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Ultimately, it seems as though injury to the NMJ is a culmination of mutant protein aggregation at the presynaptic nerve terminal, presynaptic cholinergic dysfunction, impaired axonal transport, reduced synaptic acetylcholinesterase, and diseased muscle itself, among others [292]

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That experience is more common than most clinics prepare their patients for, and understanding why it happens can be the difference between pushing through intel