{'fraction_non_alphanumeric': 0.014705882352941176, 'fraction_numerical': 0.0, 'mean_word_length': 5.730769230769231, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Recent advances in the pharmacological control of experimental allergic encephalomyelitis (EAE) and the implications for multiple sclerosis treatment

The autoimmune, cell-mediated condition experimental allergic encephalomyelitis (EAE) is the representative model for the inflammatory central nervous system disease MS. EAE has been extensively employed to determine the efficacy of pharmacological agents that may be of ultimate use in the treatment of MS. A wide variety of drugs has been examined for activity in EAE but, over the last decade, three groups of compounds have emerged with clear and reproducible ability to modify significantly the onset and progression of the disease. The immunosuppressants, the modulators of catecholamine activity and the antineoplastic agents have convincingly altered the course of EAE and, as a consequence, provided understanding of the mechanisms of disease expression and offered further insight into the pathogenesis of MS. The article stresses the usefulness of EAE as a model to identify prospective pharmacological treatments for MS and, in particular, considers those compounds subsequently assessed for their ability to interfere with the progression of the human disease.