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Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice.
Curr Alzheimer Res. 2018; 15(11):1053-1061.CA

Abstract

BACKGROUND

Mice co-expressing human amyloid precursor protein with the Swedish mutation (APPswe) and exon-9-deleted presenilin (PS1dE9) has become one of the most widely used mouse models for studying Alzheimer's disease (AD) pathogenesis and preclinical studies of AD therapeutic approaches.

OBJECTIVE

In this study, we systematically investigated cognitive decline, amyloid-β (Aβ) deposition and cerebral or Aβ serum levels as well as the relationships among these measures in APPswe/PS1dE9 transgenic mice.

METHOD

APPswe/PS1dE9 mice were separated into four equal age cohorts (4, 6, 9, and 12 months). We assessed cognitive capacity, deposited plaques, and the levels of Aβ40/Aβ42 in brain tissue and serum of mice at different ages.

RESULTS

APPswe/PS1dE9 mice exhibited declined memory beginning at 6 months of age, with cognitive capacity remarkably impaired at 12-months. Coincidently, amyloid deposits began to develop in transgenic mice brain at 6-months and increased with age. In addition, Aβ42 levels in brains of APPswe/ PS1dE9 mice increased with age with no parallel increase in Aβ40. The concentration of serum Aβ42 declined from 4 to 6 months of age, but a similar age-dependent decrease was not observed for Aβ40.

CONCLUSION

APPswe/PS1dE9 transgenic mice began to develop amyloid plaques at 6 months of age and exhibited a corresponding impairment of spatial learning capacity. Serum Aβ42 level decreased remarkably from 4 to 6 months, at which stage Aβ42 began to accumulate in the brain and deposit as plaques.

Authors+Show Affiliations

National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China. Laboratory of Pathogenic Microbiology and Immunology, College of life science, Jilin Agricultural University, Changchun 130118, China.National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China.National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China.National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China. Key Laboratory for Molecular Enzymology and Engineering, the Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China. Key Laboratory for Molecular Enzymology and Engineering, the Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China. Key Laboratory for Molecular Enzymology and Engineering, the Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China. Key Laboratory for Molecular Enzymology and Engineering, the Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China. Key Laboratory for Molecular Enzymology and Engineering, the Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China. Key Laboratory for Molecular Enzymology and Engineering, the Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29984654

Citation

Fu, Lu, et al. "Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice." Current Alzheimer Research, vol. 15, no. 11, 2018, pp. 1053-1061.
Fu L, Sun Y, Guo Y, et al. Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice. Curr Alzheimer Res. 2018;15(11):1053-1061.
Fu, L., Sun, Y., Guo, Y., Yu, B., Zhang, H., Wu, J., Yu, X., Wu, H., & Kong, W. (2018). Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice. Current Alzheimer Research, 15(11), 1053-1061. https://doi.org/10.2174/1567205015666180709112327
Fu L, et al. Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice. Curr Alzheimer Res. 2018;15(11):1053-1061. PubMed PMID: 29984654.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice. AU - Fu,Lu, AU - Sun,Yao, AU - Guo,Yongqing, AU - Yu,Bin, AU - Zhang,Haihong, AU - Wu,Jiaxin, AU - Yu,Xianghui, AU - Wu,Hui, AU - Kong,Wei, PY - 2018/03/12/received PY - 2018/05/09/revised PY - 2018/07/05/accepted PY - 2018/7/10/pubmed PY - 2019/10/18/medline PY - 2018/7/10/entrez KW - APPswe/PS1dE9 transgenic mice KW - Alzheimer`s disease KW - amyloid deposition KW - cerebral Aβ42 KW - cognitive decline KW - serum Aβ42. SP - 1053 EP - 1061 JF - Current Alzheimer research JO - Curr Alzheimer Res VL - 15 IS - 11 N2 - BACKGROUND: Mice co-expressing human amyloid precursor protein with the Swedish mutation (APPswe) and exon-9-deleted presenilin (PS1dE9) has become one of the most widely used mouse models for studying Alzheimer's disease (AD) pathogenesis and preclinical studies of AD therapeutic approaches. OBJECTIVE: In this study, we systematically investigated cognitive decline, amyloid-β (Aβ) deposition and cerebral or Aβ serum levels as well as the relationships among these measures in APPswe/PS1dE9 transgenic mice. METHOD: APPswe/PS1dE9 mice were separated into four equal age cohorts (4, 6, 9, and 12 months). We assessed cognitive capacity, deposited plaques, and the levels of Aβ40/Aβ42 in brain tissue and serum of mice at different ages. RESULTS: APPswe/PS1dE9 mice exhibited declined memory beginning at 6 months of age, with cognitive capacity remarkably impaired at 12-months. Coincidently, amyloid deposits began to develop in transgenic mice brain at 6-months and increased with age. In addition, Aβ42 levels in brains of APPswe/ PS1dE9 mice increased with age with no parallel increase in Aβ40. The concentration of serum Aβ42 declined from 4 to 6 months of age, but a similar age-dependent decrease was not observed for Aβ40. CONCLUSION: APPswe/PS1dE9 transgenic mice began to develop amyloid plaques at 6 months of age and exhibited a corresponding impairment of spatial learning capacity. Serum Aβ42 level decreased remarkably from 4 to 6 months, at which stage Aβ42 began to accumulate in the brain and deposit as plaques. SN - 1875-5828 UR - https://www.unboundmedicine.com/medline/citation/29984654/Progressive_Spatial_Memory_Impairment_Brain_Amyloid_Deposition_and_Changes_in_Serum_Amyloid_Levels_as_a_Function_of_Age_in_APPswe/PS1dE9_Mice_ L2 - http://www.eurekaselect.com/163619/article DB - PRIME DP - Unbound Medicine ER -