correlates with dense-core amyloid plaque burden in Alzheimer disease mouse models[J]. Journal of Pathology, 2009, 219(2):173-181. [39] Ghosal K, Stathopoulos A, Pimplikar SW.APP intracellular domain impairs adult neurogenesis in transgenic mice by inducing neuroinflammation[J/OL]. PLoS One, 2010, 5(7):e11866. [40] Ando K, Leroy K, Heraud C, et al.Accelerated Human Mutant Tau Aggregation by Knocking Out Murine Tau in a Transgenic Mouse Model[J]. American Journal of Pathology, 2011, 178(2):803-816. [41] Takeuchi H, Iba M, Inoue H, et al. P301S mutant human Tau transgenic mice manifest early symptoms of human tauopathies with dementia and altered sensorimotor gating[J]. PLoS One, 2011, 6(6):e21050.Epub. [42] Fischer A, Sananbenesi F, Wang XY, et al.Recovery of learning and memory is associated with chromatin remodelling[J]. Nature, 2007, 447(7141):178-182. [43] Zhu L, Yu JC, Shi QQ, et al.Strain- and age-related alteration of proteins in the brain of SAMP8 and SAMR1 mice[J]. Journal of Alzheimers Disease, 2011,23(4):641-654. [44] John S, Thangapandian S, Sakkiah S, et al.Potent bace-1 inhibitor design using pharmacophore modeling, in silico screening and molecular docking studies[J]. BMC Bioinformatics, 2011, 12(Suppl 1):S28. [45] Ooi CP, Loke SC, Yassin Z, et al. Carbohydrates for improving the cognitive performance of independent-living older adults with normal cognition or mild cognitive impairment[J]. Cochrane Database Syst Rev, 2011, 4(CD007220. [46] Lee KS, Divis PC, Zakaria SK, et al.Plasmodium knowlesi: Reservoir Hosts and Tracking the Emergence in Humans and Macaques[J]. PLoS Pathog, 2011, 7(4):e1002015. [47] Yan Q, Zhang J, Liu H, et al.Anti-inflammatory drug therapy alters beta-amyloid processing and deposition in an animal model of Alzheimer's disease[J]. J Neurosci, 2003, 23(20):7504-7509. [48] Lleo A, Berezovska O, Herl L, et al.Nonsteroidal anti-inflammatory drugs lower Abeta42 and change presenilin 1 conformation[J]. Nat Med, 2004, 10(10):1065-1066. [49] Citron M.Beta-secretase inhibition for the treatment of Alzheimer's disease--promise and challenge[J]. Trends Pharmacol Sci, 2004, 25(2):92-97. [50] Gnjec A, Fonte JA, Atwood C, et al.Transition metal chelator therapy-a potential treatment for Alzheimer's disease?[J]. Front Biosci, 2002, 7:d1016-1023. [51] Cherny RA, Atwood CS, Xilinas ME, et al.Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice[J]. Neuron, 2001, 30(3):665-676. [52] Lee JY, Cole TB, Palmiter RD, et al.Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic mice[J]. Proc Natl Acad Sci USA, 2002, 99(11):7705-7710. [53] Ritchie CW, Bush AI, Mackinnon A, et al.Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting Abeta amyloid deposition and toxicity in Alzheimer disease: a pilot phase 2 clinical trial[J]. Archives of Neurology, 2003, 60(12):1685-1691. [54] Morgan D, Diamond DM, Gottschall PE, et al.A beta peptide vaccination prevents memory loss in an animal model of Alzheimer's disease[J]. Nature, 2000, 408(6815):982-985. [55] Lombardo JA, Stern EA, McLellan ME, et al. Amyloid-beta antibody treatment leads to rapid normalization of plaque-induced neuritic alterations[J]. J Neurosci, 2003, 23(34):10879-10883. [56] Oddo S, Billings L, Kesslak JP, et al.Abeta immunotherapy leads to clearance of early, but not late, hyperphosphorylated tau aggregates via the proteasome[J]. Neuron, 2004, 43(3):321-332. [57] Cattepoel S, Hanenberg M, Kulic L, et al.Chronic Intranasal Treatment with an Anti-Aβ<sub>30-42</sub> scFv Antibody Ameliorates Amyloid Pathology in a Transgenic Mouse Model of Alzheimer's Disease[J]. PLoS ONE, 2011, 6(4):e18296. [58] Nicoll JA, Wilkinson D, Holmes C, et al.Neuropathology of human Alzheimer disease after immunization with amyloid-beta peptide: a case report[J]. Nat Med, 2003, 9(4):448-452. [59] Hock C, Konietzko U, Streffer JR, et al.Antibodies against beta-amyloid slow cognitive decline in Alzheimer's disease[J]. Neuron, 2003, 38(4):547-554. [60] Wang A, Das P, Switzer RC, et al.Robust amyloid clearance in a mouse model of alzheimer's disease provides novel insights into the mechanism of amyloid-beta immunotherapy[J]. Journal of Neuroscience, 2011, 31(11):4124-4136. [61] Marchesi VT.Alzheimer's dementia begins as a disease of small blood vessels, damaged by oxidative-induced inflammation and dysregulated amyloid metabolism: implications for early detection and therapy[J]. Faseb Journal, 2011,25(1):5-13. [62] Singh JCH, Alagarsamy V, Kumar SS, et al.Neurotransmitter metabolic enzymes and antioxidant status on Alzheimer's disease induced mice treated with Alpinia galanga (L.) Willd[J]. Phytotherapy Research, 2011,25(7):1061-1067. [63] Budimir A.Metal ions, Alzheimer's disease and chelation therapy[J]. Acta Pharmaceutica, 2011, 61(1):1-14. [64] Oehlrich D, Berthelot DJC, Gijsen HJM. gamma-Secretase Modulators as Potential Disease Modifying Anti-Alzheimer's Drugs[J]. Journal of Medicinal Chemistry, 2011, 54(3):669-698. [65] Vassar R.Alzheimer's therapy: a BACE in the hand?[J]. Nature Medicine, 2011, 17(8):932-933. [66] Medina M, Avila J.Glycogen synthase kinase-3 (GSK-3) inhibitors for the treatment of Alzheimer's disease[J]. Current Pharmaceutical Design, 2010, 16(25):2790-2798. |