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Related Concept Videos

Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

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Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which...
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Myasthenia Gravis: Diagnostic Tests01:15

Myasthenia Gravis: Diagnostic Tests

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Myasthenia gravis is an autoimmune condition affecting neuromuscular transmission, causing generalized weakness in skeletal muscles. Initial diagnoses rely on patients' signs, symptoms, and medical history. The challenge lies in distinguishing myasthenia from other muscular dystrophies. An important diagnostic feature is the significant improvement of symptoms after administering anticholinesterase inhibitors.
The edrophonium test is a diagnostic tool for myasthenia gravis. It involves...
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Chemical Synapses01:26

Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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Chemical Synapses01:26

Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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Indirect-Acting Cholinergic Agonists: Pharmacological Actions01:30

Indirect-Acting Cholinergic Agonists: Pharmacological Actions

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Indirect-acting cholinergic agonists, also known as anticholinesterases, exert their pharmacological effects by enhancing cholinergic transmission in various body parts, including the neuromuscular junction, autonomic cholinergic synapses, and the brain.
At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...
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Disorders of the Skeletal Muscle01:28

Disorders of the Skeletal Muscle

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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
Musculoskeletal disorders
Musculoskeletal disorders involve injuries and conditions affecting the skeletal muscles and associated connective tissues. These disorders can arise from acute biomechanical stresses or chronic overuse and can occur across different age groups. Common injuries include sprains, fractures, and muscular strains, often resulting from...
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Related Experiment Video

Updated: Dec 17, 2025

Antigenic Liposomes for Generation of Disease-specific Antibodies
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Complement Inhibitor Therapy for Myasthenia Gravis.

Khaled Albazli1, Henry J Kaminski1, James F Howard2

  • 1Department of Neurology, George Washington University, Washington, DC, United States.

Frontiers in Immunology
|June 26, 2020
PubMed
Summary

Complement activation drives myasthenia gravis (MG) pathology. Inhibiting complement, particularly C5 with eculizumab, is an effective therapy for acetylcholine receptor antibody-positive MG.

Keywords:
C5complementeculizumabmyasthenia (myasthenia gravis—MG)zilucoplan

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Last Updated: Dec 17, 2025

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Area of Science:

  • Immunology
  • Neurology
  • Pharmacology

Background:

  • Complement activation is a key factor in myasthenia gravis (MG) pathogenesis.
  • The terminal complement component, membrane attack complex (MAC), is present at neuromuscular junctions in MG patients.
  • Acetylcholine receptor antibody-positive (AChR+) MG is driven by complement activation.

Purpose of the Study:

  • To review the role of complement activation in MG.
  • To discuss complement inhibition as a therapeutic strategy for MG.
  • To present the current state of knowledge on complement inhibitors in MG treatment.

Main Methods:

  • Review of historical data and current research on complement in MG.
  • Analysis of preclinical studies on complement inhibition.
  • Evaluation of clinical trial data for complement inhibitors, including eculizumab.

Main Results:

  • Experimental autoimmune MG models show dependence on the complement system.
  • Complement inhibition is a validated therapeutic approach for MG.
  • Eculizumab, a C5 inhibitor, is FDA-approved for AChR+ MG based on Phase 3 trial efficacy.

Conclusions:

  • Complement activation is a critical driver of pathology in myasthenia gravis.
  • Complement inhibitors, such as eculizumab, represent a significant therapeutic advancement for AChR+ MG.
  • Next-generation complement inhibitors are under development and nearing evaluation.