دورية أكاديمية
أعرض في EDS

Synaptic Pathophysiology and Treatment of Lambert-Eaton Myasthenic Syndrome.

التفاصيل البيبلوغرافية
العنوان: Synaptic Pathophysiology and Treatment of Lambert-Eaton Myasthenic Syndrome.
المؤلفون: Tarr TB; Department of Neuroscience, Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, 15260, USA., Wipf P, Meriney SD
المصدر: Molecular neurobiology [Mol Neurobiol] 2015 Aug; Vol. 52 (1), pp. 456-63. Date of Electronic Publication: 2014 Sep 09.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
اللغة: English
بيانات الدورية: Publisher: Humana Press Country of Publication: United States NLM ID: 8900963 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-1182 (Electronic) Linking ISSN: 08937648 NLM ISO Abbreviation: Mol Neurobiol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Clifton, NJ : Humana Press, c1987-
مواضيع طبية MeSH: Lambert-Eaton Myasthenic Syndrome/*physiopathology , Lambert-Eaton Myasthenic Syndrome/*therapy , Synapses/*pathology, Animals ; Humans ; Lambert-Eaton Myasthenic Syndrome/drug therapy ; Neuromuscular Junction/drug effects ; Neuromuscular Junction/physiopathology ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Synapses/drug effects
مستخلص: Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease that disrupts the normally reliable neurotransmission at the neuromuscular junction (NMJ). This disruption is thought to result from an autoantibody-mediated removal of a subset of the P/Q-type Ca(2+) channels involved with neurotransmitter release. With less neurotransmitter release at the NMJ, LEMS patients experience debilitating muscle weakness. The underlying cause of LEMS in slightly more than half of all patients is small cell lung cancer, and cancer therapy is the priority for these patients. In the remaining cases, the cause of LEMS is unknown, and these patients often rely on symptomatic treatment options, as there is no cure. However, current symptomatic treatment options, such as 3,4-diaminopyridine (3,4-DAP), can have significant dose-limiting side effects; thus, additional treatment approaches would benefit LEMS patients. Recent studies introduced a novel Ca(2+) channel agonist (GV-58) as a potential therapeutic alternative for LEMS. Additionally, this work has shown that GV-58 and 3,4-DAP interact in a supra-additive manner to completely restore the magnitude of neurotransmitter release at the NMJs of a LEMS mouse model. In this review, we discuss synaptic mechanisms for reliability at the NMJ and how these mechanisms are disrupted in LEMS. We then discuss the current treatment options for LEMS patients, while also considering recent work demonstrating the therapeutic potential of GV-58 alone and in combination with 3,4-DAP.
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معلومات مُعتمدة: P50 GM067082 United States GM NIGMS NIH HHS; GM067082 United States GM NIGMS NIH HHS
المشرفين على المادة: 0 (Neuroprotective Agents)
تواريخ الأحداث: Date Created: 20140909 Date Completed: 20160517 Latest Revision: 20211021
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC4362862
DOI: 10.1007/s12035-014-8887-2
PMID: 25195700
قاعدة البيانات: MEDLINE
الوصف
تدمد:1559-1182
DOI:10.1007/s12035-014-8887-2