Yesterday I participated in another clinical study.
Like the other studies I have contributed to, it was aimed at better understanding the identification and causes of Parkinson’s, as opposed to a clinical trial for a new drug.
There have been many drug trials over recent decades but few of them have been successful. One of the most recent medicines to be licensed for use in treating Parkinson’s was the one that I use, pramipexole, which was studied in 1992 and approved by the European Medicines Agency and the US Federal Drug Administration in 1997. But pramipexole is similar to other dopamine agonists, and this class of drug was introduced in the 1950s, along with the two main other treatments for Parkinson’s, levodopa and monoamine oxidase inhibitors (or MAOIs, not to be confused with moais, which are the enigmatic statues on Easter Island). So, the drugs used to treat Parkinson’s today are essentially the same as 60 years ago*.
However, none of the treatments available tackle the cause of Parkinson’s. As I have mentioned a few times previously, this is simply because the true cause is unknown. So there are many studies now trying to fill that knowledge gap. Central to this is the thesis that Parkinson’s probably comes in several varieties (see previous post The science behind neurodegeneration) and hence has several causes. It is quite possible that, had some of the recent drug trials been targeted at people only with a particular variety of Parkinson’s, then some of them would have worked.
The study I participated in was a curious mixture of cutting edge science, subjective clinical observation, and copious old-fashioned form filling.
I was surprised to see no less than a dozen vials waiting to be filled with my blood, but the extraction of the life sustaining liquid from my vein was simple enough and gave me quite a bit of time to chat to the doctor about his research into mitochondrial dysfunction, and my whisky theory.
There were endless tests on my movement, some of them videoed for quality control, and endless questions about my symptoms, medication, mood and so on.
There was also a drawing test and a cognitive test.
The cognitive test was simple enough:
- Name these animals (I was shown pictures of a lion, a rhinoceros and a camel – or was it a dromedary…?)
- Name as many words beginning with the letter F as possible in a minute
- Memorise this list of words: red, church, velvet, daisy, face
- Listen to this list of numbers then repeat them: 2, 1, 8, 5, 4
- Repeat this sentence: “the cat always hid under the couch when dogs were in the room”
- Say the months of the year backwards
- Where are you and what is the date today?
- Close your eyes and, starting at 100, continue subtracting 7
Not a big deal you might think. But I have two A grade A-levels in Maths and Further Maths. Mathematics was, and still is, my favourite subject. I even still read maths books from time to time. And as for mental arithmetic, when I was aged 8 I would have no problem reeling off subtractions of 7, and I could probably have translated it into French at the same time: quatre-vingt-treize, quatre-vingt-six, soixante-dix-neuf, …
I can’t deny that I have had some mild cognitive decline since first experiencing Parkinson’s symptoms. I notice it sometimes at work and when chatting to Clara in the evenings. Short attention span, can't find the right words, difficult to follow a complex discussion. Maybe natural ageing, maybe fatigue. Or perhaps something more insidious.
I didn’t dwell on it, and I left the study in a positive mood. As always, I was happy to have made another small contribution to moving the world forward.
There are 10 million people across the globe waiting for a breakthrough. After two generations since the last major breakthrough this will eventually happen, but it will require the collective efforts of neurologists, neuroscientists, research assistants – and willing study volunteers.
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* These Parkinson’s
drugs all treat the effect of Parkinson’s, which is a lack of dopamine (that in
turn leads to a myriad of motor and non-motor symptoms). In crude terms:
- Levodopa helps the brain to generate more dopamine with its existing neurons
- MAOIs slow down the natural breakdown of dopamine so that what dopamine there is goes further
- Dopamine agonists are a kind of artificial dopamine
