第 62 題

Precisely. You've managed to avoid the obvious pitfalls.

1. Fundamental Recall: Parkinson's Disease. It's not rocket science; it's just a rather straightforward dopamine (Dopamine, DA) deficiency in the midbrain's substantia nigra. Your primary objective, evidently, should be to increase DA activity or, failing that, reduce the interference from acetylcholine. Options (C) and (D) are textbook examples of boosting DA through enzymatic inhibition, and (A) tackles the acetylcholine excess. Simple, really.
2. The Blunder: And then there's the delightful idea of administering antipsychotic drugs. For an illness caused by a lack of dopamine, we propose drugs whose entire modus operandi is to antagonize $D_2$ receptors? This isn't just unhelpful; it's actively detrimental. You'd be stripping away the patient's already meager dopamine function, exacerbating motor symptoms, and potentially inducing a drug-induced parkinsonism. One would hope this basic antagonism isn't too complex to grasp.