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APOE epsilon-4 allele and cytokine production in Alzheimer's disease.

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Title: APOE epsilon-4 allele and cytokine production in Alzheimer's disease.
Authors: Olgiati, Paolo, Politis, Antonis, Malitas, Petros, Albani, Diego, Dusi, Sabrina, Polito, Letizia, De Mauro, Stefania, Zisaki, Aikaterini, Piperi, Christina, Stamouli, Evangelia, Mailis, Antonis, Batelli, Sara, Forloni, Gianluigi, De Ronchi, Diana, Kalofoutis, Anastasios, Liappas, Ioannis, Serretti, Alessandro
Source: International Journal of Geriatric Psychiatry. Apr2010, Vol. 25 Issue 4, p338-344. 7p. 2 Charts.
Subjects: Genetics of Alzheimer's disease, Apolipoprotein E4, Cytokine genetics, Inflammatory mediators
Abstract: Objective: The APOE epsilon-4 allele has consistently emerged as a susceptibility factor for Alzheimer's disease (AD). Pro-inflammatory cytokines are detectable at abnormal levels in AD, and are thought to play a pathophysiological role. Animal studies have shown dose-dependent correlations between the number of APOE epsilon-4 alleles and the levels of pro-inflammatory cytokines. The aims of this study were to investigate the influence of APOE genotypes on TNF-o:, IL-6, and IL-lß secreted by peripheral blood mononuclear cells (PBMC) from human patients with AD and to analyze the correlation between cytokine production and AD clinical features. Methods: Outpatients with AD (w—40) were clinically evaluated for cognitive decline (MMSE) and psychiatric symptoms (Cornell Scale for Depression in Dementia; Neuropsychiatric Inventory) and genotyped for APOE variants. PBMCs were isolated from the donors and used to assess spontaneous and PMA-stimulated secretion of TNF-o:, IL-6, and IL-1/3. Cytokine production was determined by immuno-enzymatic assays (ELISA). Results: In comparison with their counterparts without APOE4, patients with at least one copy of the APOE epsilon-4 allele showed higher spontaneous (p —0.037) and PMA-induced (p —0.039) production of IL-lß after controlling for clinical variables. Significant correlations were reported between NPI scores (psychotic symptoms) and IL-6 production. Conclusion: These preliminary findings suggest the involvement of inflammatory response in the pathogenic effect of the APOE epsilon-4 allele in AD, although their replication in larger samples is mandatory. The modest correlations between pro-inflammatory cytokines released at peripheral level and AD features emphasizes the need for further research to elucidate the role of neuroinflammation in pathophysiology of AD. Copyright © 2009 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]
Copyright of International Journal of Geriatric Psychiatry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Label: Title
  Group: Ti
  Data: APOE epsilon-4 allele and cytokine production in Alzheimer's disease.
