A patient presents to the clinic complaining of chronic exhaustion. HPI reveals that the patient feels fine in the morning, however as the day progresses, he feels weak. Physical examination shows ptosis (lazy eyelid), and difficulty smiling. Muscle resistance is low. Further tests reveal that the patient is suffering from Myasthenia Gravis, which is an autoimmune disorder that destroys acetylcholine receptors in the neuromuscular junction.

What is the pathophysiology of this disease, starting from the neuromuscular junction? Why is this patient feeling weak?
a) Destruction of acetylcholinesterase enzymes, causing decreased acetylcholine breakdown
b) Autoantibodies against voltage-gated calcium channels, leading to impaired muscle contraction
c) Reduction in acetylcholine release due to autoimmune attack on presynaptic vesicles
d) Autoimmune destruction of acetylcholine receptors, impairing neuromuscular transmission