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The Journal of Neuroscience, December 24, 2008, 28(52):14189-14201; doi:10.1523/JNEUROSCI.4453-08.2008

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Neurobiology of Disease
Recovery from Chronic Demyelination by Thyroid Hormone Therapy: Myelinogenesis Induction and Assessment by Diffusion Tensor Magnetic Resonance Imaging

Laura-Adela Harsan,^1,2 Jérôme Steibel,¹ Anita Zaremba,³ Arnaud Agin,¹ Rémy Sapin,¹ Patrick Poulet,¹ Blandine Guignard,¹ Nathalie Parizel,¹ Daniel Grucker,¹ Nelly Boehm,⁴ Robert H. Miller,³ and M. Said Ghandour¹

¹UMR 7191, Laboratoire d'Imagerie et de Neurosciences Cognitives, Faculté de Médecine, Université Louis Pasteur and Centre National de la Recherche Scientifique, 67085 Strasbourg, France, ²Medical Physics, Department of Diagnostic Radiology, University Hospital, 79106 Freiburg, Germany, ³Case Western Reserve University, Department of Neurosciences, School of Medicine, Cleveland, Ohio 44106, and ⁴INSERM U666 and Service Central de Microscopie Electronique, Faculté de Médecine, Université Louis Pasteur, 67085 Strasbourg, France

Correspondence should be addressed to Dr. M. Said Ghandour, UMR 7191, Centre National de la Recherche Scientifique/Université Louis Pasteur, Faculté de Médecine, 11 rue Humann, 67085 Strasbourg, France. Email: ghandour{at}neurochem.u-strasbg.fr

The failure of the remyelination processes in multiple sclerosis contributes to the formation of chronic demyelinated plaques that lead to severe neurological deficits. Long-term cuprizone treatment of C57BL/6 mice resulted in pronounced white matter pathology characterized by oligodendrocyte depletion, irreversible demyelination and persistent functional deficits after cuprizone withdrawal. The use of a combination of in vivo diffusion tensor magnetic resonance imaging (DT-MRI) and histological analyses allowed for an accurate longitudinal assessment of demyelination. Injection of triiodothyronine (T₃) hormone over a 3 week interval after cuprizone withdrawal progressively restored the normal DT-MRI phenotype accompanied by an improvement of clinical signs and remyelination. The effects of T₃ were not restricted to the later stages of remyelination but increased the expression of sonic hedgehog and the numbers of Olig2⁺ and PSA-NCAM⁺ precursors and proliferative cells. Our findings establish a role for T₃ as an inducer of oligodendrocyte progenitor cells in adult mouse brain following chronic demyelination.

Key words: myelin; oligodendrocytes; demyelination therapy; gliotoxic agent; DT-MRI; myelin repair

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Received Sept. 17, 2008; accepted Oct. 27, 2008.

Correspondence should be addressed to Dr. M. Said Ghandour, UMR 7191, Centre National de la Recherche Scientifique/Université Louis Pasteur, Faculté de Médecine, 11 rue Humann, 67085 Strasbourg, France. Email: ghandour{at}neurochem.u-strasbg.fr

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