Volume 43 Issue 6
Nov.  2022
Turn off MathJax
Article Contents
Zhi-Ya Chen, Yan Zhang. Animal models of Alzheimer’s disease: Applications, evaluation, and perspectives. Zoological Research, 2022, 43(6): 1026-1040. doi: 10.24272/j.issn.2095-8137.2022.289
Citation: Zhi-Ya Chen, Yan Zhang. Animal models of Alzheimer’s disease: Applications, evaluation, and perspectives. Zoological Research, 2022, 43(6): 1026-1040. doi: 10.24272/j.issn.2095-8137.2022.289

Animal models of Alzheimer’s disease: Applications, evaluation, and perspectives

doi: 10.24272/j.issn.2095-8137.2022.289
The authors declare that they have no competing interests.
Y.Z. and Z.Y.C. conceptualized the study and drafted the manuscript. All authors read and approved the final version of the manuscript.
Funds:  This work was supported by the National Science and Technology Innovation 2030-Major Program of “Brain Science and Brain-Like Research” (2022ZD0211800), National Natural Science Foundation of China (NSFC) General Research Grants (81971679, 32020103007, 32088101, 21727806), Ministry of Science and Technology (2018YFA0507600, 2017YFA0503600), and Qidong-PKU SLS Innovation Fund (2016000663, 2017000246)
More Information
  • Corresponding author: E-mail: yanzhang@pku.edu.cn
  • Received Date: 2022-10-19
  • Accepted Date: 2022-10-31
  • Published Online: 2022-10-31
  • Publish Date: 2022-11-18
  • Although great advances in elucidating the molecular basis and pathogenesis of Alzheimer’s disease (AD) have been made and multifarious novel therapeutic approaches have been developed, AD remains an incurable disease. Evidence shows that AD neuropathology occurs decades before clinical presentation. AD is divided into three stages: preclinical stage, mild cognitive impairment (MCI), and AD dementia. In the natural world, some animals, such as non-human primates (NHPs) and canines, can develop spontaneous AD-like dementia. However, most animals do not develop AD. With the development of transgenic techniques, both invertebrate and vertebrate animals have been employed to uncover the mechanisms of AD and study treatment methods. Most AD research focuses on early-onset familial AD (FAD) because FAD is associated with specific genetic mutations. However, there are no well-established late-onset sporadic AD (SAD) animal models because SAD is not directly linked to any genetic mutation, and multiple environmental factors are involved. Moreover, the widely used animal models are not able to sufficiently recapitulate the pathological events that occur in the MCI or preclinical stages. This review summarizes the common models used to study AD, from yeast to NHP models, and discusses the different applications, evaluation methods, and challenges related to AD animal models, as well as prospects for the evolution of future studies.
  • The authors declare that they have no competing interests.
    Y.Z. and Z.Y.C. conceptualized the study and drafted the manuscript. All authors read and approved the final version of the manuscript.
  • loading
  • [1]
    Adalbert R, Nogradi A, Babetto E, Janeckova L, Walker SA, Kerschensteiner M, et al. 2009. Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies. Brain, 132(Pt 2): 402–416.
    [2]
    Ahlijanian MK, Barrezueta NX, Williams RD, Jakowski A, Kowsz KP, McCarthy S, et al. 2000. Hyperphosphorylated tau and neurofilament and cytoskeletal disruptions in mice overexpressing human p25, an activator of cdk5. Proceedings of the National Academy of Sciences of the United States of America, 97(6): 2910−2915. doi: 10.1073/pnas.040577797
    [3]
    Albert MS, Dekosky ST, Dickson D, Dubois B, Feldman HH, Fox NC, et al. 2011. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia:Translational Research & Clinical Interventions, 7(3): 270−279.
    [4]
    Alzheimer's Association. 2013. 2013 Alzheimer's disease facts and figures. Alzheimer's & Dementia, 9(2): 208−245.
    [5]
    Ankarcrona M, Mangialasche F, Winblad B. 2010. Rethinking Alzheimer's disease therapy: are mitochondria the key?. Journal of Alzheimer's Disease, 20 Suppl 2: S579–S590.
    [6]
    Arendt T, Holzer M, Fruth R, Brückner MK, Gärtner U. 1998. Phosphorylation of Tau, Aβ-formation, and apoptosis after in vivo inhibition of PP-1 and PP-2A. Neurobiology of Aging, 19(1): 3−13. doi: 10.1016/S0197-4580(98)00003-7
    [7]
    Bagriantsev S, Liebman S. 2006. Modulation of Aβ42 low-n oligomerization using a novel yeast reporter system. BMC Biology, 4(1): 32. doi: 10.1186/1741-7007-4-32
    [8]
    Bain MJ, Hart BL, Cliff KD, Ruehl WW. 2001. Predicting behavioral changes associated with age-related cognitive impairment in dogs. Journal of the American Veterinary Medical Association, 218(11): 1792−1795. doi: 10.2460/javma.2001.218.1792
    [9]
    Bassett DE, Boguski MS, Hieter P. 1996. Yeast genes and human disease. Nature, 379(6566): 589−590. doi: 10.1038/379589a0
    [10]
    Bennett DA, Schneider JA, Arvanitakis Z, Kelly JF, Aggarwal NT, Shah RC, et al. 2006. Neuropathology of older persons without cognitive impairment from two community-based studies. Neurology, 66(12): 1837−1844. doi: 10.1212/01.wnl.0000219668.47116.e6
    [11]
    Bennett V. 1992. Ankyrins. Adaptors between diverse plasma membrane proteins and the cytoplasm. The Journal of Biological Chemistry, 267(13): 8703−8706. doi: 10.1016/S0021-9258(19)50333-7
    [12]
    Best JD, Berghmans S, Hunt JJFG, Clarke SC, Fleming A, Goldsmith P, et al. 2008. Non-associative learning in larval zebrafish. Neuropsychopharmacology, 33(5): 1206−1215. doi: 10.1038/sj.npp.1301489
    [13]
    Blaser R, Gerlai R. 2006. Behavioral phenotyping in zebrafish: comparison of three behavioral quantification methods. Behavior Research Methods, 38(3): 456−469. doi: 10.3758/BF03192800
    [14]
    Blazquez-Llorca L, Valero-Freitag S, Rodrigues EF, Merchán-Pérez Á, Rodríguez JR, Dorostkar MM, et al. 2017. High plasticity of axonal pathology in Alzheimer’s disease mouse models. Acta Neuropathologica Communications, 5(1): 14. doi: 10.1186/s40478-017-0415-y
    [15]
    Borràs D, Ferrer I, Pumarola M. 1999. Age-related changes in the brain of the dog. Veterinary Pathology, 36(3): 202−211. doi: 10.1354/vp.36-3-202
    [16]
    Bouzidi M, Tricaud N, Giraud P, Kordeli E, Caillol G, Deleuze C, et al. 2002. Interaction of the Nav1.2a subunit of the voltage-dependent sodium channel with nodal ankyrinG: In vitro mapping of the interacting domains and association in synaptosomes. The Journal of Biological Chemistry, 277(32): 28996−29004. doi: 10.1074/jbc.M201760200
    [17]
    Braak H, Braak E. 1995. Staging of Alzheimer's disease-related neurofibrillary changes. Neurobiology of Aging, 16(3): 271−278. doi: 10.1016/0197-4580(95)00021-6
    [18]
    Braidy N, Muñoz P, Palacios AG, Castellano-Gonzalez G, Inestrosa NC, Chung RS, et al. 2012. Recent rodent models for Alzheimer's disease: clinical implications and basic research. Journal of Neural Transmission, 119(2): 173−195. doi: 10.1007/s00702-011-0731-5
    [19]
    Braidy N, Poljak A, Jayasena T, Mansour H, Inestrosa NC, Sachdev P. 2015. Accelerating Alzheimer's research through 'natural' animal models. Current Opinion in Psychiatry, 28(2): 155−164. doi: 10.1097/YCO.0000000000000137
    [20]
    Bu GJ. 2009. Apolipoprotein E and its receptors in Alzheimer’s disease: pathways, pathogenesis and therapy. Nature Reviews Neuroscience, 10(5): 333–344.
