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Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia
BACKGROUND AND AIMS: Similar clinical and pathological features have been observed in Alzheimer's disease (AD) and Parkinson's disease with dementia (PDD). Both the peroxisome proliferator-activated receptor-γ (PPAR-γ) gene and the peroxisome proliferator-activated receptor-γ coactivator-1...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
S. Karger AG
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670632/ https://www.ncbi.nlm.nih.gov/pubmed/23741228 http://dx.doi.org/10.1159/000351419 |
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author | Shibata, Nobuto Motoi, Yumiko Tomiyama, Hiroyuki Ohnuma, Tohru Kuerban, Bolati Tomson, Katrin Komatsu, Miwa Shimazaki, Hiromi Hattori, Nobutaka Arai, Heii |
author_facet | Shibata, Nobuto Motoi, Yumiko Tomiyama, Hiroyuki Ohnuma, Tohru Kuerban, Bolati Tomson, Katrin Komatsu, Miwa Shimazaki, Hiromi Hattori, Nobutaka Arai, Heii |
author_sort | Shibata, Nobuto |
collection | PubMed |
description | BACKGROUND AND AIMS: Similar clinical and pathological features have been observed in Alzheimer's disease (AD) and Parkinson's disease with dementia (PDD). Both the peroxisome proliferator-activated receptor-γ (PPAR-γ) gene and the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) gene are candidates modifying the risk for both diseases. The aim of this study was to clarify whether common single nucleotide polymorphisms (SNPs) of the PPAR-γ gene and the PGC-1α gene affect the onset of AD and PDD genetically. METHODS: Four exonic SNPs of both genes (rs1801282 and rs3856806 of the PPAR-γ gene, rs3736265 and rs8192678 of the PGC-1α gene) were genotyped in 171 AD patients, 136 age-matched controls and 53 PDD patients. Haplotype analysis and logistic regression analysis with apolipoprotein E (APO E) status were performed for AD. RESULTS: There was no statistical difference between AD cases and controls for the 4 SNPs, nor was there any statistical difference between PDD cases and controls for the 4 SNPs. We could not find any synergetic associations between these SNPs, APO E4 and AD. CONCLUSIONS: The 4 SNPs studied here did not influence the risk for AD in a Japanese population. As the number of PDD cases was small, comprehensive genetic studies considering diabetes would be needed. |
format | Online Article Text |
id | pubmed-3670632 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | S. Karger AG |
record_format | MEDLINE/PubMed |
spelling | pubmed-36706322013-06-05 Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia Shibata, Nobuto Motoi, Yumiko Tomiyama, Hiroyuki Ohnuma, Tohru Kuerban, Bolati Tomson, Katrin Komatsu, Miwa Shimazaki, Hiromi Hattori, Nobutaka Arai, Heii Dement Geriatr Cogn Dis Extra Original Research Article BACKGROUND AND AIMS: Similar clinical and pathological features have been observed in Alzheimer's disease (AD) and Parkinson's disease with dementia (PDD). Both the peroxisome proliferator-activated receptor-γ (PPAR-γ) gene and the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) gene are candidates modifying the risk for both diseases. The aim of this study was to clarify whether common single nucleotide polymorphisms (SNPs) of the PPAR-γ gene and the PGC-1α gene affect the onset of AD and PDD genetically. METHODS: Four exonic SNPs of both genes (rs1801282 and rs3856806 of the PPAR-γ gene, rs3736265 and rs8192678 of the PGC-1α gene) were genotyped in 171 AD patients, 136 age-matched controls and 53 PDD patients. Haplotype analysis and logistic regression analysis with apolipoprotein E (APO E) status were performed for AD. RESULTS: There was no statistical difference between AD cases and controls for the 4 SNPs, nor was there any statistical difference between PDD cases and controls for the 4 SNPs. We could not find any synergetic associations between these SNPs, APO E4 and AD. CONCLUSIONS: The 4 SNPs studied here did not influence the risk for AD in a Japanese population. As the number of PDD cases was small, comprehensive genetic studies considering diabetes would be needed. S. Karger AG 2013-05-18 /pmc/articles/PMC3670632/ /pubmed/23741228 http://dx.doi.org/10.1159/000351419 Text en Copyright © 2013 by S. Karger AG, Basel http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Users may download, print and share this work on the Internet for noncommercial purposes only, provided the original work is properly cited, and a link to the original work on http://www.karger.com and the terms of this license are included in any shared versions. |
spellingShingle | Original Research Article Shibata, Nobuto Motoi, Yumiko Tomiyama, Hiroyuki Ohnuma, Tohru Kuerban, Bolati Tomson, Katrin Komatsu, Miwa Shimazaki, Hiromi Hattori, Nobutaka Arai, Heii Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia |
title | Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia |
title_full | Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia |
title_fullStr | Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia |
title_full_unstemmed | Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia |
title_short | Lack of Genetic Associations of PPAR-γ and PGC-1α with Alzheimer's Disease and Parkinson's Disease with Dementia |
title_sort | lack of genetic associations of ppar-γ and pgc-1α with alzheimer's disease and parkinson's disease with dementia |
topic | Original Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670632/ https://www.ncbi.nlm.nih.gov/pubmed/23741228 http://dx.doi.org/10.1159/000351419 |
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