Foundation for Alzheimer's Research (SAO/FRA) Belgium

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Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease.

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 . .
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