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Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer’s Disease patients: A pilot study
Decreased Choline Acetyltransferase (ChAT) brain level is one of the main biochemical disorders in Alzheimer’s Disease (AD). In rodents, recent data show that the CHAT gene can be regulated by a neural restrictive silencer factor (NRSF). The aim of the present work was to evaluate the gene and prote...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Sociedade Brasileira de Genética
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3615522/ https://www.ncbi.nlm.nih.gov/pubmed/23569405 http://dx.doi.org/10.1590/S1415-47572013000100005 |
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author | González-Castañeda, Rocío E. Sánchez-González, Víctor J. Flores-Soto, Mario Vázquez-Camacho, Gonzalo Macías-Islas, Miguel A. Ortiz, Genaro G. |
author_facet | González-Castañeda, Rocío E. Sánchez-González, Víctor J. Flores-Soto, Mario Vázquez-Camacho, Gonzalo Macías-Islas, Miguel A. Ortiz, Genaro G. |
author_sort | González-Castañeda, Rocío E. |
collection | PubMed |
description | Decreased Choline Acetyltransferase (ChAT) brain level is one of the main biochemical disorders in Alzheimer’s Disease (AD). In rodents, recent data show that the CHAT gene can be regulated by a neural restrictive silencer factor (NRSF). The aim of the present work was to evaluate the gene and protein expression of CHAT and NRSF in frontal, temporal, entorhinal and parietal cortices of AD patient brains. Four brains from patients with AD and four brains from subjects without dementia were studied. Cerebral tissues were obtained and processed by the guanidine isothiocyanate method for RNA extraction. CHAT and NRSF gene and protein expression were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. CHAT gene expression levels were 39% lower in AD patients as compared to the control group (p < 0.05, U test). ChAT protein levels were reduced by 17% (p = 0.02, U test). NRSF gene expression levels were 86% higher in the AD group (p = 0.001, U test) as compared to the control group. In the AD subjects, the NRSF protein levels were 57% higher (p > 0.05, U test) than in the control subjects. These findings suggest for the first time that in the brain of AD patients high NRSF protein levels are related to low CHAT gene expression levels. |
format | Online Article Text |
id | pubmed-3615522 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Sociedade Brasileira de Genética |
record_format | MEDLINE/PubMed |
spelling | pubmed-36155222013-04-08 Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer’s Disease patients: A pilot study González-Castañeda, Rocío E. Sánchez-González, Víctor J. Flores-Soto, Mario Vázquez-Camacho, Gonzalo Macías-Islas, Miguel A. Ortiz, Genaro G. Genet Mol Biol Human and Medical Genetics Decreased Choline Acetyltransferase (ChAT) brain level is one of the main biochemical disorders in Alzheimer’s Disease (AD). In rodents, recent data show that the CHAT gene can be regulated by a neural restrictive silencer factor (NRSF). The aim of the present work was to evaluate the gene and protein expression of CHAT and NRSF in frontal, temporal, entorhinal and parietal cortices of AD patient brains. Four brains from patients with AD and four brains from subjects without dementia were studied. Cerebral tissues were obtained and processed by the guanidine isothiocyanate method for RNA extraction. CHAT and NRSF gene and protein expression were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. CHAT gene expression levels were 39% lower in AD patients as compared to the control group (p < 0.05, U test). ChAT protein levels were reduced by 17% (p = 0.02, U test). NRSF gene expression levels were 86% higher in the AD group (p = 0.001, U test) as compared to the control group. In the AD subjects, the NRSF protein levels were 57% higher (p > 0.05, U test) than in the control subjects. These findings suggest for the first time that in the brain of AD patients high NRSF protein levels are related to low CHAT gene expression levels. Sociedade Brasileira de Genética 2013-03-04 2013-03 /pmc/articles/PMC3615522/ /pubmed/23569405 http://dx.doi.org/10.1590/S1415-47572013000100005 Text en Copyright © 2013, Sociedade Brasileira de Genética. License information: This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Human and Medical Genetics González-Castañeda, Rocío E. Sánchez-González, Víctor J. Flores-Soto, Mario Vázquez-Camacho, Gonzalo Macías-Islas, Miguel A. Ortiz, Genaro G. Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer’s Disease patients: A pilot study |
title | Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer’s Disease patients: A pilot study |
title_full | Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer’s Disease patients: A pilot study |
title_fullStr | Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer’s Disease patients: A pilot study |
title_full_unstemmed | Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer’s Disease patients: A pilot study |
title_short | Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer’s Disease patients: A pilot study |
title_sort | neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of alzheimer’s disease patients: a pilot study |
topic | Human and Medical Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3615522/ https://www.ncbi.nlm.nih.gov/pubmed/23569405 http://dx.doi.org/10.1590/S1415-47572013000100005 |
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