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+874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease

In the recent years, several cytokines have been associated with Alzheimer's disease (AD) development and progression and many studies have correlated this risk with polymorphisms in the genes encoding these molecules. Also the type 1 cytokine interferon (IFN)-γ belongs to a cytokine class that...

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Autores principales: Galimberti, Lorenza, Arosio, Beatrice, Calabresi, Carmen, Scurati, Silvia, Hamilton, Susanna, Carpini, Simona Delli, Vergani, Carlo, Annoni, Giorgio
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2004
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC544959/
https://www.ncbi.nlm.nih.gov/pubmed/15679925
http://dx.doi.org/10.1186/1742-4933-1-6
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author Galimberti, Lorenza
Arosio, Beatrice
Calabresi, Carmen
Scurati, Silvia
Hamilton, Susanna
Carpini, Simona Delli
Vergani, Carlo
Annoni, Giorgio
author_facet Galimberti, Lorenza
Arosio, Beatrice
Calabresi, Carmen
Scurati, Silvia
Hamilton, Susanna
Carpini, Simona Delli
Vergani, Carlo
Annoni, Giorgio
author_sort Galimberti, Lorenza
collection PubMed
description In the recent years, several cytokines have been associated with Alzheimer's disease (AD) development and progression and many studies have correlated this risk with polymorphisms in the genes encoding these molecules. Also the type 1 cytokine interferon (IFN)-γ belongs to a cytokine class that affects the immune function; in fact it plays a major role in defence against viruses and intracellular pathogens but also in the induction of the immune-mediated inflammatory response. The aim of this study was to evaluate the role of IFN-γ in AD by studying the association of +874T→A IFN-γ gene polymorphism with AD. We included in this study 115 AD patients (70 women, 45 men, mean age 80) and 90 sex and age-matched healthy controls (HC, 51 women, 39 men, mean age 82) from northern Italy. Genomic DNA was extracted with the salting-out method from whole blood of all subjects; the genotyping at IFN-γ loci was assessed with ARMS-PCR. The data obtained from the +874T→A IFN-γ gene polymorphism analysis of AD patients and HC lack of any statistically significant differences also when stratified according to gender. In conclusion these results confirm the previous shown lack of association between +874T→A IFN-γ gene polymorphism and the risk of AD. However, other polymorphisms have been demonstrated to influence IFN-γ transcription and since natural killer cells of AD patients show higher production of the cytokine, further analysis will be necessary to clarify the role of this gene in the pathogenesis of the disease.
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spelling pubmed-5449592005-01-26 +874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease Galimberti, Lorenza Arosio, Beatrice Calabresi, Carmen Scurati, Silvia Hamilton, Susanna Carpini, Simona Delli Vergani, Carlo Annoni, Giorgio Immun Ageing Short Report In the recent years, several cytokines have been associated with Alzheimer's disease (AD) development and progression and many studies have correlated this risk with polymorphisms in the genes encoding these molecules. Also the type 1 cytokine interferon (IFN)-γ belongs to a cytokine class that affects the immune function; in fact it plays a major role in defence against viruses and intracellular pathogens but also in the induction of the immune-mediated inflammatory response. The aim of this study was to evaluate the role of IFN-γ in AD by studying the association of +874T→A IFN-γ gene polymorphism with AD. We included in this study 115 AD patients (70 women, 45 men, mean age 80) and 90 sex and age-matched healthy controls (HC, 51 women, 39 men, mean age 82) from northern Italy. Genomic DNA was extracted with the salting-out method from whole blood of all subjects; the genotyping at IFN-γ loci was assessed with ARMS-PCR. The data obtained from the +874T→A IFN-γ gene polymorphism analysis of AD patients and HC lack of any statistically significant differences also when stratified according to gender. In conclusion these results confirm the previous shown lack of association between +874T→A IFN-γ gene polymorphism and the risk of AD. However, other polymorphisms have been demonstrated to influence IFN-γ transcription and since natural killer cells of AD patients show higher production of the cytokine, further analysis will be necessary to clarify the role of this gene in the pathogenesis of the disease. BioMed Central 2004-11-12 /pmc/articles/PMC544959/ /pubmed/15679925 http://dx.doi.org/10.1186/1742-4933-1-6 Text en Copyright © 2004 Galimberti et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Short Report
Galimberti, Lorenza
Arosio, Beatrice
Calabresi, Carmen
Scurati, Silvia
Hamilton, Susanna
Carpini, Simona Delli
Vergani, Carlo
Annoni, Giorgio
+874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease
title +874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease
title_full +874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease
title_fullStr +874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease
title_full_unstemmed +874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease
title_short +874(T→A) single nucleotide gene polymorphism does not represent a risk factor for Alzheimer's disease
title_sort +874(t→a) single nucleotide gene polymorphism does not represent a risk factor for alzheimer's disease
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC544959/
https://www.ncbi.nlm.nih.gov/pubmed/15679925
http://dx.doi.org/10.1186/1742-4933-1-6
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