Tumor necrosis factor α augments amyloid β protein (25–35) induced apoptosis in human cells
Section snippets
Acknowledgements
This work was supported by a grant of the Austrian Society of Geriatrics and Gerontology as well as by the `Hans und Blanca Moser Stiftung', Vienna, Austria. We are also grateful to G. Wick for his continuous support and G. Adolf (Bender, Vienna, Austria) for kindly providing TNFα.
References (22)
- et al.
Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis
Neuron
(1994) - et al.
Tumor necrosis factor-α pretreatment is protective in a rat model of myocardial ischemia-reperfusion injury
Biochem. Biophys. Res. Commun.
(1992) - et al.
Interaction of Alzheimer β-amyloid peptide with the human monocytic cell line THP-1 results in a protein kinase C-dependent secretion of tumor necrosis factor-α
Brain Res.
(1997) - et al.
Cellular signaling of TGFβ, TNF-α and βAPP in brain injury responses and Alzheimer's disease
Brain Res. Rev.
(1997) - et al.
The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases
Brain Res. Rev.
(1995) - et al.
A rapid and simple method for measuring thymocyte apoptosis by propidium iodide staining and flow cytometry
J. Immunol. Methods
(1991) - et al.
Amyloid β protein (25–35) increases cellular APP and inhibits the secretion of APPs in human extraneuronal cells
Exp. Cell Res.
(1997) - et al.
T cells from rejected human kidney allografts respond to heat shock protein 72
Transplant. Immunol.
(1996) - et al.
Tumor necrosis factor-α and β protect neurons against amyloid β-peptide toxicity: evidence for involvement of a κB-binding factor and attenuation of peroxide and Ca2+-accumulation
Proc. Natl. Acad. Sci. USA
(1995) - et al.
Altered neuronal and microglial responses to brain injury in mice lacking TNF receptors
Nature Med.
(1996)
Tumor necrosis factor-α potentiates glutamate neurotoxicity in human fetal brain cell cultures
Dev. Neurosci.
Cited by (45)
Adalimumab improves cognitive impairment, exerts neuroprotective effects and attenuates neuroinflammation in an Aβ<inf>1-40</inf>-injected mouse model of Alzheimer's disease
2019, CytotherapyCitation Excerpt :Overexpression of TNF-α in the APP/PS1 transgenic mouse model is neurotoxic and plays an important role in the progression of AD [8]. Additional studies have indicated that increases of TNF-α in the brain impair cognitive performance in the Y-maze test [28], and that Aβ-treated neurons exhibit increased apoptosis via increased TNF-α expression [29]. In another animal model of AD, increased TNF-α enhances Aβ and tau pathology [30].
Anti-TNF-α reduces amyloid plaques and tau phosphorylation and induces CD11c-positive dendritic-like cell in the APP/PS1 transgenic mouse brains
2011, Brain ResearchCitation Excerpt :However, more studies suggest neurotoxic roles of TNF-α. TNF-α increases apoptosis of neurons treated with Aβ (Blasko et al., 1997) and may increase Aβ production through upregulation of both β-secretase expression (Yamamoto et al., 2007) and γ-secretase activity (Liao et al., 2004; Kuo et al. 2008), as well as the expression of APP (Lahiri et al., 2003). Knock-out of TNF-α receptor 1 prevents Aβ generation and learning deficits (He et al., 2007).
Phenotypic and functional changes in glial cells as a function of age
2002, Neurobiology of Aging