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  Data: <searchLink fieldCode="AR" term="%22Olgiati%2C+Paolo%22">Olgiati, Paolo</searchLink><br /><searchLink fieldCode="AR" term="%22Politis%2C+Antonis%22">Politis, Antonis</searchLink><br /><searchLink fieldCode="AR" term="%22Malitas%2C+Petros%22">Malitas, Petros</searchLink><br /><searchLink fieldCode="AR" term="%22Albani%2C+Diego%22">Albani, Diego</searchLink><br /><searchLink fieldCode="AR" term="%22Dusi%2C+Sabrina%22">Dusi, Sabrina</searchLink><br /><searchLink fieldCode="AR" term="%22Polito%2C+Letizia%22">Polito, Letizia</searchLink><br /><searchLink fieldCode="AR" term="%22De+Mauro%2C+Stefania%22">De Mauro, Stefania</searchLink><br /><searchLink fieldCode="AR" term="%22Zisaki%2C+Aikaterini%22">Zisaki, Aikaterini</searchLink><br /><searchLink fieldCode="AR" term="%22Piperi%2C+Christina%22">Piperi, Christina</searchLink><br /><searchLink fieldCode="AR" term="%22Stamouli%2C+Evangelia%22">Stamouli, Evangelia</searchLink><br /><searchLink fieldCode="AR" term="%22Mailis%2C+Antonis%22">Mailis, Antonis</searchLink><br /><searchLink fieldCode="AR" term="%22Batelli%2C+Sara%22">Batelli, Sara</searchLink><br /><searchLink fieldCode="AR" term="%22Forloni%2C+Gianluigi%22">Forloni, Gianluigi</searchLink><br /><searchLink fieldCode="AR" term="%22De+Ronchi%2C+Diana%22">De Ronchi, Diana</searchLink><br /><searchLink fieldCode="AR" term="%22Kalofoutis%2C+Anastasios%22">Kalofoutis, Anastasios</searchLink><br /><searchLink fieldCode="AR" term="%22Liappas%2C+Ioannis%22">Liappas, Ioannis</searchLink><br /><searchLink fieldCode="AR" term="%22Serretti%2C+Alessandro%22">Serretti, Alessandro</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22International+Journal+of+Geriatric+Psychiatry%22">International Journal of Geriatric Psychiatry</searchLink>. Apr2010, Vol. 25 Issue 4, p338-344. 7p. 2 Charts.
– Name: Subject
  Label: Subjects
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  Data: <searchLink fieldCode="DE" term="%22Genetics+of+Alzheimer's+disease%22">Genetics of Alzheimer's disease</searchLink><br /><searchLink fieldCode="DE" term="%22Apolipoprotein+E4%22">Apolipoprotein E4</searchLink><br /><searchLink fieldCode="DE" term="%22Cytokine+genetics%22">Cytokine genetics</searchLink><br /><searchLink fieldCode="DE" term="%22Inflammatory+mediators%22">Inflammatory mediators</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Objective: The APOE epsilon-4 allele has consistently emerged as a susceptibility factor for Alzheimer's disease (AD). Pro-inflammatory cytokines are detectable at abnormal levels in AD, and are thought to play a pathophysiological role. Animal studies have shown dose-dependent correlations between the number of APOE epsilon-4 alleles and the levels of pro-inflammatory cytokines. The aims of this study were to investigate the influence of APOE genotypes on TNF-o:, IL-6, and IL-lß secreted by peripheral blood mononuclear cells (PBMC) from human patients with AD and to analyze the correlation between cytokine production and AD clinical features. Methods: Outpatients with AD (w—40) were clinically evaluated for cognitive decline (MMSE) and psychiatric symptoms (Cornell Scale for Depression in Dementia; Neuropsychiatric Inventory) and genotyped for APOE variants. PBMCs were isolated from the donors and used to assess spontaneous and PMA-stimulated secretion of TNF-o:, IL-6, and IL-1/3. Cytokine production was determined by immuno-enzymatic assays (ELISA). Results: In comparison with their counterparts without APOE4, patients with at least one copy of the APOE epsilon-4 allele showed higher spontaneous (p —0.037) and PMA-induced (p —0.039) production of IL-lß after controlling for clinical variables. Significant correlations were reported between NPI scores (psychotic symptoms) and IL-6 production. Conclusion: These preliminary findings suggest the involvement of inflammatory response in the pathogenic effect of the APOE epsilon-4 allele in AD, although their replication in larger samples is mandatory. The modest correlations between pro-inflammatory cytokines released at peripheral level and AD features emphasizes the need for further research to elucidate the role of neuroinflammation in pathophysiology of AD. Copyright © 2009 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of International Journal of Geriatric Psychiatry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1002/gps.2344
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      – Code: eng
        Text: English
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        PageCount: 7
        StartPage: 338
    Subjects:
      – SubjectFull: Genetics of Alzheimer's disease
        Type: general
      – SubjectFull: Apolipoprotein E4
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      – SubjectFull: Cytokine genetics
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      – SubjectFull: Inflammatory mediators
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