Parkinson’s disease is a progressive motor disorder which can take its toll on mental health and overall wellness. Caused by the loss of dopamine-producing neurons in the brain (primarily in the substantia nigra), Parkinson’s is the second most common neurodegenerative disorder after Alzheimer’s disease, and it is estimated that Parkinson’s affects the wellbeing of up to 10 million people worldwide. There is currently no drug that has been shown unequivocally to cure the disease or slow its progression, so what can treatments do for your wellbeing?
Levodopa/carbidopa – This is the gold standard therapy for symptomatic treatment of Parkinson’s, but levodopa is associated with long-term motor complications (such as motor fluctuations and dyskinesias), low blood pressure, arrhythmias, gastrointestinal problems, nausea, hair loss, sleep disorders, confusion, anxiety and hallucinations. The treatment also has a “wearing off effect” in patients who use levodopa for more than four years, and so patients must either increase their dosage or frequency (and face an increased risk of dyskinesia) or turn to alternative therapies.
Dopamine agonists – These drugs work differently to levodopa, in that they do not change into dopamine, but rather mimic the effect of dopamine in the brain. Dopamine agonists aren’t as effective as levodopa, but they do last longer in the brain and their effects do not wane over time. These treatments make up approximately 70% of the marketed therapies for Parkinson’s, but dopamine agonists unfortunately come with similar unpleasant side effects to levodopa/carbidopa.
MAO B inhibitors – An enzyme in your brain, known as Monoamine oxidase B (MAO B) breaks down dopamine, and so MAO B inhibitors block this breakdown, which slows your loss of dopamine and several of the side effects associated with Parkinson’s. If your disease is in the early stages, you’re likely to be treated with MAO B inhibitors initially.
Adenosine A2A receptor antagonists – These work to modulate the production of dopamine, glutamine and serotonin in specific regions of your brain, without increasing your risk of dyskinesia.
COMT inhibitors – COMT (or catechol O-methyltransferase) converts levodopa in the periphery to 3-O-methyl-DOPA (3-OMD), which is a metabolite that cannot be converted to dopamine. This metabolite then accumulates in plasma during levodopa therapy, reducing bioavailability of levodopa. Therefore, COMT inhibitors allow a larger amount of levodopa to reach your brain and consequently raise dopamine levels. This treatment is always taken in combination with levodopa.
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