The biological workings of highly aggressive viruses could hold the key to the treatment of another devastating condition.
Research by Cambridge-based scientists, published in the Journal of Experimental Medicine last week shows that the replicative functions of viruses like rabies and herpes could be used as a treatment for the neurodegenerative Parkinson’s Disease.
Presently, all treatments are entirely symptomatic, unable to halt the progress of the disease in any way and sometimes producing unwanted side-effects ranging from vomiting and dizziness to hallucination and edema.
However, the research carried out by Professor John Sinclair and colleagues within the University Department of Medicine, in conjunction with Professor Roger Barker and colleagues from the Cambridge Centre for Brain Repair could provide a vital breakthrough for the 120,000 sufferers within the UK and those around the world.
When replicating within the body, these viruses protect the mitochondria of host cells for a period of up to five days, allowing the virus to replicate. The protein responsible, beta2.7, was injected into rats suffering from a disease much like Parkinson’s in humans. When motor and brain function tests were performed on the rats injected, they outperformed their counterparts who had not been injected.
Crucially, their levels of dopaminergic neurons, those known to be damaged by Parkinson’s in humans, were also higher than their counterparts. It is notable too that the treatment was beneficial both before and after the formation of lesions on the brain alike to those evident in cases of PD, suggesting that it can be preventative as well as therapeutic and even be developed to counter other neurological diseases.
Professor Barker explained the multiple apparent advantages, stating that, “It can be delivered through an injection direct into the bloodstream… This makes it much easier to use than any other putative disease-modifying therapies such as growth factors which have to be injected directly into the brain”.
“This new agent also appears to be non-immunogenic- in other words it does not trigger an immune response so it can be used repeatedly and should still retain its potency. Finally, it appears to go only to the brain and nowhere else in the body and then to only target cells that are unwell”.
Clearly, while these results are vastly encouraging and provide much hope for the future, any euphoric reaction in the medical field would be premature. As Professor Sinclair told Cambridge News, “Our results with rat models are tremendously encouraging, but we need to do a lot more in terms of refining and optimising the therapy before it could be used in patients… What we have established is proof of principle – essentially showing that this is a truly novel and highly promising pathway”.
Though this medical development is clearly still in its embryonic stages, there is no doubt that it could eventually provide extraordinary benefits to thoseafflicted by Parkinson’s, and potentially sufferers of other debilitative conditions too.