期刊
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY
卷 38, 期 5, 页码 454-470出版社
WILEY
DOI: 10.1111/j.1365-2990.2011.01228.x
关键词
experimental allergic encephalomyelitis; neuroprotection; remyelination; somatosensory evoked potentials; thyroid hormone
资金
- AFaR, Associazione Fatebenefratelli per la Ricerca, Roma
M. L. Dell'Acqua, L. Lorenzini, G. D'Intino, S. Sivilia, P. Pasqualetti, V. Panetta, M. Paradisi, M. M. Filippi, C. Baiguera, M. Pizzi, L. Giardino, P. M. Rossini and L. Calza (2012) Neuropathology and Applied Neurobiology38, 454470 Functional and molecular evidence of myelin- and neuroprotection by thyroid hormone administration in experimental allergic encephalomyelitis 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据