|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Since immunohistochemical studies indicated the presence of interleukin-6 in the cortices of patients with Alzheimer's disease, we were interested in the eventual biological effects of this cytokine on neuronal cells.
|
8392518 |
1993 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Interleukin-6 (IL-6) has previously been shown to participate in neurodegenerative processes including Alzheimer's disease.
|
8550818 |
1995 |
|
Alzheimer's Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The mechanisms leading to increased IL-6 levels in brains of AD patients are still unknown.
|
8627294 |
1996 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
We could not demonstrate altered CSF concentrations of IL-6 that may indicate an inflammatory response or capability to support neuronal survival in the central nervous system (CNS) of first-degree relatives and patients with AD.
|
9218628 |
1997 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Prostaglandins (PGs) and cytokines, such as interleukin-1 (IL-1) and interleukin-6 (IL-6), have been implicated in the etiopathology of various inflammatory and degenerative disorders, including Alzheimer's disease (AD) and prion diseases.
|
9003059 |
1997 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Because IL-6 has been implicated in the etiopathology of different human diseases including multiple myeloma, rheumatoid arthritis, multiple sclerosis, acquired immunodeficiency syndrome dementia complex, and Alzheimer's disease, its inhibition may be of therapeutic interest.
|
9523575 |
1998 |
|
Alzheimer's Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The capacity for sIL-6R to enhance IL-6 function and broaden the IL-6 target cell population in the brain has implications for the regulation of beta-APP expression in disease states such as Alzheimer's disease where elevations in brain IL-6 levels have been reported.
|
9645958 |
1998 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results suggest a possible link between the release of PGs from activated microglia and the astrocytic synthesis of IL-6, which itself may affect neuronal cells, as hypothesized for Alzheimer's disease.
|
9850935 |
1998 |
|
Alzheimer's Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Since IFN-gamma is apparently lacking in the brain parenchyma, and amyloid plaque-associated cytokines (IL-1beta, IL-6, TNF-alpha) do not stimulate C1-Inh expression in vitro, the nature of the stimulus responsible for neuronal C1-Inh expression in AD brains remains to be investigated.
|
9754962 |
1998 |
|
Alzheimer's Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Taken together, these findings indicate that OSM or IL-6.sIL-6 complexes may regulate ACT expression in human astrocytes and thus directly or indirectly contribute to the pathogenesis of Alzheimer's disease.
|
9461605 |
1998 |
|
Alzheimer's Disease
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Our results support an association of the C allele of the IL-6 genotype with a delayed initial onset and reduced disease risk and indicate that genetically determined alterations of the immune response may modify the course of AD.
|
10319892 |
1999 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
However, haplotype analysis showed a strong linkage disequilibrium between IL-6vntr and IL-6prom and demonstrated an interaction between IL-6vntr and IL-6prom which modifies AD risk.
|
10739887 |
2000 |
|
Alzheimer's Disease
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We performed a genetic screening of sporadic, late-onset AD cases and age-matched controls to evaluate the role of Cat D and IL-6 polymorphisms in AD.
|
10869806 |
2000 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
The C5a complement activation peptide increases IL-1beta and IL-6 release from amyloid-beta primed human monocytes: implications for Alzheimer's disease.
|
10996210 |
2000 |
|
Alzheimer's Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Since activated microglia and astrocytes play a role in the process of neuronal degeneration in AD, the cytokine/growth factor-regulated expression of beta-catenin in human neural cell lines, including NTera2 teratocarcinoma-derived differentiated neurons (NTera2-N), IMR-32 neuroblastoma, SKN-SH neuroblastoma and U-373MG astrocytoma, was studied quantitatively following exposure to epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, interferon (IFN)-gamma, transforming growth factor (TGF)-beta1, dibutyryl cyclic adenosine 3',5'-cyclic monophosphate (cAMP) (dbcAMP) or phorbol 12-myristate 13-acetate (PMA).
|
10935448 |
2000 |
|
Alzheimer's Disease
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, the age-associated rise in IL-6 has been linked to lymphoproliferative disorders, multiple myeloma, osteoporosis, and Alzheimer's disease.
|
10774463 |
2000 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
In vivo studies and clinical trials with recombinant adenovirus have suggested a role for interleukin 6 (IL-6) in the inflammatory reaction that follows Ad-infection.
|
10894265 |
2000 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
In vivo, prevention of contact system activation beside the reduction of kallikrein generation, can also decrease the activation of complement system and the release of interleukin-6, both factors being considered to play an important role in the inflammatory reactions in AD brain.
|
11589915 |
2001 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
IL-6 in cerebellum was detectable in all AD and DS patients, but only three out of nine controls.
|
11258753 |
2001 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Thus, prevention of contact system activation, beside diminishing the recruitment of glial cells and microvascular permeability, can also decrease the activation of complement system and the release of IL6, both factors being considered to play an important role in the inflammatory reactions in AD brain.
|
11164277 |
2001 |
|
Alzheimer's Disease
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
In particular, the data suggesting that several IL-1 and IL-6 gene polymorphisms can contribute to the risk of developing AD are reviewed.
|
11442299 |
2001 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Additionally cytokines, such as interleukin-1alpha (IL-1alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) are co-localized to senile plaques, a neuropathological hallmark of AD.
|
12399113 |
2002 |
|
Alzheimer's Disease
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These findings suggest that the IL-6prom G allele which may affect plasma IL-6 concentration might be a risk factor for sporadic AD in Japanese.
|
11992567 |
2002 |
|
Alzheimer's Disease
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Our data indicate that the IL-6 gene polymorphism is associated with AD in Italians and confirm that IL-6 is crucial in the pathophysiology of neurodegenerative disorders.
|
12352619 |
2002 |
|
Alzheimer's Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Are there interactions of other genes with IL6 that affect the development and progression of AD?
|
11754993 |
2002 |