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Cerebrospinal fluid (CSF) levels of interleukin (IL)-6, IL-11 and leukaemia inhibitory factor (LIF) were evaluated in 43 patients with Alzheimer's disease (AD) and 24 patients with frontotemporal lobar degeneration (FTLD) as compared with 30 agematched controls (CON), and correlated with clinical and demographic data and with CSF biomarkers amyloid beta (A(More)
Specific proinflammatory alleles are associated with higher risk of Alzheimer disease (AD) in different onset age. The homozygosis for the A allele of -1082 polymorphism (G/A) of interleukin-10 (IL-10) promotes a higher risk of AD and reduced IL-10 generation in peripheral cells after amyloid stimulation. In this paper we analysed genotype and allele(More)
Transforming growth factor-beta1 (TGF-beta1) acts as an immunosuppressant by inhibiting the expression of several pro-inflammatory cytokines. Its gene contains single nucleotide polymorphisms (SNPs) at codon +10 (T-->C) and +25 (G-->C) that appear to influence the level of expression of TGF-beta1. We investigated these SNPs in 198 healthy controls (HC), 193(More)
Pro-inflammatory cytokines and acute-phase proteins play an important role in Alzheimer's disease (AD) neurodegeneration, and common polymorphisms of genes controlling their production have been shown to be associated with AD. Tumor necrosis factor (TNF)-alpha is an inflammatory cytokine involved in the local immune response occurring in the central nervous(More)
We investigated the effect of long-term, peripheral treatment with enoxaparin, a low molecular weight heparin, in transgenic mice overexpressing human amyloid precursor protein(751). Enoxaparin (6 IU per mouse intraperitoneally, three times a week for 6 months) significantly lowered the number and the area occupied by cortical beta-amyloid deposits and the(More)
In our case-control study we analyzed two functional IL18 gene promoter polymorphisms (-137G/C and -607C/A) and an additional polymorphism at position -656 (G/T) in Alzheimer patients and healthy controls in order to verify the involvement of these genetic variations in the onset of Alzheimer disease. No significant differences were detected for the three(More)
In the pathogenesis of Alzheimer disease (AD), it has been proposed that the anti-inflammatory interleukins such as IL-10 regulate beta-amyloid-induced microglial inflammatory responses inhibiting the proinflammatory cytokine IL-6. Since the promoters of the IL-10 and IL-6 genes show single nucleotide polymorphisms (SNPs) (IL-10: -1082 G --> A; IL-6: -174 G(More)
Studies on primates have shown that visual and spatial perceptual analysis depends on two separate neural pathways, associated with the processing of "what" and "where" an object is (visual characteristics and spatial coordinates, respectively). Similar dichotomies have been proposed by cognitive psychologists (e.g., the contrast between visual and spatial(More)
Although moderate fibrosis is a histological hallmark of the aging liver, the molecular mechanisms underlying this phenomenon are little known. Here, we provide a comprehensive description of hepatic collagen expression and metabolism during natural aging in rats. Interstitial collagen accumulated significantly in the oldest animals, mainly in the(More)
OBJECTIVE The immune system (IS) plays a key role in the mechanisms underlying major depression (MD) and pro-inflammatory cytokines seem to be particularly involved in the pathogenesis of the disease. There is growing evidence of a relationship between commonly studied single nucleotide polymorphisms (SNPs) in cytokine genes and an increased risk of MD.The(More)