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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Gene expression profile of amyloid beta protein-injected mouse model for Alzheimer disease
Ling-na Kong1, Ping-ping Zuo, Liang Mu
1Department of Pharmacology, School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100005, China.
Aim:
To investigate the gene expression profile changes in the cerebral cortex of mice injected icv with amyloid beta-protein (Abeta) fragment 25-35 using cDNA microarray.
Methods:
Balb/c mice were randomly divided into a control group and Abeta-treated group. The Morris water maze test was performed to detect the effect of Abeta-injection on the learning and memory of mice. Atlas Mouse 1.2 Expression Arrays containing 1176 genes were used to investigate the gene expression pattern of each group.
Results:
The gene expression profiles showed that 19 genes including TBX1, NF-kB, AP-1/c-Jun, cadherin, integrin, erb-B2, and FGFR1 were up-regulated after 2 weeks of icv administration of Abeta; while 12 genes were down-regulated, including NGF, glucose phosphate isomerase 1, AT motif binding factor 1, Na+/K+-ATPase, and Akt.
Conclusions:
The results provide important leads for pursuing a more complete understanding of the molecular events of Abeta-injection into mice with Alzheimer disease.
Insights
Amyloid beta-protein (Abeta) fragment 25-35 injection altered gene expression in mouse cerebral cortex, impacting learning and memory. This study identifies key up-regulated and down-regulated genes relevant to Alzheimer disease.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Alzheimer disease is characterized by amyloid beta-protein (Abeta) accumulation.
- Understanding the molecular mechanisms of Abeta toxicity is crucial for developing treatments.
Purpose of the Study:
- To investigate gene expression profile changes in the cerebral cortex of mice injected with Abeta fragment 25-35.
- To identify specific genes affected by Abeta administration relevant to Alzheimer disease pathology.
Main Methods:
- Balb/c mice were administered Abeta fragment 25-35 intracerebroventricularly (icv).
- Morris water maze test assessed learning and memory deficits.
- cDNA microarray analysis (Atlas Mouse 1.2 Expression Arrays) was used to profile gene expression of 1176 genes.
Main Results:
- Abeta injection led to significant changes in gene expression within 2 weeks.
- 19 genes were upregulated, including TBX1, NF-kB, AP-1/c-Jun, cadherin, integrin, erb-B2, and FGFR1.
- 12 genes were downregulated, including NGF, glucose phosphate isomerase 1, AT motif binding factor 1, Na+/K+-ATPase, and Akt.
Conclusions:
- Abeta fragment 25-35 administration induces distinct gene expression alterations in the mouse cerebral cortex.
- These findings offer insights into the molecular events underlying Abeta-induced neurotoxicity and Alzheimer disease.
- Identified gene changes provide potential targets for future therapeutic interventions.
