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Scientists discover the earliest signs of Parkinson's disease in the brain



About 100 people have a rare mutation in a gene called SNCA that puts them at almost safe risk of getting Parkinson's disease. This makes them ideal subjects for studying the root causes of this debilitating condition. Most of these people live in the northern Peloponnese in Greece, and a handful lives in Campania, Italy. We were fortunate enough to have 14 of these people agreed to travel to London so we could study their brains.

More than 6 million people have global Parkinson's disease; It is the second most common neurodegenerative disorder after Alzheimer's disease.

The symptoms that worsen over time include motor symptoms such as stiffness, slowness and shaking, as well as non-motor symptoms, such as memory problems. Researchers have tried to find a reliable marker for the disease so that the risky persons can be identified before the engine's symptoms start.

There is no cure for Parkinson's disease, but the symptoms are treated with substances that restore a brain chemical called dopamine to normal levels. Dopamine has long been regarded as a prime sinner in Parkinson's disease, as low levels cause problems with movement. But another brain chemical called serotonin is also implicated in the disease.

But we did not know how early and to what extent changes in serotonin occur and if these changes are related to disease outbreaks. To help answer this, we needed to study the Greek and Italian topics with the SNCA gene mutation.

Studying these gene carriers before developing Parkinson's disease is a unique opportunity to understand what comes first in the cascade of events that ultimately lead to a diagnosis of Parkinson's disease. This knowledge is critical so we can develop sensitive markers to track the progress of the disease.

People with the mutation tend to show symptoms of Parkinson's disease in their 40's or 50's, so we wanted to study topics in their 20's and 30's. to see if there were any brain changes a decade or more before the symptoms started.

Seven of our volunteers who kindly visited our laboratory for ten days with brain formation and neurological tests had no motor symptoms and seven had been diagnosed with Parkinson's disease.

We also examined 25 patients with sporadic Parkinson's disease (Parkinson's disease without a genetic cause) and 25 healthy volunteers.

All participants had three brain scans: one for measuring dopamine, one for measuring serotonin and another for studying anatomical regions of the brain.

We also conducted a number of clinical tests to investigate motor and non-motor symptoms. The volunteers had an electronic device on their wrists for seven days to pick up any movement associated with Parkinson's disease ̵

1; motion that might be too subtle to be discovered by a naked eye neurologist.

These tests confirmed that the seven individuals with the gene mutation who had no motor symptoms were actually Parkinson's free.

Early serotonin loss

Comparison of data from the various groups allowed us to measure the severity of dopamine and serotonin loss at various stages of the disease, from people without symptoms to persons with diagnosis.

It also allowed us to compare changes seen in gene carriers with changes seen in those with sporadic Parkinson's disease. This helped us translate our findings into gene carriers into the more common sporadic form of Parkinson's disease.

We discovered that gene carriers without symptoms had depleted serotonin while their dopamine neurons appeared to remain intact. So the changes in the serotonin system that we identified are likely to begin very early and before the onset of motor symptoms for some years.

Our study, published in the Lancet Neurology suggests that changes in the serotonin system come first, occurring many years before patients show symptoms. This important finding could lead to the development of new drugs to slow down or even stop disease progression.

Our findings also suggest that brain scans of the serotonin system could be used as a tool for screening and monitoring disease progression. But these scans are expensive so we need more work to develop affordable technology.

We also need more research into genetic forms of Parkinson's, which could further unlock the earliest changes underlying this terrible disease.  The Conversation [19659003] Heather Wilson, Research Assistant, King's College London and Marios Politis, Lily Safra Professor of Neurology and Neuroimaging, King's College London.

This article was reissued from The Conversation under a Creative Commons license. Read the original article.


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