Critical thinking of Alzheimer's transgenic mouse model: current research and future perspective

被引：6

作者：

Li, Xinyue ^{[1
,2
]}

Quan, Meina ^{[1
,2
,3
]}

Wei, Yiping ^{[1
,2
]}

Wang, Wei ^{[1
,2
,3
]}

Xu, Lingzhi ^{[1
,2
]}

Wang, Qi ^{[1
,2
,3
]}

Jia, Jianping ^{[1
,2
,3
,4
,5
,6
,7
]}

机构：

[1] Capital Med Univ, Innovat Ctr Neurol Disorders, Beijing 100053, Peoples R China

[2] Capital Med Univ, Xuanwu Hosp, Dept Neurol, Beijing 100053, Peoples R China

[3] Natl Med Ctr Neurol Dis & Natl Clin Res Ctr Geria, Beijing 100053, Peoples R China

[4] Beijing Key Lab Geriatr Cognit Disorders, Beijing 100053, Peoples R China

[5] Capital Med Univ, Clin Ctr Neurodegenerat Dis & Memory Impairment, Beijing 100053, Peoples R China

[6] Capital Med Univ, Beijing Inst Brain Disorders, Collaborat Innovat Ctr Brain Disorders, Ctr Alzheimers Dis, Beijing 100053, Peoples R China

[7] Minist Educ, Key Lab Neurodegenerat Dis, Beijing 100053, Peoples R China

来源：

SCIENCE CHINA-LIFE SCIENCES | 2023年 / 66卷 / 12期

基金：

中国国家自然科学基金;

关键词：

Alzheimer's disease; transgenic mouse model; amyloid-beta oligomers; multi-target therapy; AMYLOID-PRECURSOR-PROTEIN; LONG-TERM POTENTIATION; A-BETA-DEPOSITION; NEUROFIBRILLARY TANGLE FORMATION; SPATIAL MEMORY DEFICIT; COGNITIVE DEFICITS; KNOCK-IN; SYNAPTIC PLASTICITY; MUTANT PRESENILIN-1; NEURONAL LOSS;

D O I：

10.1007/s11427-022-2357-x

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Transgenic models are useful tools for studying the pathogenesis of and drug development for Alzheimer's Disease (AD). AD models are constructed usually using overexpression or knock-in of multiple pathogenic gene mutations from familial AD. Each transgenic model has its unique behavioral and pathological features. This review summarizes the research progress of transgenic mouse models, and their progress in the unique mechanism of amyloid-beta oligomers, including the first transgenic mouse model built in China based on a single gene mutation (PSEN1 V97L) found in Chinese familial AD. We further summarized the preclinical findings of drugs using the models, and their future application in exploring the upstream mechanisms and multitarget drug development in AD.

引用

页码：2711 / 2754

页数：44

共 380 条

[1] Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies [J].

Adalbert, Robert ;

Nogradi, Antal ;

Babetto, Elisabetta ;

Janeckova, Lucie ;

Walker, Simon A. ;

Kerschensteiner, Martin ;

Misgeld, Thomas ;

Coleman, Michael P. .

BRAIN, 2009, 132 :402-416

[2] Use of Caenorhabditis elegans as a model to study Alzheimer's disease and other neurodegenerative diseases [J].

Alexander, Adanna G. ;

Marfil, Vanessa ;

Li, Chris .

FRONTIERS IN GENETICS, 2014, 5

[3] Longitudinal cognitive decline in autosomal-dominant Alzheimer's disease varies with mutations in APP and PSEN1 genes [J].

Almkvist, Ove ;

Rodriguez-Vieitez, Elena ;

Thordardottir, Steinunn ;

Nordberg, Agneta ;

Viitanen, Matti ;

Lannfelt, Lars ;

Graff, Caroline .

NEUROBIOLOGY OF AGING, 2019, 82 :40-47

[4] Exenatide alleviates mitochondrial dysfunction and cognitive impairment in the 5 x FAD mouse model of Alzheimer's disease [J].

