Open AccessMetformin-induced AMPK activation stimulates remyelination through induction of neurotrophic factors, downregulation of NogoA and recruitment of Olig2+ precursor cells in the cuprizone murine model of multiple sclerosis
Author(s) -
Fariba Houshmand,
Mahmood Barati,
Fereshteh Golab,
Samaneh Ramezani-sefidar,
Sara Tanbakooie,
Mahsa Tabatabaei,
Masoomeh Amiri,
Nima Sanadgol
Publication year - 2019
Publication title -
daru
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.645
H-Index - 42
eISSN - 2008-2231
pISSN - 1560-8115
DOI - 10.1007/s40199-019-00286-z
Subject(s) - remyelination , olig2 , ampk , metformin , neuroprotection , multiple sclerosis , neurotrophic factors , myelin , neuroregeneration , medicine , oligodendrocyte , cancer research , neuroscience , endocrinology , microbiology and biotechnology , biology , immunology , central nervous system , diabetes mellitus , protein kinase a , phosphorylation , receptor
Oligodendrocytes (OLGs) damage and myelin distraction is considered as a critical step in many neurological disorders especially multiple sclerosis (MS). Cuprizone (cup) animal model of MS targets OLGs degeneration and frequently used to the mechanistic understanding of de- and remyelination. The aim of this study was exploring the effects of metformin on the OLGs regeneration, myelin repair and profile of neurotrophic factors in the mice brain after cup-induced acute demyelination.