    [21]
    Buckwalter MS, Wyss-Coray T. 2004. Modelling neuroinflammatory phenotypes in vivo. Journal of Neuroinflammation, 1(1): 10.
    [22]
    Burton MD, Johnson RW. 2012. Interleukin-6 trans-signaling in the senescent mouse brain is involved in infection-related deficits in contextual fear conditioning. Brain, Behavior, and Immunity, 26(5): 732−738. doi: 10.1016/j.bbi.2011.10.008
    [23]
    Calhoun AJ, Tong AD, Pokala N, Fitzpatrick JAJ, Sharpee TO, Chalasani SH. 2015. Neural Mechanisms for Evaluating Environmental Variability in Caenorhabditis elegans. Neuron, 86(2): 428–441.
    [24]
    Casas-Tinto S, Zhang Y, Sanchez-Garcia J, Gomez-Velazquez M, Rincon-Limas DE, Fernandez-Funez P. 2011. The ER stress factor XBP1s prevents amyloid-β neurotoxicity. Human Molecular Genetics, 20(11): 2144−2160. doi: 10.1093/hmg/ddr100
    [25]
    Castellani RJ, Perry G. 2012. Pathogenesis and disease-modifying therapy in Alzheimer's disease: the flat line of progress. Archives of Medical Research, 43(8): 694−698. doi: 10.1016/j.arcmed.2012.09.009
    [26]
    Chambers JK, Uchida K, Nakayama H. 2012. White matter myelin loss in the brains of aged dogs. Experimental Gerontology, 47(3): 263−269. doi: 10.1016/j.exger.2011.12.003
    [27]
    Chang DC. 2006. Neural circuits underlying circadian behavior in Drosophila melanogaster. Behavioural Processes, 71(2–3): 211–225.
    [28]
    Chen GQ, Chen KS, Knox J, Inglis J, Bernard A, Martin SJ, et al. 2000. A learning deficit related to age and β-amyloid plaques in a mouse model of Alzheimer's disease. Nature, 408(6815): 975−979. doi: 10.1038/35050103
    [29]
    Chen MQ, Martins RN, Lardelli M. 2009. Complex splicing and neural expression of duplicated tau genes in zebrafish embryos. Journal of Alzheimer's Disease, 18(2): 305−317. doi: 10.3233/JAD-2009-1145
    [30]
    Chen R, Tilley MR, Wei H, Zhou FW, Zhou FM, Ching S, et al. 2006. Abolished cocaine reward in mice with a cocaine-insensitive dopamine transporter. Proceedings of the National Academy of Sciences of the United States of America, 103(24): 9333−9338. doi: 10.1073/pnas.0600905103
    [31]
    Chishti MA, Yang DS, Janus C, Phinney AL, Horne P, Pearson J, et al. 2001. Early-onset amyloid deposition and cognitive deficits in transgenic mice expressing a double mutant form of amyloid precursor protein 695. The Journal of Biological Chemistry, 276(24): 21562−21570. doi: 10.1074/jbc.M100710200
    [32]
    Cohen PTW, Brewis ND, Hughes V, Mann DJ. 1990. Protein serine/threonine phosphatases; an expanding family. FEBS Letters, 268(2): 355−359. doi: 10.1016/0014-5793(90)81285-V
    [33]
    Cohen RM, Rezai-Zadeh K, Weitz TM, Rentsendorj A, Gate D, Spivak I, et al. 2013. A transgenic alzheimer rat with plaques, tau pathology, behavioral impairment, oligomeric Aβ, and frank neuronal loss. The Journal of Neuroscience, 33(15): 6245−6256. doi: 10.1523/JNEUROSCI.3672-12.2013
    [34]
    Cook SJ, Jarrell TA, Brittin CA, Wang Y, Bloniarz AE, Yakovlev MA, et al. 2019. Whole-animal connectomes of both Caenorhabditis elegans sexes. Nature, 571(7763): 63−71. doi: 10.1038/s41586-019-1352-7
    [35]
    Costa AP, Tramontina AC, Biasibetti R, Batassini C, Lopes MW, Wartchow KM, et al. 2012. Neuroglial alterations in rats submitted to the okadaic acid-induced model of dementia. Behavioural Brain Research, 226(2): 420−427. doi: 10.1016/j.bbr.2011.09.035
    [36]
    David Muyllaert DT, Kremer A, Sennvik K, Borghgraef P, Devijver H, Dewachter I, et al. 2008. Neurodegeneration and neuroinflammation in cdk5/p25-inducible mice: a model for hippocampal sclerosis and neocortical degeneration. Alzheimer's & Dementia, 4(Supplement): T185−T186.
    [37]
    do Carmo S, Cuello AC. 2013. Modeling Alzheimer's disease in transgenic rats. Molecular Neurodegeneration, 8: 37. doi: 10.1186/1750-1326-8-37
    [38]
    Drummond E, Wisniewski T. 2017. Alzheimer's disease: experimental models and reality. Acta Neuropathologica, 133(2): 155−175. doi: 10.1007/s00401-016-1662-x
    [39]
    Dubois B, Feldman HH, Jacova C, Dekosky ST, Barberger-Gateau P, Cummings J, et al. 2007. Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS-ADRDA criteria. The Lancet Neurology, 6(8): 734−746. doi: 10.1016/S1474-4422(07)70178-3
    [40]
    Duyckaerts C, Potier MC, Delatour PB. 2008. Alzheimer disease models and human neuropathology: similarities and differences. Acta Neuropathologica, 115(1): 5−38. doi: 10.1007/s00401-007-0312-8
    [41]
    Edbauer D, Kaether C, Steiner H, Haass C. 2004. Co-expression of nicastrin and presenilin rescues a loss of function mutant of APH-1. The Journal of Biological Chemistry, 279(36): 37311−37315. doi: 10.1074/jbc.M406228200
    [42]
    Edbauer D, Winkler E, Regula JT, Pesold B, Steiner H, Haass C. 2003. Reconstitution of γ-secretase activity. Nature Cell Biology, 5(5): 486−488. doi: 10.1038/ncb960
    [43]
    Eikelenboom P, van Exel E, Hoozemans JJM, Veerhuis R, Rozemuller AJM, van Gool W. 2010. Neuroinflammation - an early event in both the history and pathogenesis of Alzheimer's disease. Neurodegenerative Diseases, 7(1–3): 38–41.