An, Jingjing ;

Zhou, Yu ;

Zhang, Mengjun ;

Xie, Yunzhen ;

Ke, Sujie ;

Liu, Libin ;

Pan, Xiaodong ;

Chen, Zhou .

BEHAVIOURAL BRAIN RESEARCH, 2019, 370

[5] Tryptophan-tyrosine dipeptide improves tau-related symptoms in tauopathy mice [J].

Ano, Yasuhisa ;

Takaichi, Yuta ;

Ohya, Rena ;

Uchida, Kazuyuki ;

Nakayama, Hiroyuki ;

Takashima, Akihiko .

NUTRITIONAL NEUROSCIENCE, 2023, 26 (08) :766-777

[6] RAGE potentiates Aβ-induced perturbation of neuronal function in transgenic mice [J].

Arancio, O ;

Zhang, HP ;

Chen, X ;

Lin, C ;

Trinchese, F ;

Puzzo, D ;

Liu, SM ;

Hegde, A ;

Yan, SF ;

Stern, A ;

Luddy, JS ;

Lue, LF ;

Walker, DG ;

Roher, A ;

Buttini, M ;

Mucke, L ;

Li, WY ;

Schmidt, AM ;

Kindy, M ;

Hyslop, PA ;

Stern, DM ;

Du Yan, SS .

EMBO JOURNAL, 2004, 23 (20) :4096-4105

[7] Progressive, age-related behavioral impairments in transgenic mice carrying both mutant amyloid precursor protein and presenilin-1 transgenes [J].

Arendash, GW ;

King, DL ;

Gordon, MN ;

Morgan, D ;

Hatcher, JM ;

Hope, CE ;

Diamond, DM .

BRAIN RESEARCH, 2001, 891 (1-2) :42-53

[8] The Swedish dilemma - the almost exclusive use of APPswe-based mouse models impedes adequate evaluation of alternative β-secretases [J].

Armbrust, Fred ;

Bickenbach, Kira ;

Marengo, Liana ;

Pietrzik, Claus ;

Becker-Pauly, Christoph .

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2022, 1869 (03)

[9] Generation of a humanized Aβ expressing mouse demonstrating aspects of Alzheimer's disease-like pathology [J].

Baglietto-Vargas, David ;

Forner, Stefania ;

Cai, Lena ;

Martini, Alessandra C. ;

Trujillo-Estrada, Laura ;

Swarup, Vivek ;

Marie Minh Thu Nguyen ;

Kelly Do Huynh ;

Javonillo, Dominic, I ;

Kristine Minh Tran ;

Phan, Jimmy ;

Jiang, Shan ;

Kramar, Eniko A. ;

Nunez-Diaz, Cristina ;

Balderrama-Gutierrez, Gabriela ;

Garcia, Franklin ;

Childs, Jessica ;

Rodriguez-Ortiz, Carlos J. ;

Antonio Garcia-Leon, Juan ;

Kitazawa, Masashi ;

Shahnawaz, Mohammad ;

Matheos, Dina P. ;

Ma, Xinyi ;

Da Cunha, Celia ;

Walls, Ken C. ;

Ager, Rahasson R. ;

Soto, Claudio ;

Gutierrez, Antonia ;

Moreno-Gonzalez, Ines ;

Mortazavi, Ali ;

Tenner, Andrea J. ;

MacGregor, Grant R. ;

Wood, Marcelo ;

Green, Kim N. ;

LaFerla, Frank M. .

NATURE COMMUNICATIONS, 2021, 12 (01)

[10] Functional phonotype in transgenic mice expressing mutant human presenilin-1 [J].

Barrow, PA ;

Empson, RM ;

Gladwell, SJ ;

Anderson, CM ;

Killick, R ;

Yu, X ;

Jefferys, JGR ;

Duff, K .

NEUROBIOLOGY OF DISEASE, 2000, 7 (02) :119-126

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