Amyloid Deposition and Inflammation in APPswe/PS1dE9 Mouse Model of Alzheimer's Disease
文献类型：期刊论文
| 作者 | Ruan, LF; Kang, ZJ; Pei, G; Le, YY |
| 刊名 | CURRENT ALZHEIMER RESEARCH
 |
| 出版日期 | 2009 |
| 卷号 | 6期号:6页码:531-540 |
| 关键词 | Alzheimer's disease APPswe/PS1dE9 transgenic mouse amyloid deposition inflammation microglia astrocyte neuron |
| 通讯作者 | Le, YY (reprint author), Chinese Acad Sci, SIBS, Inst Nutr Sci, Grad Sch,Key Lab Nutr & Metab, 294 Taiyuan Rd, Shanghai 200031, Peoples R China.,yyle@sibs.ac.cn |
| 英文摘要 | Alzheimer's disease (AD) is characterized by amyloid plaques and neurofibrillary tangles associated with chronic inflammation. APPswe/PS1dE9 is an AD mouse model bearing mutant transgenes of amyloid precursor protein and presenilin-1. Amyloid deposition is present in this mouse model at early stage of life. However, the progression of inflammation and its relationship with amyloid deposition have not been characterized. Here we showed that amyloid plaques were present at 4 months of age and increased with age. CD11b-positive microglia clusters appeared in hippocampus and neocortex at 4 months of age and increased with age. Clustered glial fibrillary acidic protein (GFAP)-positive astrocytes were observed in hippocampus and cortex after 6 months of age and increased with age. Double staining with CD11b/GFAP antibody and thioflavin S showed clustered microglia and astrocytes were in close association with amyloid plaques. Expression of TNF-alpha was detected at 8 months of age, while IL-1 beta IL-6 and MCP-1 at 10 months. These cytokines increased with age. Double immunostaining of cell specific marker and cytokine indicated TNF-alpha, IL-1 beta, IL-6 and MCP-1 were expressed by activated microglia and a small part of activated astrocytes. MCP-1 was also expressed by neurons, which support recent finding that MCP-1 expression was increased in neurons of AD patient. These results demonstrate amyloid plaques and its associated inflammatory response developed at early stage of life and progressively increased with age, both activated glia and neurons are involved in chronic inflammation in AD. APPswe/PS1dE9 model provides a mean for studying the mechanisms and novel therapeutics for AD. |
| 学科主题 | Neurosciences & Neurology |
| 类目[WOS] | Clinical Neurology ; Neurosciences |
| 关键词[WOS] | TUMOR-NECROSIS-FACTOR ; COMPLEMENT CONTROL PROTEIN ; MONOCYTE CHEMOATTRACTANT PROTEIN-1 ; MILD COGNITIVE IMPAIRMENT ; NITRIC-OXIDE SYNTHASE ; A-BETA-DEPOSITION ; TRANSGENIC MICE ; PRECURSOR-PROTEIN ; MEMORY DEFICITS ; IN-VITRO |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000271344600008 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.143/handle/331003/1201]  |
| 专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
| 推荐引用方式 GB/T 7714 | Ruan, LF,Kang, ZJ,Pei, G,et al. Amyloid Deposition and Inflammation in APPswe/PS1dE9 Mouse Model of Alzheimer's Disease[J]. CURRENT ALZHEIMER RESEARCH,2009,6(6):531-540. |
| APA | Ruan, LF,Kang, ZJ,Pei, G,&Le, YY.(2009).Amyloid Deposition and Inflammation in APPswe/PS1dE9 Mouse Model of Alzheimer's Disease.CURRENT ALZHEIMER RESEARCH,6(6),531-540. |
| MLA | Ruan, LF,et al."Amyloid Deposition and Inflammation in APPswe/PS1dE9 Mouse Model of Alzheimer's Disease".CURRENT ALZHEIMER RESEARCH 6.6(2009):531-540. |
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