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Researchers Identify Mechanism Related to Sporadic Parkinson’s Disease

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Researchers Identify Mechanism Related to Sporadic Parkinson’s Disease

A research team from the Taub Institute at CUMC (Columbia University Medical Center) managed to identify the main mechanism that causes the progressive movement disorder in sporadic Parkinson’s disease patients. This new discovery could bring new therapeutic targets for patients that have Parkinson’s disease. Researchers analyzed tissue from the human brain. The study was published in the journal Nature Communications.

Precedent studies on heritable forms of Parkinson’s disease have shown that a very important role in the onset and development of the disease is played by a protein called alpha-synuclein. Patients that have a higher number of alpha-synuclein gene copies will produce a higher quantity of this protein, thus damaging their neurons. The effect of the protein can be best seen in dopamine neurons. These neurons are located in the substantia nigra (in the mesencephalon, or midbrain) and are responsible for the control of normal movement. Parkinson’s patients also show an excess of alpha-synuclein aggregates in the brain.

Due to the fact that the majority of Parkinson’s disease patients do not have a rare familial mutation, the question about why these patients have an excess of alpha-synuclein protein arises. The loss of dopamine neurons caused by the excess of this proteins is responsible for the onset of the disease.

Parkinson disease

Parkinson disease

 Through the use of multiple techniques that include gene-network mapping and gene-expression analysis, the researchers from the CUMC, managed to reveal the way alpha-synuclein contributes to the onset of sporadic Parkinson’s disease. “It turns out multiple different alpha-synuclein transcript forms are generated during the initial step in making the disease protein; our study implicates the longer transcript forms as the major culprits”, said professor Asa Abeliovich, who is also the lead author of the study. She added that some particular variants of these alpha-synuclein genes were discovered to increase the risk of sporadic Parkinson’s disease onset.

Dr Abeliovich adds that the study wasn’t based on animal models, instead it was based on a detailed analysis of tissue taken from human patients. The longer forms of the alpha-synuclein gene were found to be specific to human patients, as well as some of the genetic variants that are in close connection to the onset of the disease. The research team also showed that if patients are exposed to environmental toxins that are related to Parkinson’s disease, there is an increase in alpha-synuclein.

The results of the study show that if a drug is capable of reducing the amount of alpha-synuclein transcripts, it could have a major impact in the future treatment of the disease. The research team is currently studying several drug candidates with this property.

Another finding of the study was that of high levels on alpha-synuclein in the blood samples taken from patients that were suffering from sporadic Parkinson’s disease. The blood samples from the control group were did not show the same high levels. Dr Abeliovich concludes that this could lead to using alpha-synuclein as a biomarker for Parkinson’s in the near future.