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

doi:10.1007/s11427-022-2357-x

Review

. 2023 Dec;66(12):2711-2754.

doi: 10.1007/s11427-022-2357-x. Epub 2023 Jul 17.

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

Xinyue Li^#¹, Meina Quan^#^{1

2}, Yiping Wei¹, Wei Wang^{1

2}, Lingzhi Xu¹, Qi Wang^{1

2}, Jianping Jia^{3

4

5

6

7

8}

Affiliations

¹ Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
² National Medical Center for Neurological Diseases and National Clinical Research Center for Geriatric Diseases, Beijing, 100053, China.
³ Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. jiajp@vip.126.com.
⁴ National Medical Center for Neurological Diseases and National Clinical Research Center for Geriatric Diseases, Beijing, 100053, China. jiajp@vip.126.com.
⁵ Beijing Key Laboratory of Geriatric Cognitive Disorders, Beijing, 100053, China. jiajp@vip.126.com.
⁶ Clinical Center for Neurodegenerative Disease and Memory Impairment, Capital Medical University, Beijing, 100053, China. jiajp@vip.126.com.
⁷ Center of Alzheimer's Disease, Beijing Institute of Brain Disorders, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, 100053, China. jiajp@vip.126.com.
⁸ Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing, 100053, China. jiajp@vip.126.com.

^# Contributed equally.

PMID: 37480469
DOI: 10.1007/s11427-022-2357-x

Review

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

Xinyue Li et al. Sci China Life Sci. 2023 Dec.

. 2023 Dec;66(12):2711-2754.

doi: 10.1007/s11427-022-2357-x. Epub 2023 Jul 17.

Authors

Xinyue Li^#¹, Meina Quan^#^{1

2}, Yiping Wei¹, Wei Wang^{1

2}, Lingzhi Xu¹, Qi Wang^{1

2}, Jianping Jia^{3

4

5

6

7

8}

Affiliations

¹ Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
² National Medical Center for Neurological Diseases and National Clinical Research Center for Geriatric Diseases, Beijing, 100053, China.
³ Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. jiajp@vip.126.com.
⁴ National Medical Center for Neurological Diseases and National Clinical Research Center for Geriatric Diseases, Beijing, 100053, China. jiajp@vip.126.com.
⁵ Beijing Key Laboratory of Geriatric Cognitive Disorders, Beijing, 100053, China. jiajp@vip.126.com.
⁶ Clinical Center for Neurodegenerative Disease and Memory Impairment, Capital Medical University, Beijing, 100053, China. jiajp@vip.126.com.
⁷ Center of Alzheimer's Disease, Beijing Institute of Brain Disorders, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, 100053, China. jiajp@vip.126.com.
⁸ Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing, 100053, China. jiajp@vip.126.com.

^# Contributed equally.

PMID: 37480469
DOI: 10.1007/s11427-022-2357-x

Abstract

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-β 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.

Keywords: Alzheimer’s disease; amyloid-β oligomers; multi-target therapy; transgenic mouse model.

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References

1. Adalbert, R., Nogradi, A., Babetto, E., Janeckova, L., Walker, S.A., Kerschensteiner, M., Misgeld, T., and Coleman, M.P. (2009). Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies. Brain 132, 402–416. - PubMed
1. Alexander, A.G., Marfil, V., and Li, C. (2014). Use of Caenorhabditis elegans as a model to study Alzheimer’s disease and other neurodegenerative diseases. Front Genet 5, 279. - PubMed - PMC
1. Almkvist, O., Rodriguez-Vieitez, E., Thordardottir, S., Nordberg, A., Viitanen, M., Lannfelt, L., and Graff, C. (2019). Longitudinal cognitive decline in autosomal-dominant Alzheimer’s disease varies with mutations in APP and PSEN1 genes. Neurobiol Aging 82, 40–47. - PubMed
1. An, J., Zhou, Y., Zhang, M., Xie, Y., Ke, S., Liu, L., Pan, X., and Chen, Z. (2019). Exenatide alleviates mitochondrial dysfunction and cognitive impairment in the 5×FAD mouse model of Alzheimer’s disease. Behav Brain Res 370, 111932. - PubMed
1. Ano, Y., Takaichi, Y., Ohya, R., Uchida, K., Nakayama, H., and Takashima, A. (2023). Tryptophan-tyrosine dipeptide improves tau-related symptoms in tauopathy mice. Nutr Neurosci 26, 766–777. - PubMed

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[1] Adalbert, R., Nogradi, A., Babetto, E., Janeckova, L., Walker, S.A., Kerschensteiner, M., Misgeld, T., and Coleman, M.P. (2009). Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies. Brain 132, 402–416. - PubMed

[2] Adalbert, R., Nogradi, A., Babetto, E., Janeckova, L., Walker, S.A., Kerschensteiner, M., Misgeld, T., and Coleman, M.P. (2009). Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies. Brain 132, 402–416. - PubMed

[3] Alexander, A.G., Marfil, V., and Li, C. (2014). Use of Caenorhabditis elegans as a model to study Alzheimer’s disease and other neurodegenerative diseases. Front Genet 5, 279. - PubMed - PMC

[4] Alexander, A.G., Marfil, V., and Li, C. (2014). Use of Caenorhabditis elegans as a model to study Alzheimer’s disease and other neurodegenerative diseases. Front Genet 5, 279. - PubMed - PMC

[5] Almkvist, O., Rodriguez-Vieitez, E., Thordardottir, S., Nordberg, A., Viitanen, M., Lannfelt, L., and Graff, C. (2019). Longitudinal cognitive decline in autosomal-dominant Alzheimer’s disease varies with mutations in APP and PSEN1 genes. Neurobiol Aging 82, 40–47. - PubMed

[6] Almkvist, O., Rodriguez-Vieitez, E., Thordardottir, S., Nordberg, A., Viitanen, M., Lannfelt, L., and Graff, C. (2019). Longitudinal cognitive decline in autosomal-dominant Alzheimer’s disease varies with mutations in APP and PSEN1 genes. Neurobiol Aging 82, 40–47. - PubMed

[7] An, J., Zhou, Y., Zhang, M., Xie, Y., Ke, S., Liu, L., Pan, X., and Chen, Z. (2019). Exenatide alleviates mitochondrial dysfunction and cognitive impairment in the 5×FAD mouse model of Alzheimer’s disease. Behav Brain Res 370, 111932. - PubMed

[8] An, J., Zhou, Y., Zhang, M., Xie, Y., Ke, S., Liu, L., Pan, X., and Chen, Z. (2019). Exenatide alleviates mitochondrial dysfunction and cognitive impairment in the 5×FAD mouse model of Alzheimer’s disease. Behav Brain Res 370, 111932. - PubMed

[9] Ano, Y., Takaichi, Y., Ohya, R., Uchida, K., Nakayama, H., and Takashima, A. (2023). Tryptophan-tyrosine dipeptide improves tau-related symptoms in tauopathy mice. Nutr Neurosci 26, 766–777. - PubMed

[10] Ano, Y., Takaichi, Y., Ohya, R., Uchida, K., Nakayama, H., and Takashima, A. (2023). Tryptophan-tyrosine dipeptide improves tau-related symptoms in tauopathy mice. Nutr Neurosci 26, 766–777. - PubMed

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

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

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