    [44]
    Epis R, Gardoni F, Marcello E, Genazzani A, Canonico PL, di Luca M. 2010. Searching for new animal models of Alzheimer's disease. European Journal of Pharmacology, 626(1): 57−63. doi: 10.1016/j.ejphar.2009.10.020
    [45]
    Fan Y, Luo RC, Su LY, Xiang Q, Yu DD, Xu L, et al. 2018. Does the genetic feature of the chinese tree shrew (Tupaia Belangeri Chinensis) support its potential as a viable model for Alzheimer's disease research?. Journal of Alzheimer's Disease, 61(3): 1015−1028. doi: 10.3233/JAD-170594
    [46]
    Fast R, Schütt T, Toft N, Møller A, Berendt M. 2013. An observational study with long-term follow-up of canine cognitive dysfunction: clinical characteristics, survival, and risk factors. Journal of Veterinary Internal Medicine, 27(4): 822−829. doi: 10.1111/jvim.12109
    [47]
    Finelli A, Kelkar A, Song HJ, Yang HD, Konsolaki M. 2004. A model for studying Alzheimer's Aβ42-induced toxicity in Drosophila melanogaster. Molecular and Cellular Neuroscience, 26(3): 365–375.
    [48]
    Fischer A, Sananbenesi F, Pang PT, Lu B, Tsai LH. 2005. Opposing roles of transient and prolonged expression of p25 in synaptic plasticity and hippocampus-dependent memory. Neuron, 48(5): 825−838. doi: 10.1016/j.neuron.2005.10.033
    [49]
    Flood DG, Lin YG, Lang DM, Trusko SP, Hirsch JD, Savage MJ, et al. 2009. A transgenic rat model of Alzheimer's disease with extracellular Aβ deposition. Neurobiology of Aging, 30(7): 1078−1090. doi: 10.1016/j.neurobiolaging.2007.10.006
    [50]
    Flood DG, Reaume AG, Dorfman KS, Lin YG, Lang DM, Trusko SP, et al. 2002. FAD mutant PS-1 gene-targeted mice: increased Aβ42 and Aβ deposition without APP overproduction. Neurobiology of Aging, 23(3): 335−348. doi: 10.1016/S0197-4580(01)00330-X
    [51]
    Folwell J, Cowan CM, Ubhi KK, Shiabh H, Newman TA, Shepherd D, et al. 2010. Aβ exacerbates the neuronal dysfunction caused by human tau expression in a Drosophila model of Alzheimer's disease. Experimental Neurology, 223(2): 401−409. doi: 10.1016/j.expneurol.2009.09.014
    [52]
    Forny-Germano L, Silva NMLE, Batista AF, Brito-Moreira J, Gralle M, Boehnke SE, et al. 2014. Alzheimer's disease-like pathology induced by amyloid-β oligomers in nonhuman primates. The Journal of Neuroscience, 34(41): 13629−13643. doi: 10.1523/JNEUROSCI.1353-14.2014
    [53]
    Foury F. 1997. Human genetic diseases: a cross-talk between man and yeast. Gene, 195(1): 1−10. doi: 10.1016/S0378-1119(97)00140-6
    [54]
    Futai E, Yagishita S, Ishiura S. 2009. Nicastrin is dispensable for γ-secretase protease activity in the presence of specific presenilin mutations. The Journal of Biological Chemistry, 284(19): 13013−13022. doi: 10.1074/jbc.M807653200
    [55]
    Games D, Adams D, Alessandrini R, Barbour R, Borthelette P, Blackwell C, et al. 1995. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein. Nature, 373(6514): 523−527. doi: 10.1038/373523a0
    [56]
    Gary C, Lam S, Hérard AS, Koch JE, Petit F, Gipchtein P, et al. 2019. Encephalopathy induced by Alzheimer brain inoculation in a non-human primate. Acta Neuropathologica Communications, 7(1): 126. doi: 10.1186/s40478-019-0771-x
    [57]
    Geddes JW, Bondada V, Keller JN. 1994. Effects of intrahippocampal colchicine administration on the levels and localization of microtubule-associated proteins, tau and MAP2. Brain Research, 633(1–2): 1–8.
    [58]
    Gerlai R. 2003. Zebra fish: an uncharted behavior genetic model. Behavior Genetics, 33(5): 461−468. doi: 10.1023/A:1025762314250
    [59]
    Giaever G. 2003. A chemical genomics approach to understanding drug action. Trends in Pharmacological Sciences, 24(9): 444−446. doi: 10.1016/S0165-6147(03)00225-6
    [60]
    Gillis C, Mirzaei F, Potashman M, Ikram MA, Maserejian N. 2019. The incidence of mild cognitive impairment: a systematic review and data synthesis. Alzheimer's & Dementia, 11(1): 248−256.
    [61]
    Graybeal JJ, Bozzelli PL, Graybeal LL, Groeber CM, McKnight P, Cox D, et al. 2015. Human ApoE ε4 alters circadian rhythm activity, IL-1β, and GFAP in CRND8 mice. Journal of Alzheimer's Disease, 43(3): 823−834.
    [62]
    Greenspan RJ, van Swinderen B. 2004. Cognitive consonance: complex brain functions in the fruit fly and its relatives. Trends in Neurosciences, 27(12): 707−711. doi: 10.1016/j.tins.2004.10.002
    [63]
    Greeve I, Kretzschmar D, Tschäpe JA, Beyn A, Brellinger C, Schweizer M, et al. 2004. Age-dependent neurodegeneration and alzheimer-amyloid plaque formation in transgenic Drosophila. The Journal of Neuroscience, 24(16): 3899–3906.
    [64]
    Griffin EF, Scopel SE, Stephen CA, Holzhauer AC, Vaji MA, Tuckey RA, et al. 2019. ApoE-associated modulation of neuroprotection from Aβ-mediated neurodegeneration in transgenic Caenorhabditis elegans. Disease Models & Mechanisms, 12(2): dmm037218.
    [65]
    Groth C, Nornes S, McCarty R, Tamme R, Lardelli M. 2002. Identification of a second presenilin gene in zebrafish with similarity to the human Alzheimer's disease gene Presenilin2. Development Genes and Evolution, 212(10): 486–490.
