2014 Fiscal Year Final Research Report
Identification of target molecules related the progression of Alzheimer's disease
Project/Area Number |
24310144
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Medical genome science
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Research Institution | Niigata University |
Principal Investigator |
KUWANO Ryozo 新潟大学, 脳研究所, フェロー (20111734)
|
Co-Investigator(Kenkyū-buntansha) |
IKEUCHI Takeshi 新潟大学, 脳研究所, 教授 (20372469)
|
Co-Investigator(Renkei-kenkyūsha) |
MIYASHITA Akinori 新潟大学, 脳研究所, 助教 (60323995)
NAKAYA Akihiro 新潟大学, 研究推進機構, 准教授 (60301149)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Keywords | アルツハイマー病 / ゲノム / 脳組織 / ターゲット分子 / 染色体 / 培養細胞 / 遺伝子発現 / リスク遺伝子 |
Outline of Final Research Achievements |
Major neuropathological features of Alzheimer’s disease are senile plaques and neurofibrillary tangles .To identify genes relevant to neuropathological expansion defined by the Braak stage, we conducted whole-genome exon array analysis with 213 human postmortem brain tissues from the entorhinal, temporal and frontal cortices of 71 brain-donor subjects. We identified eight mRNAs and 5 non-coding RNAs associated with the progression of the characteristic lesion of Alzheimer’ disease brain diagnosed by Braak stage.We hypothesized that the phenotype-associated SNPs may spatially contact with distal genomic loci and may lead to regulate the gene expression. To analyze the relationship between the gene expression profiles by exon array and the higher-order chromatin structure data, we used the tethered conformation capture (TCC) method in the human neuroblastoma cell line, SK-N-SH, and the glioma cell line, U-251MG.
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Free Research Field |
神経分子遺伝学
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