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Immune gene tied to Parkinson\'s disease identified. While hereditary gene mutations have long been known to play a role in familial Parkinson\'s disease, researchers have now identified a new immune regulating gene tied to Parkinson\'s disease.
While hereditary gene mutations have long been known to play a role in familial Parkinson's disease, researchers have now identified a new immune regulating gene tied to Parkinson's disease. The researchers found that non-inheritable PD may be caused by functional changes in the immune regulating gene Interferon-beta (IFN beta).
Treatment with IFN beta gene therapy successfully prevented neuronal death and disease effects in an experimental model of PD, the findings showed. "When we introduced IFNbeta-gene therapy, we could prevent neuronal death and disease development. Our hope is that this knowledge will enable development of more effective treatment of PD,a¿ said one of the researchers Shohreh Issazadeh-Navikas, professor at University of Copenhagen, Denmark.
An estimated seven to ten million people worldwide are living with Parkinson's disease (PD), which is an incurable and progressive disease of the nervous system affecting movement and cognitive function, the study pointed out. The human brain consists of approximately 100 billion neurons, which coordinate activities in all parts of the body and the researchers discovered that the immune gene IFN beta plays a vital role in keeping neurons healthy.
"We found that IFN beta is essential for neurons ability to recycle waste proteins. Without this, the waste proteins accumulate in disease-associated structures called Lewy bodies and with time the neurons die," first author Patrick Ejlerskov, assistant professor at University of Copenhagen noted.
The research team found that mice missing this gene developed Lewy bodies in parts of the brain, which control body movement and restoration of memory, and as a result they developed disease and clinical signs similar to patients with PD and dementia with Lewy bodies. (The study was published in the journal Cell.)
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