    [66]
    Hall AM, Roberson ED. 2012. Mouse models of Alzheimer's disease. Brain Research Bulletin, 88(1): 3−12. doi: 10.1016/j.brainresbull.2011.11.017
    [67]
    Hardy J, Selkoe DJ. 2002. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science, 297(5580): 353−356. doi: 10.1126/science.1072994
    [68]
    Hauser PS, Narayanaswami V, Ryan RO. 2011. Apolipoprotein E: from lipid transport to neurobiology. Progress in Lipid Research, 50(1): 62−74. doi: 10.1016/j.plipres.2010.09.001
    [69]
    He RQ, Lu J, Miao JY. 2010. Formaldehyde stress. Science China Life Sciences, 53(12): 1399−1404. doi: 10.1007/s11427-010-4112-3
    [70]
    Heuer E, Rosen RF, Cintron A, Walker LC. 2012. Nonhuman primate models of alzheimer-like cerebral proteopathy. Current Pharmaceutical Design, 18(8): 1159−1169. doi: 10.2174/138161212799315885
    [71]
    Hickman-Davis JM, Davis IC. 2006. Transgenic mice. Paediatric Respiratory Reviews, 7(1): 49−53. doi: 10.1016/j.prrv.2005.09.005
    [72]
    Ho L, Osaka H, Aisen PS, Pasinetti GM. 1998. Induction of cyclooxygenase (COX)-2 but not COX-1 gene expression in apoptotic cell death. Journal of Neuroimmunology, 89(1–2): 142–149.
    [73]
    Holcomb L, Gordon MN, McGowan E, Yu X, Benkovic S, Jantzen P, et al. 1998. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes. Nature Medicine, 4(1): 97−100. doi: 10.1038/nm0198-097
    [74]
    Holtzman DM, Bales KR, Wu S, Bhat P, Parsadanian M, Fagan AM, et al. 1999. Expression of human apolipoprotein E reduces amyloid-β deposition in a mouse model of Alzheimer's disease. Journal of Clinical Investigation, 103(6): R15−R21. doi: 10.1172/JCI6179
    [75]
    Howe K, Clark MD, Torroja CF, Torrance J, Berthelot C, Muffato M, et al. 2013. The zebrafish reference genome sequence and its relationship to the human genome. Nature, 496(7446): 498−503. doi: 10.1038/nature12111
    [76]
    Hsiao K, Chapman P, Nilsen S, Eckman C, Harigaya Y, Younkin S, et al. 1996. Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice. Science, 274(5284): 99−103. doi: 10.1126/science.274.5284.99
    [77]
    Hughes SR, Goyal S, Sun JE, Gonzalez-DeWhitt P, Fortes MA, Riedel NG, et al. 1996. Two-hybrid system as a model to study the interaction of beta-amyloid peptide monomers. Proceedings of the National Academy of Sciences of the United States of America, 93(5): 2065−2070. doi: 10.1073/pnas.93.5.2065
    [78]
    Inestrosa NC, Reyes AE, Chacón M, Cerpa W, Villalón A, Montiel J, et al. 2005. Human-like rodent amyloid-β-peptide determines Alzheimer pathology in aged wild-type Octodon degu. Neurobiology of Aging, 26(7): 1023–1028.
    [79]
    Jack Jr CR, Albert MS, Knopman DS, Mckhann GM, Sperling RA, Carrillo MC, et al. 2011. Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia, 7(3): 257−262.
    [80]
    Jackson GR, Wiedau-Pazos M, Sang TK, Wagle N, Brown CA, Massachi S, et al. 2002. Human wild-type tau interacts with wingless pathway components and produces neurofibrillary pathology in Drosophila. Neuron, 34(4): 509–519.
    [81]
    Jacob HJ, Kwitek AE. 2002. Rat genetics: attachign physiology and pharmacology to the genome. Nature Reviews Genetics, 3(1): 33−42. doi: 10.1038/nrg702
    [82]
    Jenkins PM, Vasavda C, Hostettler J, Davis JQ, Abdi K, Bennett V. 2013. E-cadherin polarity is determined by a multifunction motif mediating lateral membrane retention through ankyrin-G and apical-lateral transcytosis through clathrin. The Journal of Biological Chemistry, 288(20): 14018−14031. doi: 10.1074/jbc.M113.454439
    [83]
    Jessen F, Amariglio RE, Buckley RF, van der Flier WM, Han Y, Molinuevo JL, et al. 2020. The characterisation of subjective cognitive decline. The Lancet Neurology, 19(3): 271−278. doi: 10.1016/S1474-4422(19)30368-0
    [84]
    Johnstone EM, Chaney MO, Norris FH, Pascual R, Little SP. 1991. Conservation of the sequence of the Alzheimer's disease amyloid peptide in dog, polar bear and five other mammals by cross-species polymerase chain reaction analysis. Molecular Brain Research, 10(4): 299−305. doi: 10.1016/0169-328X(91)90088-F
    [85]
    Jones SL, Korobova F, Svitkina T. 2014. Axon initial segment cytoskeleton comprises a multiprotein submembranous coat containing sparse actin filaments. Journal of Cell Biology, 205(1): 67−81. doi: 10.1083/jcb.201401045
    [86]
    Kalueff AV, Echevarria DJ, Stewart MA. 2014a. Gaining translational momentum: More zebrafish models for neuroscience research. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 55: 1−6. doi: 10.1016/j.pnpbp.2014.01.022
    [87]
    Kalueff AV, Stewart AM, Gerlai R. 2014b. Zebrafish as an emerging model for studying complex brain disorders. Trends in Pharmacological Sciences, 35(2): 63−75. doi: 10.1016/j.tips.2013.12.002
    [88]
    Kamat PK, Tota S, Rai S, Swarnkar S, Shukla R, Nath C. 2012. A study on neuroinflammatory marker in brain areas of okadaic acid (ICV) induced memory impaired rats. Life Sciences, 90(19–20): 713–720.
    [89]
    Kamat PK, Tota S, Saxena G, Shukla R, Nath C. 2010. Okadaic acid (ICV) induced memory impairment in rats: a suitable experimental model to test anti-dementia activity. Brain Research, 1309: 66−74. doi: 10.1016/j.brainres.2009.10.064
    [90]
    Karran E, Mercken M, de Strooper B. 2011. The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics. Nature Reviews Drug Discovery, 10(9): 698−712. doi: 10.1038/nrd3505
    [91]
    Kim W, Underwood RS, Greenwald I, Shaye DD. 2018. OrthoList 2: a new comparative genomic analysis of human and Caenorhabditis elegans genes. Genetics, 210(2): 445−461. doi: 10.1534/genetics.118.301307
    [92]
    Kimura M, Toth LA, Agostini H, Cady AB, Majde JA, Krueger JM. 1994. Comparison of acute phase responses induced in rabbits by lipopolysaccharide and double-stranded RNA. American Journal of Physiology, 267(6 Pt 2): R1596–R1605.
    [93]
    Kinsella GJ, Mullaly E, Rand E, Ong B, Burton C, Price S, et al. 2009. Early intervention for mild cognitive impairment: a randomised controlled trial. Journal of Neurology, Neurosurgery, and Psychiatry, 80(7): 730−736. doi: 10.1136/jnnp.2008.148346
    [94]
    Knight D, Iliadi K, Charlton MP, Atwood HL, Boulianne GL. 2007. Presynaptic plasticity and associative learning are impaired in a Drosophila presenilin null mutant. Developmental Neurobiology, 67(12): 1598−1613. doi: 10.1002/dneu.20532
    [95]
    Krstic D, Knuesel I. 2013. Deciphering the mechanism underlying late-onset Alzheimer disease. Nature Reviews Neurology, 9(1): 25−34. doi: 10.1038/nrneurol.2012.236
    [96]
    Krstic D, Madhusudan A, Doehner J, Vogel P, Notter T, Imhof C, et al. 2012. Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice. Journal of Neuroinflammation, 9: 151. doi: 10.1186/1742-2094-9-151
    [97]
    Kumar A, Seghal N, Naidu PS, Padi SS, Goyal R. 2007. Colchicines-induced neurotoxicity as an animal model of sporadic dementia of Alzheimer's type. Pharmacological Reports, 59(3): 274−283.
