TY - JOUR
T1 - Axonal damage is reduced following glatiramer acetate treatment in C57/bl mice with chronic-induced experimental autoimmune encephalomyelitis
AU - Gilgun-Sherki, Yossi
AU - Panet, Hana
AU - Holdengreber, Vered
AU - Mosberg-Galili, Ronit
AU - Offen, Daniel
N1 - Funding Information:
This work was performed in partial fulfillment of the requirements for a Ph.D. degree of Yossi Gilgun-Sherki, Sackler Faculty of Medicine, Tel Aviv University, Israel. Supported, in part, by the Israel Ministry of Health (D.O.) and the National Parkinson Foundation, USA (E.M.).
PY - 2003/10/1
Y1 - 2003/10/1
N2 - Glatiramer acetate (GA) is efficacious in reducing demyelinating-associated exacerbations in patients with relapsing-remitting multiple sclerosis (RRMS) and in several experimental autoimmune encephalomyelitis (EAE) models. Here we report that GA reduced the clinical and pathological signs of mice in chronic EAE induced by myelin oligodendrocyte glycoprotein (MOG). GA-treated mice demonstrated only mild focal inflammation, and less demyelination, compared with controls. Moreover, we also found minimal axonal disruption, as assessed by silver staining, antibodies against amyloid precursor protein (APP) and non-phosphorylated neurofilaments (SMI-32), in the GA-treated group. In conclusion, our study demonstrated for the first time that axonal damage is reduced following GA treatment in C57/bl mice with chronic MOG-induced EAE.
AB - Glatiramer acetate (GA) is efficacious in reducing demyelinating-associated exacerbations in patients with relapsing-remitting multiple sclerosis (RRMS) and in several experimental autoimmune encephalomyelitis (EAE) models. Here we report that GA reduced the clinical and pathological signs of mice in chronic EAE induced by myelin oligodendrocyte glycoprotein (MOG). GA-treated mice demonstrated only mild focal inflammation, and less demyelination, compared with controls. Moreover, we also found minimal axonal disruption, as assessed by silver staining, antibodies against amyloid precursor protein (APP) and non-phosphorylated neurofilaments (SMI-32), in the GA-treated group. In conclusion, our study demonstrated for the first time that axonal damage is reduced following GA treatment in C57/bl mice with chronic MOG-induced EAE.
KW - Axonal damage
KW - Experimental autoimmune encephalomyelitis (EAE)
KW - Glatiramer acetate
KW - Multiple sclerosis (MS)
KW - Myelin oligodendrocyte glycoprotein (MOG)
UR - http://www.scopus.com/inward/record.url?scp=0141516543&partnerID=8YFLogxK
U2 - 10.1016/S0168-0102(03)00217-7
DO - 10.1016/S0168-0102(03)00217-7
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AN - SCOPUS:0141516543
SN - 0168-0102
VL - 47
SP - 201
EP - 207
JO - Neuroscience Research
JF - Neuroscience Research
IS - 2
ER -