TRPA1 deficiency is protective in cuprizone-induced demyelination-A new target against oligodendrocyte apoptosis

Multiple sclerosis is a chronic inflammatory, demyelinating degenerative disease of the central nervous system. Current treatments target pathological immune responses to counteract the inflammatory processes. However, these drugs do not restrain the long‐term progression of clinical disability. For...

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Veröffentlicht in:	Glia 2016-12, Vol.64 (12), p.2166-2180
Hauptverfasser:	Sághy, Éva, Sipos, Éva, Ács, Péter, Bölcskei, Kata, Pohóczky, Krisztina, Kemény, Ágnes, Sándor, Zoltán, Szőke, Éva, Sétáló Jr, György, Komoly, Sámuel, Pintér, Erika
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenomatous Polyposis Coli - metabolism Animals Apoptosis Apoptosis - drug effects Apoptosis - genetics bcl-2 Homologous Antagonist-Killer Protein - metabolism Body Weight - drug effects Brain - drug effects Brain - metabolism Brain - pathology cuprizone Cuprizone - toxicity Demyelinating Diseases - chemically induced Demyelinating Diseases - genetics Demyelinating Diseases - pathology demyelination Disease Models, Animal Fibroblast Growth Factor 2 - metabolism Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Gliosis - chemically induced Gliosis - genetics Kinases MAPK Mice Mice, Knockout Monoamine Oxidase Inhibitors - toxicity Multiple sclerosis Myelin Basic Protein - metabolism Nerve Tissue Proteins - metabolism Nervous system oligodendrocyte Oligodendroglia - drug effects Signal Transduction - drug effects Signal Transduction - physiology TRPA1 TRPA1 Cation Channel - deficiency TRPA1 Cation Channel - genetics TRPA1 Cation Channel - metabolism
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