    [98]
    Landsberg GM, Nichol J, Araujo JA. 2012. Cognitive dysfunction syndrome: a disease of canine and feline brain aging. Veterinary Clinics of North America:Small Animal Practice, 42(4): 749−768. doi: 10.1016/j.cvsm.2012.04.003
    [99]
    Le Brocque D, Henry A, Cappai R, Li QX, Tanner JE, Galatis D, et al. 1998. Processing of the Alzheimer's disease amyloid precursor protein in Pichia pastoris: immunodetection of α-, β-, and γ-secretase products. Biochemistry, 37(42): 14958−14965. doi: 10.1021/bi981063l
    [100]
    Leimer U, Lun K, Romig H, Walter J, Grünberg J, Brand M, et al. 1999. Zebrafish (Danio rerio) presenilin promotes aberrant amyloid β-peptide production and requires a critical aspartate residue for its function in amyloidogenesis. Biochemistry, 38(41): 13602−13609. doi: 10.1021/bi991453n
    [101]
    Leon WC, Canneva F, Partridge V, Allard S, Ferretti MT, DeWilde A, et al. 2010. A novel transgenic rat model with a full Alzheimer's-like amyloid pathology displays pre-plaque intracellular amyloid-β-associated cognitive impairment. Journal of Alzheimer's Disease, 20(1): 113−126. doi: 10.3233/JAD-2010-1349
    [102]
    Leterrier C. 2016. The axon initial segment, 50 years later: a nexus for neuronal organization and function. Current Topics in Membranes, 77: 185−233.
    [103]
    Levitan D, Greenwald I. 1995. Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimer’s disease gene. Nature, 377(6547): 351−354. doi: 10.1038/377351a0
    [104]
    Li WD, Wu YE, Min FG, Li Z, Huang JY, Huang R. 2010. A nonhuman primate model of Alzheimer's disease generated by intracranial injection of amyloid-beta42 and thiorphan. Metabolic Brain Disease, 25(3): 277−284. doi: 10.1007/s11011-010-9207-9
    [105]
    Li ZH, He XP, Li H, He RQ, Hu XT. 2020. Age-associated changes in amyloid-β and formaldehyde concentrations in cerebrospinal fluid of rhesus monkeys. Zoological Research, 41(4): 444−448. doi: 10.24272/j.issn.2095-8137.2020.088
    [106]
    Lin Y, Shan PY, Jiang WJ, Sheng C, Ma L. 2019. Subjective cognitive decline: preclinical manifestation of Alzheimer's disease. Neurological Sciences, 40(1): 41−49. doi: 10.1007/s10072-018-3620-y
    [107]
    Liu L, Orozco IJ, Planel E, Wen Y, Bretteville A, Krishnamurthy P, et al. 2008. A transgenic rat that develops Alzheimer's disease-like amyloid pathology, deficits in synaptic plasticity and cognitive impairment. Neurobiology of Disease, 31(1): 46−57. doi: 10.1016/j.nbd.2008.03.005
    [108]
    Lopez AY, Wang X, Xu M, Maheshwari A, Curry D, Lam S, et al. 2017. Ankyrin-G isoform imbalance and interneuronopathy link epilepsy and bipolar disorder. Molecular Psychiatry, 22(10): 1464−1472. doi: 10.1038/mp.2016.233
    [109]
    Lüthi U, Schaerer-Brodbeck C, Tanner S, Middendorp O, Edler K, Barberis A. 2003. Human β-secretase activity in yeast detected by a novel cellular growth selection system. Biochimica Et Biophysica Acta (BBA) - General Subjects, 1620(1–3): 167–178.
    [110]
    Mawuenyega KG, Sigurdson W, Ovod V, Munsell L, Kasten T, Morris JC, et al. 2010. Decreased clearance of CNS β-amyloid in Alzheimer's disease. Science, 330(6012): 1774. doi: 10.1126/science.1197623
    [111]
    McKhann GM, Knopman DS, Chertkow H, Hyman BT, Jack Jr CR, Kawas CH, et al. 2011. The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia, 7(3): 263−269.
    [112]
    McMartin DN, Schedlbauer LM. 1978. Effect of experimental colchicine encephalopathy on brain protein synthesis and tubulin metabolism. Journal of Neurobiology, 9(6): 453−463. doi: 10.1002/neu.480090605
    [113]
    Merino-Serrais P, Benavides-Piccione R, Blazquez-Llorca L, Kastanauskaite A, Rábano A, Avila J, et al. 2013. The influence of phospho-tau on dendritic spines of cortical pyramidal neurons in patients with Alzheimer's disease. Brain, 136(6): 1913−1928. doi: 10.1093/brain/awt088
    [114]
    Merrick SE, Demoise DC, Lee MY. 1996. Site-specific dephosphorylation of tau protein at Ser202/Thr205 in response to microtubule depolymerization in cultured human neurons involves protein phosphatase 2A. The Journal of Biological Chemistry, 271(10): 5589−5594. doi: 10.1074/jbc.271.10.5589
    [115]
    Meyer U, Nyffeler M, Engler A, Urwyler A, Schedlowski M, Knuesel I, et al. 2006. The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. The Journal of Neuroscience, 26(18): 4752−4762. doi: 10.1523/JNEUROSCI.0099-06.2006
    [116]
    Michno K, Knight D, Campussano JM, van de Hoef D, Boulianne GL. 2009. Intracellular calcium deficits in Drosophila cholinergic neurons expressing wild type or FAD-mutant Presenilin. PLoS One, 4(9): e6904.
    [117]
    Middendorp O, Ortler C, Neumann U, Paganetti P, Lüthi U, Barberis A. 2004. Yeast growth selection system for the identification of cell-active inhibitors of β-secretase. Biochimica Et Biophysica Acta (BBA) - General Subjects, 1674(1): 29–39.
