Interleukin-1α –889 C/T Polymorphism in Turkish Patients with Late-Onset Alzheimer’s Disease

Dursun, Erdinç; Gezen-Ak, Duygu; Ertan, Turan; Bılgıç, Başar; Gürvıt, Hakan; Emre, Murat; Eker, Engin; Engin, Funda; Uysal, Ömer; Yılmazer, Selma

doi:10.1159/000193627

Cited by 15 publications

(8 citation statements)

References 96 publications

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“…We selected seven commonly studied promoter SNPs in inflammatory cytokines genes that have all previously been shown to affect the production of cytokine proteins and/or, which have been associated with increased risk of several inflammatory diseases [14][15][16][17][18][19][20]: IL1A-889, IL1B-511, IL10-592, IL10-1082, IL18-137, IL18-607 and TNF-308.…”

Section: Selection Of Polymorphismsmentioning

confidence: 99%

Single nucleotide polymorphisms in inflammatory genes and the risk of early onset of lone atrial fibrillation

et al. 2010

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Section: Selection Of Polymorphismsmentioning

confidence: 99%

Single nucleotide polymorphisms in inflammatory genes and the risk of early onset of lone atrial fibrillation

et al. 2010

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“…Interleukins and tumor necrosis factors are members of a huge protein family called cytokines, which are the key elements for regulating the intensity and duration of the immune response. Thus, their expression in the CNS typically increases during inflammatory states including during neurodegeneration by microglia and astrocytes [17]. Complement activation, an important component of neuroinflammation, has been suggested to participate in almost all major neurodegenerative disorders.…”

Section: Introductionmentioning

confidence: 99%

BDNF, TNFα, HSP90, CFH, and IL-10 Serum Levels in Patients with Early or Late Onset Alzheimer's Disease or Mild Cognitive Impairment

Gezen-Ak

Dursun

Hanağası

et al. 2013

JAD

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157

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Identifying early-detection biomarkers have become an increasingly important approach in the treatment and prevention of Alzheimer's disease (AD). In this study, we investigated the potential of brain-derived neurotrophic factor (BDNF), complement factor H (CFH), tumor necrosis factor-α (TNFα), interleukin 10 (IL-10), and heat shock protein 90 (Hsp90) as serum biomarkers for AD in a cohort of the Turkish population because they have been suggested to be associated with AD. Serum BDNF, CFH, TNFα, IL-10, and Hsp90 levels in three groups of patients, early-onset AD (EOAD; age of onset < 65; n = 22), late-onset AD (LOAD; age of onset > 65; n = 54), and mild cognitive impairment (MCI) (n = 30), were compared with age-matched healthy controls (age < 65, n = 18 and age > 65; n = 32) using ELISA. The serum BDNF levels significantly decreased and TNFα levels significantly increased in the EOAD and LOAD groups compared to the age-matched healthy controls. There was a correlation between serum TNFα and IL-10 levels in the LOAD and healthy control groups. Serum CFH levels in the LOAD and MCI patients were significantly decreased compared with controls. Serum Hsp90 levels in the EOAD, LOAD, and MCI patients were significantly decreased compared with controls. The protein misfolding, the inflammatory response, and decreased neurotrophic factor synthesis are all suggested to be related to AD type brain pathology, and our results indicate these alterations might be traced from serum samples. For accurate early diagnosis of AD, it is important to determine a profile of alterations in multiple biomarkers in large-scale population studies.

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“…It consists of a broken cholesterol backbone, and it has steroid-like effects, such as regulating the expression of over 1,000 genes. Although a relatively limited number of studies have investigated the genes targeted by vitamin D in the brain [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], the probable effects of vitamin D on neurotrophic factor production, oxidative stress mechanisms, Ca 2+ homeostasis and the immune system are irrefutable. A study on hippocampal neuron cultures suggest that vitamin D promotes calcium homeostasis by decreasing the level of L-type voltage-sensitive calcium channels (LVSCC), and channel density, on the plasma membrane [2].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Vitamin D Receptor Silencing on the Expression of LVSCC-A1C and LVSCC-A1D and the Release of NGF in Cortical Neurons

2011

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BackgroundRecent studies have suggested that vitamin D can act on cells in the nervous system. Associations between polymorphisms in the vitamin D receptor (VDR), age- dependent cognitive decline, and insufficient serum 25 hydroxyvitamin D3 levels in Alzheimer's patients and elderly people with cognitive decline have been reported. We have previously shown that amyloid β (Aβ) treatment eliminates VDR protein in cortical neurons. These results suggest a potential role for vitamin D and vitamin D-mediated mechanisms in Alzheimer's disease (AD) and neurodegeneration. Vitamin D has been shown to down-regulate the L-type voltage-sensitive calcium channels, LVSCC-A1C and LVSCC-A1D, and up-regulate nerve growth factor (NGF). However, expression of these proteins when VDR is repressed is unknown. The aim of this study is to investigate LVSCC-A1C, LVSCC-A1D expression levels and NGF release in VDR-silenced primary cortical neurons prepared from Sprague-Dawley rat embryos.Methodology/Principal FindingsqRT-PCR and western blots were performed to determine VDR, LVSCC-A1C and -A1D expression levels. NGF and cytotoxicity levels were determined by ELISA. Apoptosis was determined by TUNEL. Our findings illustrate that LVSCC-A1C mRNA and protein levels increased rapidly in cortical neurons when VDR is down-regulated, whereas, LVSCC-A1D mRNA and protein levels did not change and NGF release decreased in response to VDR down-regulation. Although vitamin D regulates LVSCC-A1C through VDR, it may not regulate LVSCC-A1D through VDR.Conclusions/SignificanceOur results indicate that suppression of VDR disrupts LVSCC-A1C and NGF production. In addition, when VDR is suppressed, neurons could be vulnerable to aging and neurodegeneration, and when combined with Aβ toxicity, it is possible to explain some of the events that occur during neurodegeneration.

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Interleukin-1α –889 C/T Polymorphism in Turkish Patients with Late-Onset Alzheimer’s Disease

Cited by 15 publications

References 96 publications

Single nucleotide polymorphisms in inflammatory genes and the risk of early onset of lone atrial fibrillation

Single nucleotide polymorphisms in inflammatory genes and the risk of early onset of lone atrial fibrillation

BDNF, TNFα, HSP90, CFH, and IL-10 Serum Levels in Patients with Early or Late Onset Alzheimer's Disease or Mild Cognitive Impairment

The Effects of Vitamin D Receptor Silencing on the Expression of LVSCC-A1C and LVSCC-A1D and the Release of NGF in Cortical Neurons

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