Zobrazeno 1 - 10
of 15
pro vyhledávání: '"Oluwaseun Fatoba"'
Publikováno v:
Frontiers in Cellular Neuroscience, Vol 17 (2023)
Recently, a rising interest is given to neuroimmune communication in physiological and neuropathological conditions. Meningeal immunity is a complex immune environment housing different types of immune cells. Here, we focus on meningeal T cells, poss
Externí odkaz:
https://doaj.org/article/dda484ec669b4bf79f6f6d04590117f2
Publikováno v:
Journal of Pharmacological Sciences, Vol 144, Iss 3, Pp 102-118 (2020)
Chronic microglial activation is associated with the pathogenesis of several CNS disorders. Microglia show phenotypic diversity and functional complexity in diseased CNS. Thus, understanding the pathology-specific heterogeneity of microglial behavior
Externí odkaz:
https://doaj.org/article/7ef5e6bd038a4d6f92e56c055117f405
Publikováno v:
Frontiers in Immunology, Vol 11 (2020)
Modulation of immune activation using immunotherapy has attracted considerable attention for many years as a potential therapeutic intervention for several inflammation-associated neurodegenerative diseases. However, the efficacy of single-target imm
Externí odkaz:
https://doaj.org/article/fc20c1af572b4193b1b52d2dde1c3273
Autor:
Alina Blusch, Annika Mattukat, Jennifer König, Verian Bader, Konstanze F Winklhofer, Oluwaseun Fatoba, Carsten Saft, Gisa Ellrichmann
Publikováno v:
A: Pathogenic mechanisms.
Publikováno v:
The FEBS Journal. 289:2085-2109
The complement system, an essential tightly regulated innate immune system, is a key regulator of normal central nervous system (CNS) development and function. However, aberrant complement component expression and activation in the brain may culminat
Publikováno v:
Journal of Pharmacological Sciences, Vol 144, Iss 3, Pp 102-118 (2020)
Chronic microglial activation is associated with the pathogenesis of several CNS disorders. Microglia show phenotypic diversity and functional complexity in diseased CNS. Thus, understanding the pathology-specific heterogeneity of microglial behavior
Autor:
Simon Ebbinghaus, Christian Heid, Frank-Gerrit Klärner, Anne Steinhof, Kenny Bravo-Rodriguez, Erich E. Wanker, Tobias Vöpel, Abhishek Sharma, Elsa Sanchez-Garcia, Thomas Schrader, Shivang Vachharajani, David Gnutt, Joseph A. Loo, Gal Bitan, Oluwaseun Fatoba, Michael Nshanian, Gisa Ellrichmann, Sumit Mittal
Publikováno v:
Journal of the American Chemical Society, vol 139, iss 16
Voepel, T; Bravo-Rodriguez, K; Mittal, S; Vachharajani, S; Gnutt, D; Sharma, A; et al.(2017). Inhibition of Huntingtin Exon-1 Aggregation by the Molecular Tweezer CLR01. JOURNAL OF THE AMERICAN CHEMICAL SOCIETY, 139(16), 5640-5643. doi: 10.1021/jacs.6b11039. UCLA: Retrieved from: http://www.escholarship.org/uc/item/886087d7
Voepel, T; Bravo-Rodriguez, K; Mittal, S; Vachharajani, S; Gnutt, D; Sharma, A; et al.(2017). Inhibition of Huntingtin Exon-1 Aggregation by the Molecular Tweezer CLR01. JOURNAL OF THE AMERICAN CHEMICAL SOCIETY, 139(16), 5640-5643. doi: 10.1021/jacs.6b11039. UCLA: Retrieved from: http://www.escholarship.org/uc/item/886087d7
Huntington's disease is a neurodegenerative disorder associated with the expansion of the polyglutamine tract in the exon-1 domain of the huntingtin protein (htte1). Above a threshold of 37 glutamine residues, htte1 starts to aggregate in a nucleatio
Autor:
Michael R. Hayden, Gisa Ellrichmann, Alina Blusch, Liat Hayardeny, Christiane Reick, Carsten Saft, Janine Brunner, Ralf Gold, Konstanze F. Winklhofer, Dominik A. Sehr, Oluwaseun Fatoba
Publikováno v:
Scientific Reports
Scientific Reports, Vol 9, Iss 1, Pp 1-1 (2019)
Scientific Reports, Vol 9, Iss 1, Pp 1-1 (2019)
The transgenic mouse model R6/2 exhibits Huntington's disease (HD)-like deficits and basic pathophysiological similarities. We also used the pheochromocytoma-12 (PC12)-cell-line-model to investigate the effect of laquinimod on metabolic activity. Laq
Autor:
Gisa Ellrichmann, Oluwaseun Fatoba, Eugen Kloster, Larissa Arning, Ralf Gold, Jörg T. Epplen, Christiane Reick, Carsten Saft
Publikováno v:
Experimental neurology. 302
Huntington's disease (HD) is a monogenic inherited polyglutamine-mediated neurodegenerative disorder for which effective therapies are currently unavailable. Neuropeptide Y (NPY) has been implicated as a potential therapeutic target in several neurod
Autor:
Liat Hayardeny, Ralf Gold, Oluwaseun Fatoba, Janine Brunner, Konstanze F. Winklhofer, Michael R. Hayden, Dominik A. Sehr, Gisa Ellrichmann, Alina Blusch, Christiane Reick, Carsten Saft
Publikováno v:
Scientific Reports
Scientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
Scientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
The transgenic mouse model R6/2 exhibits Huntington’s disease (HD)-like deficits and basic pathophysiological similarities. We also used the pheochromocytoma-12 (PC12)-cell-line-model to investigate the effect of laquinimod on metabolic activity. L