Functional and molecular evidence of myelin- and neuro-protection by thyroid hormone administration in experimental allergic encephalomyelitis
| Autor: | Dell'Acqua, Maria Daniela, Lorenzini, L, D'Intino, G, Sivilia, S, Pasqualetti, P, Panetta, V, Paradisi, M, Filippi, Mauro, Baiguera, C, Pizzi, M, Giardino, L, Rossini, Paolo Maria, Calzà, L. |
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| Přispěvatelé: | ML Dell’Acqua, L Lorenzini, G D’Intino, S Sivilia, P Pasqualetti, V Panetta, M. Paradisi, MM Filippi, C. Baiguera, M Pizzi, L Giardino, PM Rossini, L Calzà |
| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Thyroid Hormones
Histology Encephalomyelitis Autoimmune Experimental Experimental Physiology (medical) Animals Experimental allergic encephalomyelitis Neuroprotection Remyelination Somatosensory evoked potentials Thyroid hormone Axons Disease Models Animal Female Myelin Sheath Neuroprotective Agents Rats Spinal Cord Triiodothyronine 2734 Neurology Neurology (clinical) Encephalomyelitis NEUROPROTECTION Animal experimental allergic encephalomyeliti thyroid hormone Settore MED/26 - NEUROLOGIA remyelination Disease Models somatosensory evoked potential Autoimmune |
| Popis: | AIMS: Recent data in mouse and rat demyelination models indicate that administration of thyroid hormone (TH) has a positive effect on the demyelination/remyelination balance. As axonal pathology has been recognized as an early neuropathological event in multiple sclerosis, and remyelination is considered a pre-eminent neuroprotective strategy, in this study we investigated whether TH administration improves nerve impulse propagation and protects axons. METHODS: We followed up the somatosensory evoked potentials (SEPs) in triiodothyronine (T3)-treated and untreated experimental allergic encephalomyelitis (EAE) Dark-Agouti female rats during the electrical stimulation of the tail nerve. T3 treatment started on the 10th day post immunization (DPI) and a pulse administration was continued until the end of the study (33 DPI). SEPs were recorded at baseline (8 DPI) and the day after each hormone/ vehicle administration. RESULTS: T3 treatment was associated with better outcome of clinical and neurophysiological parameters. SEPs latencies of the two groups behaved differently, being briefer and closer to control values (=faster impulse propagation) in T3-treated animals. The effect was evident on 24 DPI. In the same groups of animals, we also investigated axonal proteins, showing that T3 administration normalizes neurofilament immunoreactivity in the fasciculus gracilis and tau hyperphosphorylation in the lumbar spinal cord of EAE animals. No sign of plasma hyperthyroidism was found; moreover, the dysregulation of TH nuclear receptor expression observed in the spinal cord of EAE animals was corrected by T3 treatment. CONCLUSIONS: T3 supplementation results in myelin sheath protection, nerve conduction preservation and axon protection in this animal model of multiple sclerosis. |
| Databáze: | OpenAIRE |
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