Today, levodopa remains the most effective and widely prescribed pharmacological treatment for the disease.
It is often coupled with certain enzyme inhibitors, such as carbidopa (that stop the breakdown of levodopa prior to entering the brain), allowing more of it into the brain and increasing the amount of dopamine produced.
This means dopamine itself can’t be given as a medicinal treatment, since it will not be able to enter the brain.
So in 1961, levodopa – a dopamine “precursor” that is transported across the blood brain barrier into the brain and converted into dopamine – was trialled for the first time with beneficial effects.
This was followed by the application of substances to induce blistering of the skin and the insertion of small pieces of cork into these blisters to lead to pus discharge. The basis of Parkinson’s is loss of cells that normally produce the neurotransmitter dopamine in an area of the brain called the substantia nigra.
The involvement of the substantia nigra has been known since the late 19th and early 20th century.
This releases the drug over a longer period of time (four to six hours), leading to steadier levels of levodopa in the blood.
But because of the slow release, the beneficial effects of Sinemet CR may take longer to come about.
In 1960, Herbert Ehringer and Oleh Hornykiewicz discovered that dopamine was depleted in the brain of those with the disease.
Dopamine itself is not able to cross the blood-brain barrier – a protective barrier that stops pathogens and other larger molecules from entering the brain through the blood.