    [118]
    Monaco III EA. 2004. Recent evidence regarding a role for CDK5 dysregulation in alzheimers disease. Current Alzheimer Research, 1(1): 33−38. doi: 10.2174/1567205043480519
    [119]
    Moore AH, Wu M, Shaftel SS, Graham KA, O'Banion MK. 2009. Sustained expression of interleukin-1β in mouse hippocampus impairs spatial memory. Neuroscience, 164(4): 1484−1495. doi: 10.1016/j.neuroscience.2009.08.073
    [120]
    Mucke L, Masliah E, Yu GQ, Mallory M, Rockenstein EM, Tatsuno G, et al. 2000. High-level neuronal expression of Aβ1–42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation. The Journal of Neuroscience, 20(11): 4050−4058. doi: 10.1523/JNEUROSCI.20-11-04050.2000
    [121]
    Musa A, Lehrach H, Russo VE. 2001. Distinct expression patterns of two zebrafish homologues of the human APP gene during embryonic development. Development Genes and Evolution, 211(11): 563−567. doi: 10.1007/s00427-001-0189-9
    [122]
    Naj AC, Jun G, Beecham GW, Wang LS, Vardarajan BN, Buros J, et al. 2011. Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease. Nature Genetics, 43(5): 436−441. doi: 10.1038/ng.801
    [123]
    Nakamura SI, Nakayama H, Goto N, Ono F, Sakakibara I, Yoshikawa Y. 1998. Histopathological studies of senile plaques and cerebral amyloidosis in cynomolgus monkeys. Journal of Medical Primatology, 27(5): 244−252. doi: 10.1111/j.1600-0684.1998.tb00244.x
    [124]
    Näslund J, Haroutunian V, Mohs R. 2000. Correlation between elevated levels of amyloid β-peptide in the brain and cognitive decline. JAMA, 283(12): 1571−1577. doi: 10.1001/jama.283.12.1571
    [125]
    Neha, Sodhi RK, Jaggi AS, Singh N. 2014. Animal models of dementia and cognitive dysfunction. Life Sciences, 109(2): 73−86. doi: 10.1016/j.lfs.2014.05.017
    [126]
    Neilson JC, Hart BL, Cliff KD, Ruehl WW. 2001. Prevalence of behavioral changes associated with age-related cognitive impairment in dogs. Journal of the American Veterinary Medical Association, 218(11): 1787−1791. doi: 10.2460/javma.2001.218.1787
    [127]
    Nery LR, Eltz NS, Hackman C, Fonseca R, Altenhofen S, Guerra HN, et al. 2013. Brain intraventricular injection of amyloid-β in zebrafish embryo impairs cognition and increases tau phosphorylation, effects reversed by lithium. PLoS One, 9(9): e105862.
    [128]
    Nichols CD. 2006. Drosophila melanogaster neurobiology, neuropharmacology, and how the fly can inform central nervous system drug discovery. Pharmacology & Therapeutics, 112(3): 677−700.
    [129]
    Nolan MF, Malleret G, Dudman JT, Buhl DL, Santoro B, Gibbs E, et al. 2004. A behavioral role for dendritic integration: HCN1 channels constrain spatial memory and plasticity at inputs to distal dendrites of CA1 pyramidal neurons. Cell, 119(5): 719−732.
    [130]
    Oakley H, Cole SL, Logan S, Maus E, Shao P, Craft J, et al. 2006. Intraneuronal β-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. The Journal of Neuroscience, 26(40): 10129−10140. doi: 10.1523/JNEUROSCI.1202-06.2006
    [131]
    Oddo S, Caccamo A, Shepherd JD, Murphy MP, Golde TE, Kayed R, et al. 2003. Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Aβ and synaptic dysfunction. Neuron, 39(3): 409−421. doi: 10.1016/S0896-6273(03)00434-3
    [132]
    Patrick GN, Zukerberg L, Nikolic M, de la Monte S, Dikkes P, Tsai LH. 1999. Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration. Nature, 402(6762): 615−622. doi: 10.1038/45159
    [133]
    Pawlik M, Fuchs E, Walker LC, Levy E. 1999. Primate-like amyloid-β sequence but no cerebral amyloidosis in aged tree shrews. Neurobiology of Aging, 20(1): 47−51. doi: 10.1016/S0197-4580(99)00017-2
    [134]
    Petersen RC. 2004. Mild cognitive impairment as a diagnostic entity. Journal of Internal Medicine, 256(3): 183−194. doi: 10.1111/j.1365-2796.2004.01388.x
    [135]
    Picciotto MR, Wickman K. 1998. Using knockout and transgenic mice to study neurophysiology and behavior. Physiological Reviews, 78(4): 1131−1163. doi: 10.1152/physrev.1998.78.4.1131
    [136]
    Price DL, Sisodia SS, Gandy SE. 1995. Amyloid beta amyloidosis in Alzheimer's disease. Current Opinion in Neurology, 8(4): 268−274. doi: 10.1097/00019052-199508000-00004
    [137]
    Puglielli L, Tanzi RE, Kovacs DM. 2003. Alzheimer's disease: the cholesterol connection. Nature Neuroscience, 6(4): 345−351. doi: 10.1038/nn0403-345
    [138]
    Puig O, Caspary F, Rigaut G, Rutz B, Bouveret E, Bragado-Nilsson E, et al. 2001. The tandem affinity purification (TAP) method: a general procedure of protein complex purification. Methods, 24(3): 218−229. doi: 10.1006/meth.2001.1183
    [139]
    Rabin LA, Smart CM, Amariglio RE. 2017. Subjective cognitive decline in preclinical Alzheimer's disease. Annual Review of Clinical Psychology, 13: 369−396. doi: 10.1146/annurev-clinpsy-032816-045136
    [140]
    Rajasekar N, Dwivedi S, Tota SK, Kamat PK, Hanif K, Nath C, et al. 2013. Neuroprotective effect of curcumin on okadaic acid induced memory impairment in mice. European Journal of Pharmacology, 715(1–3): 381–394.
    [141]
    Rat Genome Sequencing Project Consortium. 2004. Genome sequence of the Brown Norway rat yields insights into mammalian evolution. Nature, 428(6982): 493−521. doi: 10.1038/nature02426
    [142]
    Rocha-Martins M, Cavalheiro GR, Matos-Rodrigues GE, Martins RAP. 2015. From gene targeting to genome editing: transgenic animals applications and beyond. Anais da Academia Brasileira de Ciências, 87(2 Suppl): 1323–1348.
