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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]
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Database: Psychology and Behavioral Sciences Collection
Description
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]
ISSN:08856230
DOI:10.1002/gps.2344