Scientists at the University of Cambridge have reported on a promising new concept in treating Parkinson’s. Harnessing the survival and invasive properties of two separate viruses, they hope to be able to prevent cell death in the human brain. The therapy should also be of benefit for other neurodegenerative conditions such as Alzheimer’s and Huntington’s disease.
While it is a little disturbing to read the familiar names of the two viral donors – herpes and rabies – the Cambridge news article assures its readers that “there is no danger of contracting any disease from either virus.” The team took advantage of the survival mechanism of the herpes virus and the rabies’ virus ability to cross the blood-brain barrier.
The news article describes how the survival mechanism works:
[…] common viruses – such as herpes – seek to survive and replicate in cells in the body. When these viruses invade a cell, a tiny component of the virus called the Beta2.7 gene guards the mitochondria from damage for an interval of time – typically five days – so that the virus can replicate and spread from cell to cell.
The idea seems to be that the beta2.7 gene, which is part of the herpes virus RNA, can be persuaded to protect human brain cells. The researchers, led by Professor Sinclair, successfully combined this RNA with a protein of the rabies virus. The latter was selected because “it enables the beta2.7 to cross into the brain when the whole complex is given into the circulation” (i.e. injected into the blood).
Having identified the potential offered by the virus as an agent for ‘search and rescue’, Professor Sinclair collaborated with Professor Roger Barker and colleagues at the Cambridge Centre for Brain Repair to see whether this novel protein/RNA complex could protect neurons from cell death associated with PD. Using rat models, the results have been promising […]
The Michael J. Fox Foundation are supporting further work. Sinclair is quoted as saying:
“What we have established is proof of principle – essentially showing that this is a truly novel and highly promising pathway for treating not just the dopamine cell loss in Parkinson’s but also all cell losses in this condition, as well as other chronic neurodegenerative disorders.”
From here, the path to a workable therapy available to the public is long (the translation from rat to human has to be negotiated; appropriate dosages need to be determined; clinical trials need to be completed to establish the efficacy and safety of the treatment), but the therapy seems to have several advantages, as explained by Professor Barker:
“In many ways the therapy we’ve developed is a beautiful treatment. It can be delivered through an injection direct into the bloodstream, for example into the arm of the patient. This makes it much easier to use than many 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 maintain its potency. Finally, it appears to go only into the brain and nowhere else in the body and then to target only cells that are unwell.”
Any treatment that slows or even halts the progression of this condition has got to be a good thing. Diagnoses are often made at a sufficiently early stage such that the symptoms can be coped with; what is harder to accept is the knowledge of the inevitability of future progression.
- Cambridge University news article – the main source for this post
- Abstract in the Journal of Experimental Medicine