    [143]
    Rockenstein E, Mallory M, Mante M, Sisk A, Masliaha E. 2001. Early formation of mature amyloid-β protein deposits in a mutant APP transgenic model depends on levels of Aβ1–42. The Journal of Neuroscience Research, 66(4): 573−582. doi: 10.1002/jnr.1247
    [144]
    Rusbridge C, Salguero FJ, David MA, Faller KME, Bras JT, Guerreiro RJ, et al. 2018. An aged canid with behavioral deficits exhibits blood and cerebrospinal fluid amyloid beta oligomers. Frontiers in Aging Neuroscience, 10: 7. doi: 10.3389/fnagi.2018.00007
    [145]
    Saito T, Matsuba Y, Mihira N, Takano J, Nilsson P, Itohara S, et al. 2014. Single app knock-in mouse models of Alzheimer's disease. Nature Neuroscience, 17(5): 661−663. doi: 10.1038/nn.3697
    [146]
    Sani S, Traul D, Klink A, Niaraki A, Gonzalo-Ruiz A, Wu CK, et al. 2003. Distribution, progression and chemical composition of cortical amyloid-β deposits in aged rhesus monkeys: similarities to the human. Acta Neuropathologica, 105(2): 145−156. doi: 10.1007/s00401-002-0626-5
    [147]
    Schenk D, Barbour R, Dunn W, Gordon G, Grajeda H, Guido T, et al. 1999. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature, 400(6740): 173−177. doi: 10.1038/22124
    [148]
    Schmidt F, Boltze J, Jager C, Hofmann S, Willems N, Seeger J, et al. 2015. Detection and quantification of beta-amyloid, pyroglutamyl abeta, and tau in aged canines. Journal of Neuropathology and Experimental Neurology, 74(9): 912−923. doi: 10.1097/NEN.0000000000000230
    [149]
    Schütt T, Helboe L, Pedersen LØ, Waldemar G, Berendt M, Pedersen JT. 2016. Dogs with cognitive dysfunction as a spontaneous model for early Alzheimer's disease: a translational study of neuropathological and inflammatory markers. Journal of Alzheimer's Disease, 52(2): 433−449. doi: 10.3233/JAD-151085
    [150]
    Shaye DD, Greenwald I. 2011. OrthoList: a compendium of C. elegans genes with human orthologs. PLoS One, 6(5): e20085. doi: 10.1371/journal.pone.0020085
    [151]
    Shulman JM, Feany MB. 2003. Genetic modifiers of tauopathy in drosophila. Genetics, 165(3): 1233−1242. doi: 10.1093/genetics/165.3.1233
    [152]
    Sil S, Goswami AR, Dutta G, Ghosh T. 2014. Effects of naproxen on immune responses in a colchicine-induced rat model of Alzheimer's disease. Neuroimmunomodulation, 21(6): 304−321. doi: 10.1159/000357735
    [153]
    Siwak-Tapp CT, Head E, Muggenburg BA, Milgram NW, Cotman CW. 2008. Region specific neuron loss in the aged canine hippocampus is reduced by enrichment. Neurobiology of Aging, 29(1): 39−50. doi: 10.1016/j.neurobiolaging.2006.09.018
    [154]
    Smolek T, Madari A, Farbakova J, Kandrac O, Jadhav S, Cente M, et al. 2016. Tau hyperphosphorylation in synaptosomes and neuroinflammation are associated with canine cognitive impairment. Journal of Comparative Neurology, 524(4): 874−895. doi: 10.1002/cne.23877
    [155]
    Sontag JM, Sontag E. 2014. Protein phosphatase 2A dysfunction in Alzheimer's disease. Frontiers in Molecular Neuroscience, 7: 16.
    [156]
    Sperling RA, Aisen PS, Beckett LA, Bennett DA, Craft S, Fagan AM, et al. 2011. Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia, 7(3): 280−292.
    [157]
    Spinney L. 2014. Alzheimer's disease: The forgetting gene. Nature, 510(7503): 26−28. doi: 10.1038/510026a
    [158]
    Spires TL, Meyer-Luehmann M, Stern EA, McLean PJ, Skoch J, Nguyen PT, et al. 2005. Dendritic spine abnormalities in amyloid precursor protein transgenic mice demonstrated by gene transfer and intravital multiphoton microscopy. The Journal of Neuroscience, 25(31): 7278−7287. doi: 10.1523/JNEUROSCI.1879-05.2005
    [159]
    Sturchler-Pierrat C, Abramowski D, Duke M, Wiederhold KH, Mistl C, Rothacher S, et al. 1997. Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology. Proceedings of the National Academy of Sciences of the United States of America, 94(24): 13287−13292. doi: 10.1073/pnas.94.24.13287
    [160]
    Sun XQ, Wu Y, Gu MX, Liu Z, Ma YL, Li J, et al. 2014a. Selective filtering defect at the axon initial segment in Alzheimer's disease mouse models. Proceedings of the National Academy of Sciences of the United States of America, 111(39): 14271−14276. doi: 10.1073/pnas.1411837111
    [161]
    Sun XQ, Wu Y, Gu MX, Zhang Y. 2014b. miR-342-5p decreases ankyrin G levels in Alzheimer's disease transgenic mouse models. Cell Report, 6(2): 264−270. doi: 10.1016/j.celrep.2013.12.028
    [162]
    Sundaram JR, Chan ES, Poore CP, Pareek TK, Cheong WF, Shui GH, et al. 2012. Cdk5/p25-induced cytosolic PLA2-mediated lysophosphatidylcholine production regulates neuroinflammation and triggers neurodegeneration. The Journal of Neuroscience, 32(3): 1020−1034. doi: 10.1523/JNEUROSCI.5177-11.2012
    [163]
    Suter B, Auerbach D, Stagljar I. 2006. Yeast-based functional genomics and proteomics technologies: the first 15 years and beyond. BioTechniques, 40(5): 625−644. doi: 10.2144/000112151
    [164]
    Tan FHP, Azzam G. 2017. Drosophila melanogaster: deciphering Alzheimer's disease. Malaysian Journal of Medical Sciences, 24(2): 6−20. doi: 10.21315/mjms2016.24.2.2
    [165]
    Tapia R, Peña F, Arias C. 1999. Neurotoxic and synaptic effects of okadaic acid, an inhibitor of protein phosphatases. Neurochemical Research, 24(11): 1423−1430. doi: 10.1023/A:1022588808260
    [166]
    Tapp PD, Siwak CT, Gao FQ, Chiou JY, Black SE, Head E, et al. 2004. Frontal lobe volume, function, and β-amyloid pathology in a canine model of aging. The Journal of Neuroscience, 24(38): 8205−8213. doi: 10.1523/JNEUROSCI.1339-04.2004
    [167]
    Tesson L, Cozzi J, Ménoret S, Rémy S, Usal C, Fraichard A, et al. 2005. Transgenic modifications of the rat genome. Transgenic Research, 14(5): 531−546. doi: 10.1007/s11248-005-5077-z
    [168]
    Tilson HA, Rogers BC, Grimes L, Harry GJ, Peterson NJ, Hong JS, et al. 1987. Time-dependent neurobiological effects of colchicine administered directly into the hippocampus of rats. Brain Research, 408(1–2): 163–172.
    [169]
    Toepper M. 2017. Dissociating normal aging from Alzheimer's disease: a view from cognitive neuroscience. Journal of Alzheimer's Disease, 57(2): 331−352. doi: 10.3233/JAD-161099
    [170]
    Toledano A, Álvarez MI, López-Rodríguez A, Toledano-Díaz A, Fernández-Verdecia C. 2014. Does Alzheimer disease exist in all primates? Alzheimer pathology in non-human primates and its pathophysiological implications (II). Neurología (English Edition), 29(1): 42–55.
