WPC report from Richard Windle

Ken Bowler writes: “Richard Windle is a fellow member of the Research Support Network Development Team at Parkinson’s UK. He has lodged the following report, which may be of interest”.

Here is a brief summary of my take on the latest scientific thinking as presented at WPC3. There is a disclaimer on this: I’m not a scientist, I did not attend all the sessions (this would have been impossible) so there may be other important developments that I missed. In addition I may have misunderstood or over-simplified what I have reported below.

Why do brain cells die? It has been thought for some time that abnormal behaviour of the protein alpha-synuclein within cells (folding) is associated with Parkinson’s.
Patrik Brundin gave a very eloquent presentation describing how misfolded alpha-synuclein might move from one cell to another, causing misfolding to take place in a chain-like sequence. Apparently there are researchers looking at ways of

  1. stopping the misfolded alpha-synuclein from leaving the damaged cell
  2. stopping it from entering adjacent cells and, if it does enter adjacent cells,
  3. stopping it from causing similar misfolding in those cells.

Of course there are other theories – for example involving the role of the mitochondria.

Stem cells are effectively on the back burner (so to speak). Apparently it takes up to a dozen aborted foetuses to provide sufficient material for one transplant. Work is concentrating on induced pluripotent stem cells (developed from skin cells provided by the patient), which would avoid the practical and ethical concerns about the use of foetal material. This may not be as easy as it sounds and the Transeuro project is going ahead with the first transplants using foetal material taking place ‘in the next few months.’

There was a lot of discussion about non-motor symptoms but nothing new in the treatment of these.

The notion that Parkinson’s is a syndrome rather than a single disease is now firmly on the agenda. The term ‘stratified medicine’ was mentioned more than once with a recognition that previous trials may have failed because they did not take this into account and that different treatments might be appropriate for different types of Parkinson’s.

Gene therapy is in the ascendancy as a way of ascertaining the different types and delivering treatments.

The need for a suitable bio-marker becomes all the more critical as a way of monitoring whether any of these approaches slow down or stop the progression. There is also concern about the validity of existing animal models which rely on inducing Parkinson’s using chemicals – this may not be as effective as previously thought as a way of mimicking the development of Parkinson’s in humans.

Our colleagues in the US now use the term Parkinson rather than Parkinson’s (as in I have Parkinson, not I have Parkinson’s).

Richard

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