Parkinson's disease

Parkinson’s disease is a progressive neurological condition. It involves the death of brain cells, especially those that make the signalling molecule dopamine. It is named after the English doctor James Parkinson, who published the first detailed description of the condition, An Essay on the Shaking Palsy, in 1817.

Parkinson’s begins with abnormal clumping of a protein called synuclein in the brain. The neighbouring dopamine-producing neurons then die, causing tremors, slowness and difficulty moving.

The prevailing wisdom has been that affected neurons die from a toxic reaction to synuclein deposits. However, Parkinson’s has been linked to some gene variants that affect how the immune system works – leading to an alternative theory that synuclein causes Parkinson’s by triggering the immune system to attack the brain. This would suggest that Parkinson’s disease could be an autoimmune disease.

Levodopa is the main drug used to treat many of the symptoms experienced by the 10 million people with Parkinson’s globally. Levodopa works by passing the blood-brain barrier and releasing dopamine in the brain.

Some of the drug is converted to dopamine before it gets to the brain, which can cause adverse side effects and limit the drug’s effectiveness. A particular problem is that the drug is broken down by enzymes in the gut and blood vessels. For this reason, people with Parkinson’s usually take levodopa in combination with another drug, carbidopa, that inhibits the break down.

Researchers have been working to see how much of a role the human microbiome could be playing in the varying responses people experience to levodopa.