    [171]
    Tong ZQ, Han CS, Luo WH, Wang XH, Li H, Luo HJ, et al. 2013. Accumulated hippocampal formaldehyde induces age-dependent memory decline. AGE (Dordr), 35(3): 583−596. doi: 10.1007/s11357-012-9388-8
    [172]
    Tulpule K, Dringen R. 2013. Formaldehyde in brain: an overlooked player in neurodegeneration?. Journal of Neurochemistry, 127(1): 7−21. doi: 10.1111/jnc.12356
    [173]
    Ueno K, Ohta M, Morita H, Mikuni Y, Nakajima S, Yamamoto K, et al. 2001. Trehalose sensitivity in Drosophila correlates with mutations in and expression of the gustatory receptor gene Gr5a. Current Biology, 11(18): 1451−1455. doi: 10.1016/S0960-9822(01)00450-X
    [174]
    Uno H, Walker LC. 1993. The age of biosenescence and the incidence of cerebral β‐amyloidosis in aged captive rhesus monkeys. Annals of the New York Academy of Sciences, 695(1): 232−235. doi: 10.1111/j.1749-6632.1993.tb23058.x
    [175]
    Vernier P, Kyzar EJ, Maximino C, Tierney K, Gebhardt M, Lange M, et al. 2012. Time to recognize zebrafish 'affective' behavior. Behaviour, 149(10–12): 1019–1036.
    [176]
    Vickers JC, King AE, Woodhouse A, Kirkcaldie MT, Staal JA, McCormack GH, et al. 2009. Axonopathy and cytoskeletal disruption in degenerative diseases of the central nervous system. Brain Research Bulletin, 80(4–5): 217–223.
    [177]
    von der Haar T, Jossé L, Wright P, Zenthon J, Tuite MF. 2007. Development of a novel yeast cell-based system for studying the aggregation of Alzheimer's disease-associated Aβ peptides in vivo. Neurodegenerative Diseases, 4(2–3): 136–147.
    [178]
    Voytko ML. 1999. Impairments in acquisition and reversals of two-choice discriminations by aged rhesus monkeys. Neurobiology of Aging, 20(6): 617−627. doi: 10.1016/S0197-4580(99)00097-4
    [179]
    Wang CC, Ortiz-González XR, Yum SW, Gill SM, White A, Kelter E, et al. 2018. βIV spectrinopathies cause profound intellectual disability, congenital hypotonia, and motor axonal neuropathy. The American Journal of Human Genetics, 102(6): 1158−1168. doi: 10.1016/j.ajhg.2018.04.012
    [180]
    Wang F, Chen DQ, Wu PP, Klein C, Jin CY. 2019. Formaldehyde, epigenetics, and Alzheimer's disease. Chemical Research in Toxicology, 32(5): 820−830. doi: 10.1021/acs.chemrestox.9b00090
    [181]
    Wang YM, Guan ML, Wang H, Li Y, Zhanghao K, Xi P, et al. 2021. The largest isoform of Ankyrin-G is required for lattice structure of the axon initial segment. Biochemical and Biophysical Research Communications, 578: 28−34. doi: 10.1016/j.bbrc.2021.09.017
    [182]
    Wang YM, Yang YQ, Liu YQ, Guo AY, Zhang Y. 2022a. Cognitive impairments in type 1 diabetes mellitus model mice are associated with synaptic protein disorders. Neuroscience Letters, 777: 136587. doi: 10.1016/j.neulet.2022.136587
    [183]
    Wang ZH, Xia YY, Wu ZR, Kang SS, Zhang JC, Liu P, et al. 2022b. Neuronal ApoE4 stimulates C/EBPβ activation, promoting Alzheimer's disease pathology in a mouse model. Progress in Neurobiology, 209: 102212. doi: 10.1016/j.pneurobio.2021.102212
    [184]
    Whitehouse P, Brodaty H. 2006. Mild cognitive impairment. The Lancet, 367(9527): 1979. doi: 10.1016/S0140-6736(06)68880-6
    [185]
    Wittmann CW, Wszolek MF, Shulman JM, Salvaterra PM, Lewis J, Hutton M, et al. 2001. Tauopathy in Drosophila: neurodegeneration without neurofibrillary tangles. Science, 293(5530): 711−714. doi: 10.1126/science.1062382
    [186]
    Yagishita S, Futai E, Ishiura S. 2008. In vitro reconstitution of γ-secretase activity using yeast microsomes. Biochemical and Biophysical Research Communications, 377(1): 141−145. doi: 10.1016/j.bbrc.2008.09.090
    [187]
    Yang MF, Miao JY, Rizak J, Zhai RW, Wang ZB, Huma T, et al. 2014. Alzheimer's disease and methanol toxicity (part 2): lessons from four rhesus macaques (Macaca mulatta) chronically fed methanol. Journal of Alzheimer's Disease, 41(4): 1131−1147. doi: 10.3233/JAD-131532
    [188]
    Yang R, Walder-Christensen KK, Lalani S, Yan HD, García-Prieto ID, Álvarez S, et al. 2019. Neurodevelopmental mutation of giant ankyrin-G disrupts a core mechanism for axon initial segment assembly. Proceedings of the National Academy of Sciences of the United States of America, 116(39): 19717−19726. doi: 10.1073/pnas.1909989116
    [189]
    Yao YG. 2017. Creating animal models, why not use the Chinese tree shrew (Tupaia belangeri chinensis)?. Zoological Research, 38(3): 118−126. doi: 10.24272/j.issn.2095-8137.2017.032
    [190]
    Ye MS, Zhang JY, Yu DD, Xu M, Xu L, Lv LB, et al. 2021. Comprehensive annotation of the Chinese tree shrew genome by large-scale RNA sequencing and long-read isoform sequencing. Zoological Research, 42(6): 692−709. doi: 10.24272/j.issn.2095-8137.2021.272
    [191]
    Zahorsky-Reeves J, Lawson G, Chu DK, Schimmel A, Ezell PC, Dang M, et al. 2007. Maintaining longevity in a triple transgenic rat model of Alzheimer's disease. Journal of the American Association for Laboratory Animal Science, 46(4): 124.
    [192]
    Zhai RW, Rizak J, Zheng N, He XP, Li ZH, Yin Y, et al. 2018. Alzheimer's disease-like pathologies and cognitive impairments induced by formaldehyde in non-human primates. Current Alzheimer Research, 15(14): 1304−1321. doi: 10.2174/1567205015666180904150118
    [193]
    Zhang HY, Komano H, Fuller RS, Gandy SE, Frail DE. 1994. Proteolytic processing and secretion of human β-amyloid precursor protein in yeast. Evidence for a yeast secretase activity. The Journal of Biological Chemistry, 269(45): 27799−27802. doi: 10.1016/S0021-9258(18)46854-8
    [194]
    Zhang W, Espinoza D, Hines V, Innis M, Mehta P, Miller DL. 1997. Characterization of β-amyloid peptide precursor processing by the yeast Yap3 and Mkc7 proteases. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1359(2): 110−122. doi: 10.1016/S0167-4889(97)00082-7
    [195]
    Zhu SS, Cordner ZA, Xiong JL, Chiu CT, Artola A, Zuo YN, et al. 2017. Genetic disruption of ankyrin-G in adult mouse forebrain causes cortical synapse alteration and behavior reminiscent of bipolar disorder. Proceedings of the National Academy of Sciences of the United States of America, 114(39): 10479−10484. doi: 10.1073/pnas.1700689114
    [196]
    Zlokovic BV. 2011. Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders. Nature Reviews Neuroscience, 12(12): 723−738. doi: 10.1038/nrn3114
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(2)

    Article Metrics

    Article views (3129) PDF downloads(559) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return