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The postsynaptic neuromuscular dysfunction in MG is produced by IgG autoantibodies which act by three main mechanisms: (1) direct functional blockade of the receptors, (2) antigenic modulation leading to receptor internalisation and degradation and (3) complement activation and destruction of the membrane [6]
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NAD+ / SIRT1: Associated with elevated NAD+ and SIRT1 activation in preclinical studies [2] [3]
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