Showing papers by "Giuliano Binetti published in 2005"

Circulating levels of soluble receptor for advanced glycation end products in Alzheimer disease and vascular dementia.

Abstract: Background: The receptor for advanced glycation end products (RAGE) is a cell surface receptor that has been implicated in vascular disease and neurodegeneration. Low levels of its secreted isoform, soluble RAGE (sRAGE), have been regarded as a putative risk factor for atherosclerosis. In addition, administration of sRAGE has been shown to reduce development of cerebral -amyloidosis in an Alzheimer disease mouse model. Objective: To investigate the role of sRAGE as a biological marker for Alzheimer disease and vascular dementia. Design: Cross-sectional study of 152 patients with a clinical diagnosis of Alzheimer disease, 91 with vascular dementia and 161 control subjects. Main Outcome Measure: Plasma levels of sRAGE. Results: Levels of sRAGE were significantly reduced in the plasma of patients with Alzheimer disease compared with that for those with either vascular dementia (P.05) or with controls (P.001). Conclusions: Patients with Alzheimer disease have reduced levels of sRAGE in plasma compared with patients with vascular dementia and controls. The striking reduction of circulating sRAGE in Alzheimer disease further supports a role for the RAGE axis in this clinical entity and requires further investigation. Arch Neurol. 2005;62:1734-1736

Lack of association between MnSOD gene polymorphism and sporadic Alzheimer's disease.

Abstract: Background and aims: Substantial evidence supports the hypothesis that impairment of mitochondrial function and increased oxidative damage are involved in the pathogenesis of several neurodegenerative disorders including Alzheimer’s disease (AD). Manganese Superoxide dismutase (MnSOD) plays a major role in protecting the mitochondrion from oxidative damage due to Superoxide radicals and other excited oxygen species. Recent studies have indicated that MnSOD mRNA levels are significantly increased in the lymphocytes of AD patients, supporting the role of oxidative alterations in the pathogenetic mechanism underlying this neurodegeneration. A potentially functional amino acid polymorphism (Ala-9Val) has been described in the signal sequence of enzymes associated with decreased defense capacity against oxidative stress. The object of this study was to investigate the association between this polymorphism of the MnSOD gene and AD in the Italian population. Methods: The Ala-9Val polymorphism was genotyped by PCR amplification and SSCP analysis in 227 AD patients and 198 healthy controls. Results: No significant differences in genotype or allele frequencies between cases and controls, even after stratification for APOE carrier status, were observed. Conclusions: Our data suggest that the Ala-9Val polymorphism in the MnSOD gene is not associated with genetic susceptibility in AD patients.