Increasing evidence supports a propensity towards inflammation in Alzheimer's disease (AD) pathogenesis. In our previous studies we observed high levels of IL-16, IL-18 and TGF-beta1 mRNA expression in monocyte-macrophages of the peripheral blood of AD patients. The aim of this investigation was to determine the plasma levels of IL-12, IL-16, IL-18 and TGF-beta1 in AD patients at different stages of the disease and to correlate the production of these cytokines with the disease progression. The levels of IL-12, IL-16, IL-18 and TGF-beta1 resulted higher in AD-mild patients, were slightly lower in AD-moderate patients, whereas no significant difference was observed between AD-severe patients and non-demented age-matched subjects. The correlation values between cytokine plasma levels were dependent on the disease progression. Our data indicate that plasma levels of these inflammatory molecules follow the degree of AD suggesting a gradual decline of immune responsiveness in AD.

Altered plasma cytokine levels in Alzheimer's disease: correlation with the disease progression

Motta M.;Imbesi R.;Malaguarnera L.;Di Rosa M. D. A.;F. Stivala
2007-01-01

Abstract

Increasing evidence supports a propensity towards inflammation in Alzheimer's disease (AD) pathogenesis. In our previous studies we observed high levels of IL-16, IL-18 and TGF-beta1 mRNA expression in monocyte-macrophages of the peripheral blood of AD patients. The aim of this investigation was to determine the plasma levels of IL-12, IL-16, IL-18 and TGF-beta1 in AD patients at different stages of the disease and to correlate the production of these cytokines with the disease progression. The levels of IL-12, IL-16, IL-18 and TGF-beta1 resulted higher in AD-mild patients, were slightly lower in AD-moderate patients, whereas no significant difference was observed between AD-severe patients and non-demented age-matched subjects. The correlation values between cytokine plasma levels were dependent on the disease progression. Our data indicate that plasma levels of these inflammatory molecules follow the degree of AD suggesting a gradual decline of immune responsiveness in AD.
2007
Alzheimer's disease; Interleukin-12; Interleukin-16; Interleukin-18; Transforming growth factor-beta 1; Immune response
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/26931
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