Elevated circulating tumor necrosis factor levels in Alzheimer's disease

Fillit, Howard; Ding, Wanhong; Buée, Luc; Kalman, Jill; Altstiel, Larry D.; Lawlor, Brian A.; Wolf-Klein, Giselle

doi:10.1016/0304-3940(91)90490-k

Cited by 460 publications

(270 citation statements)

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“…Regarding the CNS, microglia and astrocytes are believed to be the primary sources of TNF-␣. Evidence indicates the presence of increased levels of TNF-␣ in the brain and plasma of AD patients and an upregulation of TNFR1 have been detected in the AD brain (Fillit et al, 1991;Li et al, 2004). In addition, TNF-␣ has been implicated recently as a critical mediator of long-term potentiation (LTP) reduction by A␤ (Wang et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Medeiros¹,

Prediger²,

Passos³

et al. 2007

J. Neurosci.

269

179

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Section: Introductionmentioning

confidence: 99%

Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Medeiros¹,

Prediger²,

Passos³

et al. 2007

J. Neurosci.

269

179

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“…Microglia, which is supposed to be the resident macrophages of the brain, and atrocities are the main cells that involve in this process. In the brains of both AD individuals and transgenic animal models, it was found that Ab plaques are surrounded by activated glial cells (Bauer et al 1991;Cagnin et al 2001;Fillit et al 1991;Liu et al 2013;Varnum and Ikezu 2012). Activated microglia and astrocytes strongly secrete inflammatory components such as pro-inflammatory cytokines, chemokines, complement, macrophage inflammatory proteins, monocyte chemoattractant proteins, reactive oxygen species (ROS), nitric oxide (NO) prostaglandins, leukotrienes, thromboxanes and so on (Akiyama et al 2000;Griffin et al 1998;Mrak et al 1995;Town et al 2005;Tuppo and Arias 2005).…”

Section: Inflammation In Admentioning

confidence: 99%

“…Activated microglia and astrocytes strongly secrete inflammatory components such as pro-inflammatory cytokines, chemokines, complement, macrophage inflammatory proteins, monocyte chemoattractant proteins, reactive oxygen species (ROS), nitric oxide (NO) prostaglandins, leukotrienes, thromboxanes and so on (Akiyama et al 2000;Griffin et al 1998;Mrak et al 1995;Town et al 2005;Tuppo and Arias 2005). The released inflammatory molecules, especially some cytokines such as interleukin (IL)-18, IL-1b and tumor necrosis factor (TNF)-a, impair the balance of normal neurophysiologic condition that correlates with cognition and learning and memory (Fillit et al 1991;Gemma and Bickford 2007;Jankowsky and Patterson 1999;Liu et al 2013;Varnum and Ikezu 2012). These secreted inflammatory mediators, in turn, activate more microglia and astrocytes to produce inflammatory molecules.…”

Section: Inflammation In Admentioning

confidence: 99%

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Zhang

et al. 2015

Arch. Immunol. Ther. Exp.

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Alzheimer's disease (AD) is a complex agerelated neurodegenerative disorder of the central nervous system. Since the first description of AD in 1907, many hypotheses have been established to explain its causes. The inflammation theory is one of them. Pathological and biochemical studies of brains from AD individuals have provided solid evidence of the activation of inflammatory pathways. Furthermore, people with long-term medication of anti-inflammatory drugs have shown a reduced risk to develop the disease. After three decades of genetic study in AD, dozens of loci harboring genetic variants influencing inflammatory pathways in AD patients has been identified through genome-wide association studies (GWAS). The most well-known GWAS risk factor that is responsible for immune response and inflammation in AD development should be APOE e4 allele. However, a growing number of other GWAS risk AD candidate genes in inflammation have recently been discovered. In the present study, we try to review the inflammation in AD and immunity-associated GWAS risk genes like HLA-DRB5/DRB1, INPP5D, MEF2C, CR1, CLU and TREM2.

