Vitamin B12 Levels in Alzheimer's Disease: Association with Clinical Features and Cytokine Production

Autor: Anastasios Kalofoutis, Letizia Polito, Antonis Politis, Evangelia Stamouli, Sara Batelli, Paolo Olgiati, Antonis Mailis, Ioannis Liappas, Diana De Ronchi, Petros Malitas, Alessandra Signorini, Christina Piperi, Stefania De Mauro, Aikaterini Zisaki, Diego Albani, Gianluigi Forloni, Alessandro Serretti
Přispěvatelé: Politis A., Olgiati P., Malitas P., Albani D., Signorini A., Polito L., De Mauro S., Zisaki A., Piperi C., Stamouli E., Mailis A., Batelli S., Forloni G., De Ronchi D., Kalofoutis A., Liappas I., Serretti A.
Rok vydání: 2010
Předmět:
Zdroj: Journal of Alzheimer's Disease. 19:481-488
ISSN: 1875-8908
1387-2877
Popis: Alzheimer's disease (AD) has been associated with up-regulation of pro-inflammatory cytokines (e.g., specific gene variants for TNF-alpha; IL-6; IFN-gamma) and low plasma levels of cyanocobalamin (vitamin B12). Our goal was to relate B12 levels to AD symptoms and to expression of pro-inflammatory cytokines. Clinical manifestations were investigated for a case series of fifty-five outpatients using the MMSE, Neuropsychiatric Inventory (NPI) and Cornell Scale for Depression in Dementia (CDDS). Plasma B12 levels were measured by radioligand binding assay. Basal and PMA-stimulated levels of IFN-gamma, TNF-alpha, and IL-6 were measured by ELISPOT (PBMC culture supernatant). 47 patients were genotyped for APOE. Ten patients (18%) had their B12 levels below < 250 pg/ml. They did not statistically differ from those 45 who had normal levels in most demographic and clinical features; their MMSE scores were lower (14.7 vs 19.6 p=0.03) but not after adjustment for disease duration. A greater basal production of IL-6 was reported in patients who had low B12 levels compared to normal B12 subjects (1333 pg/ml vs 976 p< 0.01); this association was confirmed after controlling for age of onset and APOE genotype. In conclusion, low B12 level is associated with greater production of IL-6 in peripheral blood mononuclear cells. Further research is warranted to elucidate whether this neuroinflammatory effect of cobalamin is implicated in the pathophysiology of AD.
Databáze: OpenAIRE