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In vivo imaging reveals rapid astrocyte depletion and axon damage in a model of neuromyelitis optica-related pathology.

Annals of neurology

Herwerth M, Kalluri SR, Srivastava R, Kleele T, Kenet S, Illes Z, Merkler D, Bennett JL, Misgeld T, Hemmer B.
PMID: 26946517
Ann Neurol. 2016 May;79(5):794-805. doi: 10.1002/ana.24630. Epub 2016 Apr 18.

OBJECTIVE: Neuromyelitis optica (NMO) is an autoimmune disease of the central nervous system, which resembles multiple sclerosis (MS). NMO differs from MS, however, in the distribution and histology of neuroinflammatory lesions and shows a more aggressive clinical course. Moreover,...

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Herwerth M, Kalluri SR, Srivastava R, et al. In vivo imaging reveals rapid astrocyte depletion and axon damage in a model of neuromyelitis optica-related pathology. Ann Neurol. 2016;79(5):794-805doi: 10.1002/ana.24630.
Herwerth, M., Kalluri, S. R., Srivastava, R., Kleele, T., Kenet, S., Illes, Z., Merkler, D., Bennett, J. L., Misgeld, T., & Hemmer, B. (2016). In vivo imaging reveals rapid astrocyte depletion and axon damage in a model of neuromyelitis optica-related pathology. Annals of neurology, 79(5), 794-805. https://doi.org/10.1002/ana.24630
Herwerth, Marina, et al. "In vivo imaging reveals rapid astrocyte depletion and axon damage in a model of neuromyelitis optica-related pathology." Annals of neurology vol. 79,5 (2016): 794-805. doi: https://doi.org/10.1002/ana.24630
Herwerth M, Kalluri SR, Srivastava R, Kleele T, Kenet S, Illes Z, Merkler D, Bennett JL, Misgeld T, Hemmer B. In vivo imaging reveals rapid astrocyte depletion and axon damage in a model of neuromyelitis optica-related pathology. Ann Neurol. 2016 May;79(5):794-805. doi: 10.1002/ana.24630. Epub 2016 Apr 18. PMID: 26946517; PMCID: PMC5021140.
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Treatment response to cyclophosphamide, rituximab, and bortezomib in chronic immune-mediated sensorimotor neuropathies: a retrospective cohort study.

Therapeutic advances in neurological disorders

Motte J, Fisse AL, Köse N, Grüter T, Mork H, Athanasopoulos D, Fels M, Otto S, Siglienti I, Schneider-Gold C, Hellwig K, Yoon MS, Gold R, Pitarokoili K.
PMID: 33747132
Ther Adv Neurol Disord. 2021 Mar 05;14:1756286421999631. doi: 10.1177/1756286421999631. eCollection 2021.

BACKGROUND: Up to 20% of patients with chronic immune-mediated sensorimotor neuropathies (CIN) do not respond adequately to first-line therapies. However, studies on further treatment are scarce.METHODS: We analyzed retrospectively 200 CIN patients regarding disease characteristics and response to therapy...

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Motte J, Fisse AL, Köse N, et al. Treatment response to cyclophosphamide, rituximab, and bortezomib in chronic immune-mediated sensorimotor neuropathies: a retrospective cohort study. Ther Adv Neurol Disord. 2021;14:1756286421999631doi: 10.1177/1756286421999631.
Motte, J., Fisse, A. L., Köse, N., Grüter, T., Mork, H., Athanasopoulos, D., Fels, M., Otto, S., Siglienti, I., Schneider-Gold, C., Hellwig, K., Yoon, M. S., Gold, R., & Pitarokoili, K. (2021). Treatment response to cyclophosphamide, rituximab, and bortezomib in chronic immune-mediated sensorimotor neuropathies: a retrospective cohort study. Therapeutic advances in neurological disorders, 141756286421999631. https://doi.org/10.1177/1756286421999631
Motte, Jeremias, et al. "Treatment response to cyclophosphamide, rituximab, and bortezomib in chronic immune-mediated sensorimotor neuropathies: a retrospective cohort study." Therapeutic advances in neurological disorders vol. 14 (2021): 1756286421999631. doi: https://doi.org/10.1177/1756286421999631
Motte J, Fisse AL, Köse N, Grüter T, Mork H, Athanasopoulos D, Fels M, Otto S, Siglienti I, Schneider-Gold C, Hellwig K, Yoon MS, Gold R, Pitarokoili K. Treatment response to cyclophosphamide, rituximab, and bortezomib in chronic immune-mediated sensorimotor neuropathies: a retrospective cohort study. Ther Adv Neurol Disord. 2021 Mar 05;14:1756286421999631. doi: 10.1177/1756286421999631. eCollection 2021. PMID: 33747132; PMCID: PMC7940507.
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Hereditary defect of cobalamin metabolism with adolescence onset resembling multiple sclerosis: 41-year follow up in two cases.

Therapeutic advances in neurological disorders

Motte J, Kneiphof J, Straßburger-Krogias K, Pitarokoili K, Fisse AL, Kappos L, Gold R.
PMID: 31489032
Ther Adv Neurol Disord. 2019 Aug 24;12:1756286419872115. doi: 10.1177/1756286419872115. eCollection 2019.

The cblC defect is the most common inborn error of cobalamin (Cbl) metabolism. Clinical severity and presentation of the cblC defect ranges from death to mild disability. Only 71 cases of late-onset cblC defect have been described in the...

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Motte J, Kneiphof J, Straßburger-Krogias K, et al. Hereditary defect of cobalamin metabolism with adolescence onset resembling multiple sclerosis: 41-year follow up in two cases. Ther Adv Neurol Disord. 2019;12:1756286419872115doi: 10.1177/1756286419872115.
Motte, J., Kneiphof, J., Straßburger-Krogias, K., Pitarokoili, K., Fisse, A. L., Kappos, L., & Gold, R. (2019). Hereditary defect of cobalamin metabolism with adolescence onset resembling multiple sclerosis: 41-year follow up in two cases. Therapeutic advances in neurological disorders, 121756286419872115. https://doi.org/10.1177/1756286419872115
Motte, Jeremias, et al. "Hereditary defect of cobalamin metabolism with adolescence onset resembling multiple sclerosis: 41-year follow up in two cases." Therapeutic advances in neurological disorders vol. 12 (2019): 1756286419872115. doi: https://doi.org/10.1177/1756286419872115
Motte J, Kneiphof J, Straßburger-Krogias K, Pitarokoili K, Fisse AL, Kappos L, Gold R. Hereditary defect of cobalamin metabolism with adolescence onset resembling multiple sclerosis: 41-year follow up in two cases. Ther Adv Neurol Disord. 2019 Aug 24;12:1756286419872115. doi: 10.1177/1756286419872115. eCollection 2019. PMID: 31489032; PMCID: PMC6710698.
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Showing 1 to 3 of 3 entries