Contributions
Abstract: P1102
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Repairing mechanisms
Background: In multiple sclerosis (MS), axonal degeneration is critical for the development of irreversible disability and occurs during the entire course of the disease. It seems that mitochondria play an active role in axonal degeneration, and increasing evidence suggests that mitochondrial dysfunctions are involved in MS, especially in progressive MS.
Objective: To determine the influence of mitochondrial dysfunction in experimental autoimmune encephalomyelitis (EAE), we used mice lacking Parkin gene, a genetic mouse model of Parkinson's disease. Parkin is a key factor in mitochondrial quality control because recognizes and eliminates damages mitochondria from the cell through mitophagy.
Methods: Young (8-10 weeks) and middle-aged(6-8 months)Parkin-knockout(KO) mice and wild-type (WT) littermate controls were submitted to EAE induction by active immunization with MOG35-55 peptide in Complete Freund's Adjuvant.
Results: KO mice showed earlier onset and more severe EAE compared to WT. The latter developed an acute monophasic EAE, while in KO mice the disease consisted of an acute attack followed by a chronic phase of irreversible accumulation of neurological damages without relapses. Histological analysis revealed that KO mice showed more pronounced cell infiltration in the brain and spinal cord during the acute and chronic phases. Abnormal morphology of mitochondria was detected by electron microscopy in the substantia nigra of the middle-aged KO mice with EAE. Alteration in cytokines and chemokines profile as well as differences in immune cell subsets were observed during the chronic phase of the disease. T cells from KO mice in general exhibit a higher T cell proliferative response to immunized antigen throughout their lives.
Conclusions: Our results support the idea that the role of mitochondria in EAE affect acute as well as chronic recovering status and seems to be age-related.
Disclosure: financially supported by Ohara Pharmaceutical, AbbVie, Ono Pharmaceutical, Mitsubishi Tanabe Pharma, MiZ, Asahi Kasei Medical, Nihon Pharmaceutical.
Abstract: P1102
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Repairing mechanisms
Background: In multiple sclerosis (MS), axonal degeneration is critical for the development of irreversible disability and occurs during the entire course of the disease. It seems that mitochondria play an active role in axonal degeneration, and increasing evidence suggests that mitochondrial dysfunctions are involved in MS, especially in progressive MS.
Objective: To determine the influence of mitochondrial dysfunction in experimental autoimmune encephalomyelitis (EAE), we used mice lacking Parkin gene, a genetic mouse model of Parkinson's disease. Parkin is a key factor in mitochondrial quality control because recognizes and eliminates damages mitochondria from the cell through mitophagy.
Methods: Young (8-10 weeks) and middle-aged(6-8 months)Parkin-knockout(KO) mice and wild-type (WT) littermate controls were submitted to EAE induction by active immunization with MOG35-55 peptide in Complete Freund's Adjuvant.
Results: KO mice showed earlier onset and more severe EAE compared to WT. The latter developed an acute monophasic EAE, while in KO mice the disease consisted of an acute attack followed by a chronic phase of irreversible accumulation of neurological damages without relapses. Histological analysis revealed that KO mice showed more pronounced cell infiltration in the brain and spinal cord during the acute and chronic phases. Abnormal morphology of mitochondria was detected by electron microscopy in the substantia nigra of the middle-aged KO mice with EAE. Alteration in cytokines and chemokines profile as well as differences in immune cell subsets were observed during the chronic phase of the disease. T cells from KO mice in general exhibit a higher T cell proliferative response to immunized antigen throughout their lives.
Conclusions: Our results support the idea that the role of mitochondria in EAE affect acute as well as chronic recovering status and seems to be age-related.
Disclosure: financially supported by Ohara Pharmaceutical, AbbVie, Ono Pharmaceutical, Mitsubishi Tanabe Pharma, MiZ, Asahi Kasei Medical, Nihon Pharmaceutical.