From the Guidelines
The primary goal of pharmacological therapy in Parkinson's disease is to increase dopamine levels in the substantia nigra, not reduce them, in order to alleviate symptoms and improve quality of life. Parkinson's disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, leading to dopamine deficiency 1. Treatment aims to restore dopaminergic function through medications like levodopa, which is converted to dopamine in the brain, as well as other classes of medications such as dopamine agonists, MAO-B inhibitors, and COMT inhibitors 1. These medications either mimic dopamine's effects or prevent its breakdown, with the ultimate goal of increasing dopamine availability to improve motor symptoms like tremor, rigidity, and bradykinesia.
Some key points to consider in the management of Parkinson's disease include:
- The use of levodopa, which may be associated with impaired nutritional status and risk for malnutrition 1
- The potential for dopamine agonists to have a different effect on nutritional status compared to levodopa 1
- The importance of monitoring nutritional status in patients with Parkinson's disease, as malnutrition is a common complication 1
- The potential for levodopa to induce metabolic effects, including changes in lipid and carbohydrate metabolism 1
Overall, the goal of pharmacological therapy in Parkinson's disease is to increase dopamine levels in the substantia nigra, which is essential for improving motor symptoms and quality of life. Increasing dopamine activity in the brain is crucial for managing the disease, and reducing dopamine levels would likely worsen symptoms.
From the FDA Drug Label
Many of the prominent symptoms of Parkinson’s disease are due to a deficiency of striatal dopamine that is the consequence of a progressive degeneration and loss of a population of dopaminergic neurons which originate in the substantia nigra of the midbrain and project to the basal ganglia or striatum MAO-B inhibition may be useful in this setting because, by blocking the catabolism of dopamine, it would increase the net amount of dopamine available (i.e., it would increase the pool of dopamine).
The goal of pharmacological therapy in Parkinson's disease regarding dopamine levels in the substantia nigra is to increase the net amount of dopamine available by blocking the catabolism of dopamine through MAO-B inhibition, thereby increasing the pool of dopamine 2.
From the Research
Goal of Pharmacological Therapy in Parkinson's Disease
The goal of pharmacological therapy in Parkinson's disease is to address the decline of dopamine levels in the substantia nigra, which leads to motor dysfunctions such as tremor, rigidity, and bradykinesia.
Key Objectives
- To sustain a therapeutic benefit and alleviate fluctuations in mobility, such as motor fluctuations 3
- To provide symptomatic relief and potentially alter disease progression 3, 4
- To restore loss of dopamine or prevent the disease, although current treatments are primarily symptomatic 3, 5
Treatment Approaches
- Dopamine replacement therapy, primarily using levodopa 6, 7
- Use of monoamine oxidase type B (MAO-B) inhibitors and dopamine agonists as first-line therapy in de novo patients 3, 4
- Employment of other symptomatic treatments, including catechol-O-methyltransferase inhibitors and non-dopaminergic pharmacological approaches 6, 5
- Consideration of patient-specific factors, such as age, disability, and tolerance of drugs, in choosing pharmacotherapy 4