A deficiency of the brain neurotransmitter dopamine is central to Parkinson’s disease. The key problem is the gradual loss of dopamine-producing nerve cells in the substantia nigra, a region of the midbrain.
Dopamine helps regulate movement through circuits connecting the substantia nigra with the basal ganglia. As dopamine levels fall, these circuits become less effective, contributing to the characteristic motor symptoms of Parkinson’s: bradykinesia, or slowness of movement; rigidity; resting tremor; and impaired balance.
The condition is more than a simple chemical deficiency. Parkinson’s also involves abnormal accumulation of the protein alpha-synuclein, often associated with Lewy bodies, along with changes affecting both the central and peripheral nervous systems. Non-motor symptoms can include loss of smell, sleep problems, constipation, depression, and cognitive changes.
Levodopa is the most effective medication for replacing dopamine activity because it can cross the blood-brain barrier and be converted into dopamine. Dopamine itself cannot cross that barrier efficiently. Acetylcholine, serotonin, and adrenaline are important brain chemicals, but they are not the canonical answer to this question.