first of all the article is published in a journal that charges £30 - couldnt PUK make sure its funded research is published in free journals or have some way of providing more than the summary?
all the summary seems to say is that there are two types of neurons.
but the puk entry describes them as 'rogue cells' - how are they acting roguishly?
dr breen says
"The results of this study suggest that these 2 rogue cells could trigger a chain reaction that could cause a person to develop Parkinson's. "
so - these cells in the GPe send GABA to the SRN which then sends glutamatee to the SNr (is that right) - but what is there to say they are somehow doing it wrongly and thus damaging the SN cells? why think there is something wrong in the GPe rather than things just going wrong in the SN?
is there some way to get the whole story without paying £30 ?
its very frustrating.
Perhaps i am missing something but i can't see how the conclusions follow from the findings.
What article??
Fascinated but lost!
Fascinated but lost!
sorry - i mean this one
http://tinyurl.com/6ub5tb2
its not puk's fault but most of the interesting articles are in journals that demand exorbitant prices especially as they should be e-published nowadays rant rant rant rannnnnnt.
back to the article = i've always assumed that the SN (subst. nigra) was directly attacked by virus, prion etc. Now it seems something is 'rogue' about cells in the GPe (i give up typing the long names) which feeds into the SN,
(handy diagram http://tinyurl.com/8ytglmt very useful on london underground)
-why do the researchers think this?
-how is the error transmitted?
-how can this cause synuclei whatsit not to fold properly?
i' ve no idea but dont fancy spending 30pounds to find out i;ve bought a pup.
all i can gather from the synopsis is that there are two types of cells - but the puk article suggests much more - but why?
http://tinyurl.com/6ub5tb2
its not puk's fault but most of the interesting articles are in journals that demand exorbitant prices especially as they should be e-published nowadays rant rant rant rannnnnnt.
back to the article = i've always assumed that the SN (subst. nigra) was directly attacked by virus, prion etc. Now it seems something is 'rogue' about cells in the GPe (i give up typing the long names) which feeds into the SN,
(handy diagram http://tinyurl.com/8ytglmt very useful on london underground)
-why do the researchers think this?
-how is the error transmitted?
-how can this cause synuclei whatsit not to fold properly?
i' ve no idea but dont fancy spending 30pounds to find out i;ve bought a pup.
all i can gather from the synopsis is that there are two types of cells - but the puk article suggests much more - but why?
Hi Turnip
Thanks for your comments and questions.
Firstly, on the subject of open-access publishing. We do encourage our researchers to publish their findings in scientific journals that are freely available and we also offer financial help for them to do this - see our open access publishing policy here:
http://www.parkinsons.org.uk/research/for_researchers/communicating_your_research.aspx#share_your_findings
But we still have some work to do in making sure our researchers make use of the support we offer - so it's a work in progress.
Secondly, a bit more detail about the study itself. The researchers studied the brains of rats to investigate the nerve cells in a brain area called the globus pallidus external (or GPe).
Many different parts of the brain are involved in coordinating movement (as your diagram shows). We still don't fully understand how all the different parts talk to each other to produce movement but the GPe is thought to play a vital role, acting as a 'coordinating hub'. And it's sometimes described as a 'pacemaker' or regulator of the movement control system within the brain.
What's new about this research study is that they've discovered that there are two different types of cell in the GPe, which together play a vital role in keeping the 'pacemaker' working properly.
In Parkinson’s, it seems these cells stop working properly (or go rogue!). And this may unbalance the whole movement control system, resulting in the disrupted brain rhythms that cause the symptoms of the condition.
The researchers haven't yet worked out exactly how all this happens - or how things like misfolded synuclein may be involved - so the picture is far from complete. But this discovery will hopefully trigger lots of new research to understand all these things.
I hope this helps to answer your questions!!
Best wishes
Claire
Senior Research Communications Officer
Thanks for your comments and questions.
Firstly, on the subject of open-access publishing. We do encourage our researchers to publish their findings in scientific journals that are freely available and we also offer financial help for them to do this - see our open access publishing policy here:
http://www.parkinsons.org.uk/research/for_researchers/communicating_your_research.aspx#share_your_findings
But we still have some work to do in making sure our researchers make use of the support we offer - so it's a work in progress.
Secondly, a bit more detail about the study itself. The researchers studied the brains of rats to investigate the nerve cells in a brain area called the globus pallidus external (or GPe).
Many different parts of the brain are involved in coordinating movement (as your diagram shows). We still don't fully understand how all the different parts talk to each other to produce movement but the GPe is thought to play a vital role, acting as a 'coordinating hub'. And it's sometimes described as a 'pacemaker' or regulator of the movement control system within the brain.
What's new about this research study is that they've discovered that there are two different types of cell in the GPe, which together play a vital role in keeping the 'pacemaker' working properly.
In Parkinson’s, it seems these cells stop working properly (or go rogue!). And this may unbalance the whole movement control system, resulting in the disrupted brain rhythms that cause the symptoms of the condition.
The researchers haven't yet worked out exactly how all this happens - or how things like misfolded synuclein may be involved - so the picture is far from complete. But this discovery will hopefully trigger lots of new research to understand all these things.
I hope this helps to answer your questions!!
Best wishes
Claire
Senior Research Communications Officer
thanks claire, very helpful , even if ,mainly to say that much is still a mystery.
still seems somewhat circular causation. bet then again perhaps thats to be expected in a slow degenerative disease.
thanks again
still seems somewhat circular causation. bet then again perhaps thats to be expected in a slow degenerative disease.
thanks again