What causes Myasthenia gravis?

Myasthenia gravis is an autoimmune disorder characterized primarily by weakness and fatigue of the skeletal muscles. The underlying cause of this condition is the presence of antibodies that target acetylcholine receptors at the neuromuscular junction. In individuals with myasthenia gravis, the immune system mistakenly produces antibodies that block, alter, or destroy these acetylcholine receptors, which impairs the ability of acetylcholine to stimulate muscle contraction. This leads to the hallmark symptoms of muscle weakness, which typically worsens with activity and improves with rest.

Understanding the role of acetylcholine receptors is crucial; they are essential for transmitting signals from nerves to muscles. When these receptors are compromised due to antibody action, the communication between nerves and muscles is disrupted, resulting in the characteristic muscle weakness associated with the disease.

The other options do not correspond to the pathophysiology of myasthenia gravis. For instance, the destruction of peripheral nerves is not the main issue in this condition, and while neurotransmitters like serotonin and dopamine play various roles in the central nervous system, their production levels are not directly linked to the mechanisms behind myasthenia gravis. The focus on antibodies against acetylcholine receptors accurately captures the primary pathological process