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.
Keywords: Alzheimer`s disease, amyloid deposition, APPswe/PS1dE9 transgenic mice, cerebral Aβ42, cognitive decline, serum Aβ42.
Current Alzheimer Research
Title:Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice
Volume: 15 Issue: 11
Author(s): Lu Fu, Yao Sun, Yongqing Guo, Bin Yu, Haihong Zhang, Jiaxin Wu, Xianghui Yu, Hui Wu*Wei Kong*
Affiliation:
- 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
Keywords: Alzheimer`s disease, amyloid deposition, APPswe/PS1dE9 transgenic mice, cerebral Aβ42, cognitive decline, serum Aβ42.
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.
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Cite this article as:
Fu Lu , Sun Yao , Guo Yongqing , Yu Bin , Zhang Haihong , Wu Jiaxin , Yu Xianghui , Wu Hui *, Kong Wei *, 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 2018; 15 (11) . https://dx.doi.org/10.2174/1567205015666180709112327
DOI https://dx.doi.org/10.2174/1567205015666180709112327 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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