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“…Tumor necrosis factor-␣ (TNF-␣), 1 an inflammatory mediator, is recently reported to be up-regulated following brain trauma (1,2) and ischemic injury (3,4), and in multiple sclerosis (5,6), Parkinson's disease (7), and Alzheimer's disease (8). Studies have shown that TNF-␣ can elicit either a trophic or toxic effect, which is dependent on the target cell type.…”

Section: Recent Evidence Indicates That Tumor Necrosis Factor-␣ (Tnf-mentioning

confidence: 99%

Inhibition of p75 Tumor Necrosis Factor Receptor by Antisense Oligonucleotides Increases Hypoxic Injury and β-Amyloid Toxicity in Human Neuronal Cell Line

Shen

Shiosaki

1997

Journal of Biological Chemistry

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Recent evidence indicates that tumor necrosis factor-␣ (TNF-␣) is up-regulated following brain injury andin neurodegenerative disorders such as stroke, multiple sclerosis, Parkinson's disease, and Alzheimer's disease. TNF-␣ elicits its biological effects through two distinct TNF receptor (TNFR) subtypes: p55 TNFR (TNFR1) and p75 TNFR (TNFR2). Studies have demonstrated that the p55 TNFR contributes to cell death, whereas the role of the p75 TNFR in neuronal viability is unclear. To better understand the role of p75 TNFR, we treated human neuronal SH-SY5Y cells with phosphorothioate-modified antisense oligonucleotides (ASO) for p75 TNFR and established that ASO inhibited p75 TNFR expression. Treatment of SH-SY5Y cells with ASO alone did not affect cell viability, whereas treatment with both ASO and human TNF-␣ significantly increased cell death relative to treatment with TNF-␣ alone. Moreover, addition of ASO significantly increased the level of cell injury observed following hypoxic conditions or exposure of ␤-amyloid peptide. These results indicate that inhibition of p75 TNFR using ASO increases the vulnerability of neurotypic cells to insults and suggest that the p75 TNFR may not be required for normal neuronal cell viability but rather plays a protective role following injury.Tumor necrosis factor-␣ (TNF-␣), 1 an inflammatory mediator, is recently reported to be up-regulated following brain trauma (1, 2) and ischemic injury (3, 4), and in multiple sclerosis (5, 6), Parkinson's disease (7), and Alzheimer's disease (8). Studies have shown that TNF-␣ can elicit either a trophic or toxic effect, which is dependent on the target cell type. For example, TNF-␣ is toxic to human oligodendrocytes (9) and neuronal cells (10, 11), but it is trophic to rat hippocampal neurons (12). Since TNF-␣ elicits its biological effects through activation of two distinct receptors, p55 TNFR and p75 TNFR, both of which have been cloned (13-15), we hypothesized that the distinct TNF receptor subtypes might contribute to the multiple biological functions of TNF-␣. Reports indicate that the p55 TNFR may contribute to cell death (16), whereas the role of the p75 TNFR in neuronal cell function is not clear. Here we show that inhibition of p75 TNFR by antisense oligonucleotides (ASO) increased the magnitude of neuronal cell death induced by TNF-␣, hypoxic injury or ␤-amyloid peptide (A␤) as measured by lactate dehydrogenase (LDH) release. This novel finding provides evidence that the p75 TNFR might play a protective role following neuronal insult. EXPERIMENTAL PROCEDURESCell Cultures-Human neuronal-like cells, SH-SY5Y, were cultured in a 1:1 ratio of minimum Eagle's medium/F-12 medium, 15% fetal calf serum (Life Technologies, Inc.), and 10 M retinoic acid (RA, Sigma). The cells were seeded at 25,000 cells/well in a 24-well plate for cytotoxicity assays or 3 ϫ 10 6 cells in Petri dishes for radioimmunoprecipitation study. The medium was replaced every 3 days. Treatments were given to the cells in serum-free medium with 1:100 N2-supplement (Li...

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Elevated circulating tumor necrosis factor levels in Alzheimer's disease

Cited by 460 publications

References 14 publications

Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Inhibition of p75 Tumor Necrosis Factor Receptor by Antisense Oligonucleotides Increases Hypoxic Injury and β-Amyloid Toxicity in Human Neuronal Cell Line

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