A research team at University of Copenhagen, Denmark, has discovered that non-inheritable Parkinson’s disease may be caused by functional changes in the immune regulating gene Interferon-beta (IFNβ) and targeted treatment with IFNβ-gene therapy can successfully prevent its neuronal death and the disease effects.
The results, published in the journal Cell, show that the immune gene IFNβ plays a vital role in keeping neurons healthy by regulating waste management in nerve cells. The human brain consists of approximately 100 billion neurons, which coordinate activities in all parts of the body.
At Biotech Research and Innovation Centre (BRIC), University of Copenhagen, the group of Professor Shohreh Issazadeh-Navikas, who has discovered that the immune gene IFNβ plays a vital role in keeping neurons healthy, said: “We found that IFNβ 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, explains assistant professor Patrick Ejlerskov, the first author of this report.”
An estimated seven to ten million people worldwide are living with Parkinson’s disease (PD), which is an incurable and leads to progressive decline in cognitive function. More than half of PD patients develop progressive disease showing signs of dementia similar to Alzheimer’s disease.
The research team found that mice missing IFNβ 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 (DLB).
It has long been believed that hereditary gene mutations play a role in familial PD, but the new study offers one of the first models for so-called non-familial PD, which comprises the majority (90-95%) of patients suffering from PD.
Prof. Shohreh Issazadeh-Navikas says the new knowledge opens new therapeutic possibilities. “This is one of the first genes found to cause pathology and clinical features of non-familial PD and DLB, through accumulation of disease-causing proteins. It is independent of gene mutations known from familial PD and when we introduced IFNβ-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,” says professor Shohreh Issazadeh-Navikas.
Current treatments are effective at improving the early motor symptoms of the disease, however, as the disease progress, the treatment effect is lost.