Clinical meaning
Parkinson disease results from progressive loss of dopaminergic neurons in the substantia nigra pars compacta, creating a dopamine-acetylcholine imbalance in the striatum. Pharmacotherapy targets multiple points in the dopaminergic pathway: levodopa (dopamine precursor) crosses the blood-brain barrier and is converted to dopamine by aromatic L-amino acid decarboxylase (AADC); carbidopa inhibits peripheral AADC to prevent peripheral conversion and reduce nausea/hypotension; COMT inhibitors (entacapone, opicapone) block peripheral degradation of levodopa extending its half-life; MAO-B inhibitors (selegiline, rasagiline, safinamide) prevent synaptic dopamine breakdown; dopamine agonists (pramipexole, ropinirole, rotigotine) directly stimulate D2/D3 receptors; and anticholinergics (benztropine, trihexyphenidyl) restore balance by reducing cholinergic excess.