TY - JOUR
T1 - Lack of association between interleukin-1 alpha rs1800587 polymorphism and Alzheimer's disease in two independent European samples
AU - Serretti, Alessandro
AU - Olgiati, Paolo
AU - Politis, Antonis
AU - Malitas, Petros
AU - Albani, Diego
AU - Dusi, Sabrina
AU - Polito, Letizia
AU - De Mauro, Stefania
AU - Zisaki, Aikaterini
AU - Piperi, Christina
AU - Liappas, Ioannis
AU - Stamouli, Evangelia
AU - Mailis, Antonis
AU - Atti, Anna Rita
AU - Morri, Monica
AU - Ujkaj, Manjola
AU - Batelli, Sara
AU - Forloni, Gianluigi
AU - Soldatos, Costantine R.
AU - Papadimitriou, George N.
AU - De Ronchi, Diana
AU - Kalofoutis, Anastasios
PY - 2009
Y1 - 2009
N2 - Interleukin-1 (IL1) can contribute to pathophysiology of Alzheimer's disease (AD) by promoting deposition of amyloid-β in the brain. The gene encoding IL1 alpha (IL1A) has a common polymorphism in its 5' regulatory region (rs1800587) with possible functional effects. IL1A T/T genotype has been associated with AD but the overall effect is modest and negative studies have been published. The aim of this study was to investigate the association of the IL1A rs1800587 polymorphism with AD in two independent case-control groups from Greece (Athens) and Italy (Faenza and Granarolo). Preliminary results from the ongoing sample (110 patients with sporadic AD and 130 nonpsychiatric controls) showed no association between IL1A variants and AD, however C/T heterozygotes had more severe depression in AD (Cornell Scale for Depression in Dementia) compared to other genotypes (F = 4.56, d.f = 1, p = 0.037) after controlling for age, illness duration and cognitive impairment (MMSE). Despite the small sample size and the possibility of a false negative finding, our preliminary data support the hypothesis the IL1A rs1800587 variants are not associated with AD. The effect of the IL1A on depressive symptomatology warrants further investigations, however the lack of a gene-dose relationship would suggest a false positive.
AB - Interleukin-1 (IL1) can contribute to pathophysiology of Alzheimer's disease (AD) by promoting deposition of amyloid-β in the brain. The gene encoding IL1 alpha (IL1A) has a common polymorphism in its 5' regulatory region (rs1800587) with possible functional effects. IL1A T/T genotype has been associated with AD but the overall effect is modest and negative studies have been published. The aim of this study was to investigate the association of the IL1A rs1800587 polymorphism with AD in two independent case-control groups from Greece (Athens) and Italy (Faenza and Granarolo). Preliminary results from the ongoing sample (110 patients with sporadic AD and 130 nonpsychiatric controls) showed no association between IL1A variants and AD, however C/T heterozygotes had more severe depression in AD (Cornell Scale for Depression in Dementia) compared to other genotypes (F = 4.56, d.f = 1, p = 0.037) after controlling for age, illness duration and cognitive impairment (MMSE). Despite the small sample size and the possibility of a false negative finding, our preliminary data support the hypothesis the IL1A rs1800587 variants are not associated with AD. The effect of the IL1A on depressive symptomatology warrants further investigations, however the lack of a gene-dose relationship would suggest a false positive.
KW - Alzheimer's disease
KW - IL-1A gene
KW - Inflammatory cytokines
KW - Psychosis
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U2 - 10.3233/JAD-2009-0946
DO - 10.3233/JAD-2009-0946
M3 - Article
C2 - 19158434
AN - SCOPUS:58849162678
SN - 1387-2877
VL - 16
SP - 181
EP - 187
JO - Journal of Alzheimer's Disease
JF - Journal of Alzheimer's Disease
IS - 1
ER -