The influence of tumour necrosis factor- α (TNF-α) on amyloid-β (Aβ)-degrading enzymes in vitro.

Pro-inflammatory cytokines, such as tumour necrosis factor-α (TNF-α), are increased in serum and CSF in Alzheimer's disease (AD). We investigated the effect of TNF-α on gene and protein expression levels of Aβ degrading enzymes (ACE, ECE-1, ECE- 2, IDE and NEP) in vitro. Differentiated (DC) and non-differentiated (NDC) neuroblastoma cells (SH-SY5Y) were exposed to TNF-α for 15 minutes and 3 hours and protein and gene expression levels measured using western blotting or sandwich ELISA (ECE-2), and real time-PCR (RT-PCR).

Tumour necrosis factor-α (TNF-α) and miRNA expression in frontal and temporal neocortex in Alzheimer's disease and the effect of TNF-α on miRNA expression in vitro.

Micro-RNAs (miRNAs) are short non-coding RNAs capable of regulating gene expression at the translational level. A number of studies have suggested that the expression of several miRNAs is changed in AD. The pro-inflammatory cytokine tumour necrosis factor-a (TNF-α) is increased in serum and CSF in AD.

TNFR-associated factor-2 (TRAF-2) in Alzheimer's disease.

Levels of tumor necrosis factor-alpha (TNF-alpha) are increased in the brain in Alzheimer's disease (AD). The TNF-alpha/TNF-R signaling pathways involve complex interactions between several proteins, including TNF-receptor-associated factor-2 (TRAF-2). We have examined the distribution and levels of TRAF-2 in AD and control brains and also whether single nucleotide polymorphisms (SNPs) in the TRAF-2 gene are associated with AD and influence TRAF-2 expression.

Protein and gene expression of tumour necrosis factor receptors I and II and their promoter gene polymorphisms in Alzheimer's disease.

The levels of pro-inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-alpha), are increased in the brain in Alzheimer's disease (AD). Most of the biological properties of TNF-alpha are mediated through its two receptors, tumour necrosis factor receptors I and II (TNF-RI and TNF-RII). We have used immunohistochemistry, Western blotting and real time-PCR (RT-PCR) on frontal (BA 6/24) and temporal (BA 20-22) neocortex and hippocampus from AD and control brains to determine if both receptor proteins were present and expressed in AD and if sequence variations (SNPs) in the promoter regions of the two genes are associated with AD.

Neither sequence variation in the IL-10 gene promoter nor presence of IL-10 protein in the cerebral cortex is associated with Alzheimer's disease.

Interleukin 10 (IL-10) is an important anti-inflammatory cytokine produced in response to neuroinflammation and might be involved in modulating the progression of Alzheimer's disease (AD) through inhibiting the action of pro-inflammatory cytokines. We have used immunohistochemistry, Western blotting, real time-PCR (RT-PCR) on frontal (BA 6/24) and temporal (BA 20-22) neocortex and hippocampus from AD and control brains as well as genetic association analysis to address the possible involvement of IL-10 in AD. Expression of IL-10 in AD and control brains at both protein and mRNA levels were detected.

APOE promoter, ACE1 and CYP46 polymorphisms and beta-amyloid in Alzheimer's disease.

Polymorphisms in the APOE promoter, ACE1 and CYP46 genes have all been reported to be associated with Alzheimer's disease (AD). We studied the relationship of these polymorphisms to the presence of AD in 86 neuropathologically confirmed cases of AD and 58 controls. In addition, we assessed the effects of these polymorphisms on the accumulation of beta-amyloid (Abeta) in the cerebral parenchyma and vasculature.

Tumour necrosis factor-alpha gene polymorphisms and Alzheimer's disease.

Recent findings suggest that production of pro-inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-alpha), is increased in the brains of people with Alzheimer's disease (AD). We used direct sequencing methods on a section of the enhancer/promoter region and on a smaller fragment located 10.5 kb upstream of the TNF-alpha gene to respectively examine TNF-alpha polymorphisms and TNF-a and -b microsatellite alleles in a cohort of 235 post-mortem confirmed AD and 130 control cases.