Steeland, Sophie; Gorlé, Nina; Vandendriessche, Charysse; Balusu, Sriram; Brkić, Marjana; Van Cauwenberghe, Caroline; Van Imschoot, Griet; Van Wonterghem, Elien; De Rycke, Riet; Kremer, Anneke; Lippens, Saskia; Stopa, Edward; Johanson, Conrad E; Libert, Claude; Vandenbroucke, Roosmarijn E
(EMBO Press, 2018)
TY - JOUR AU - Steeland, Sophie AU - Gorlé, Nina AU - Vandendriessche, Charysse AU - Balusu, Sriram AU - Brkić, Marjana AU - Van Cauwenberghe, Caroline AU - Van Imschoot, Griet AU - Van Wonterghem, Elien AU - De Rycke, Riet AU - Kremer, Anneke AU - Lippens, Saskia AU - Stopa, Edward AU - Johanson, Conrad E AU - Libert, Claude AU - Vandenbroucke, Roosmarijn E PY - 2018 UR - http://www.ncbi.nlm.nih.gov/pubmed/29472246 UR - https://radar.ibiss.bg.ac.rs/handle/123456789/3005 AB - Alzheimer's disease (AD) is the most common form of dementia, and neuroinflammation is an important hallmark of the pathogenesis. Tumor necrosis factor (TNF) might be detrimental in AD, though the results coming from clinical trials on anti-TNF inhibitors are inconclusive. TNFR1, one of the TNF signaling receptors, contributes to the pathogenesis of AD by mediating neuronal cell death. The blood-cerebrospinal fluid (CSF) barrier consists of a monolayer of choroid plexus epithelial (CPE) cells, and AD is associated with changes in CPE cell morphology. Here, we report that TNF is the main inflammatory upstream mediator in choroid plexus tissue in AD patients. This was confirmed in two murine AD models: transgenic APP/PS1 mice and intracerebroventricular (icv) AβO injection. TNFR1 contributes to the morphological damage of CPE cells in AD, and TNFR1 abrogation reduces brain inflammation and prevents blood-CSF barrier impairment. In APP/PS1 transgenic mice, TNFR1 deficiency ameliorated amyloidosis. Ultimately, genetic and pharmacological blockage of TNFR1 rescued from the induced cognitive impairments. Our data indicate that TNFR1 is a promising therapeutic target for AD treatment. PB - EMBO Press T2 - EMBO Molecular Medicine T1 - Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease. DO - 10.15252/emmm.201708300 ER -
@article{ author = "Steeland, Sophie and Gorlé, Nina and Vandendriessche, Charysse and Balusu, Sriram and Brkić, Marjana and Van Cauwenberghe, Caroline and Van Imschoot, Griet and Van Wonterghem, Elien and De Rycke, Riet and Kremer, Anneke and Lippens, Saskia and Stopa, Edward and Johanson, Conrad E and Libert, Claude and Vandenbroucke, Roosmarijn E", year = "2018", abstract = "Alzheimer's disease (AD) is the most common form of dementia, and neuroinflammation is an important hallmark of the pathogenesis. Tumor necrosis factor (TNF) might be detrimental in AD, though the results coming from clinical trials on anti-TNF inhibitors are inconclusive. TNFR1, one of the TNF signaling receptors, contributes to the pathogenesis of AD by mediating neuronal cell death. The blood-cerebrospinal fluid (CSF) barrier consists of a monolayer of choroid plexus epithelial (CPE) cells, and AD is associated with changes in CPE cell morphology. Here, we report that TNF is the main inflammatory upstream mediator in choroid plexus tissue in AD patients. This was confirmed in two murine AD models: transgenic APP/PS1 mice and intracerebroventricular (icv) AβO injection. TNFR1 contributes to the morphological damage of CPE cells in AD, and TNFR1 abrogation reduces brain inflammation and prevents blood-CSF barrier impairment. In APP/PS1 transgenic mice, TNFR1 deficiency ameliorated amyloidosis. Ultimately, genetic and pharmacological blockage of TNFR1 rescued from the induced cognitive impairments. Our data indicate that TNFR1 is a promising therapeutic target for AD treatment.", publisher = "EMBO Press", journal = "EMBO Molecular Medicine", title = "Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease.", doi = "10.15252/emmm.201708300" }
Steeland, S., Gorlé, N., Vandendriessche, C., Balusu, S., Brkić, M., Van Cauwenberghe, C., Van Imschoot, G., Van Wonterghem, E., De Rycke, R., Kremer, A., Lippens, S., Stopa, E., Johanson, C. E., Libert, C.,& Vandenbroucke, R. E.. (2018). Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease.. in EMBO Molecular Medicine EMBO Press.. https://doi.org/10.15252/emmm.201708300
Steeland S, Gorlé N, Vandendriessche C, Balusu S, Brkić M, Van Cauwenberghe C, Van Imschoot G, Van Wonterghem E, De Rycke R, Kremer A, Lippens S, Stopa E, Johanson CE, Libert C, Vandenbroucke RE. Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease.. in EMBO Molecular Medicine. 2018;. doi:10.15252/emmm.201708300 .
Steeland, Sophie, Gorlé, Nina, Vandendriessche, Charysse, Balusu, Sriram, Brkić, Marjana, Van Cauwenberghe, Caroline, Van Imschoot, Griet, Van Wonterghem, Elien, De Rycke, Riet, Kremer, Anneke, Lippens, Saskia, Stopa, Edward, Johanson, Conrad E, Libert, Claude, Vandenbroucke, Roosmarijn E, "Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease." in EMBO Molecular Medicine (2018), https://doi.org/10.15252/emmm.201708300 . .