Today’s (experimental) post provides something new – an overview of some of the major bits of Parkinson’s-related research that were made available in January 2018.
In January of 2018, the world was rocked by news that New Zealand had become the 11th country in the world to put a rocket into orbit (no really, I’m serious. Not kidding here – Click here to read more). Firmly cementing their place in the rankings of world superpowers. In addition, they became only the second country to have a prime minister get pregnant during their term in office (in this case just 3 months into her term in office – Click here to read more about this).
In major research news, NASA and NOAA announced that 2017 was the hottest year on record globally (without an El Niño), and among the top three hottest years overall (Click here for more on this), and scientists in China reported in the journal Cell that they had created the first monkey clones, named Zhong Zhong and Hua Hua (Click here for that news)
Zhong Zhong the cute little clone. Source: BBC
People with high socioeconomic status jobs are believed to be better off in life.
New research published last week by the Centre for Disease Control, however, suggests that this may not be the case with regards to one’s risk of developing Parkinson’s disease.
In today’s post we will review the research and discuss what it means for our understanding of Parkinson’s disease.
The impact of socioeconomic status. Source: Medicalxpress
In 2013, a group of researchers at Carnegie Mellon University found a rather astonishing but very interesting association:
Children from lower socioeconomic status have shorter telomeres as adults.
Yeah, wow, strange… sorry, but what are telomeres?
Do you remember how all of your DNA is wound up tightly into 23 pairs of chromosomes? Well, telomeres are at the very ends of each of those chromosomes. They are literally the cap on each end. The name is derived from the Greek words ‘telos‘ meaning “end”, and ‘merοs‘ meaning “part”.
Telomeres are regions of repetitive nucleotide sequences (think the As, Gs, Ts, & Cs that make up your DNA) at each end of a chromosome. Their purpose seems to involve protecting the end of each chromosome from deteriorating or fusing with neighbouring chromosomes. Researchers also use their length is a marker of ageing because every time a cell divides, the telomeres on each chromosome gradually get shorter.
In 2002, deep brain stimulation (or DBS) was granted approval for the treatment of Parkinson’s disease by the US Food and Drug Administration (FDA). The historical starting point for this technology, however, dates quite far back…
Further back than many of you may be thinking actually…
In his text “Compositiones medicamentorum” (46 AD), Scribonius Largo, head physician of the Roman emperor Claudius, first suggested using pulses of electricity to treat afflictions of the mind.
Roman emperor Claudius. Source: Travelwithme
He proposed that the application of the electric ray (Torpedo nobiliana) on to the cranium could be a beneficial remedy for headaches (and no, I’m not kidding here – this was high tech at the time!).
Torpedo nobiliana. Source: Wikipedia
These Atlantic fish are known to be very capable of producing an electric discharge (approximately 200 volts). The shock is quite severe and painful – the fish get their name from the Latin “torpere,” meaning to be stiffened or paralysed, referring specifically to the response of those who try to pick these fish up – but the shock is not fatal.
Now, whether Largo was ever actually allowed to apply this treatment to the august ruler is unknown, and beyond the point. What matters here is that physicians have been considering and using this approach for a long time. And more recently, the application of it has become more refined.
What is deep brain stimulation?
The modern version of deep brain stimulation is a surgical procedure in which electrodes are implanted into the brain. It is used to treat a variety of debilitating symptoms, particularly those associated with Parkinson’s disease, such as tremor, rigidity, and walking problems.
There is a question that pops up regularly when I speak at local Parkinson’s UK support group:
‘Do you think there is a certain type of personality that is more vulnerable to Parkinson’s disease?’
And my answer:
‘This is a question that pops up regularly. It is very controversial, but there is some evidence to suggest that ‘yes’ there are certain personality traits’
Here is what we know:
In 1913, Dr Carl Camp, a neurologist at the University of Michigan, wrote in ‘Modern Treatment of Nervous and Mental Diseases’:
“It would seem that paralysis agitans affected mostly those persons whose lives had been devoted to hard work… The people who take their work to bed with them and who never come under the inhibiting influences of tobacco or alcohol are the kind that are most frequently affected. In this respect, the disease may be almost regarded as a badge of respectable endeavor”
Cited from Menza M. (2000).
Dr Carl Camp. Source: OldNews
It was the first observation that there may be personality traits are shared between people who go on to develop Parkinson’s disease. Since Dr Camp’s comment, over 100 years ago now, there are almost 100 studies that have looked at this topic and the majority of them have agreed that certain personality traits that are associated with increased risk of Parkinson’s disease.
These traits include:
- Lack of novelty seeking
And the evidence suggests that these traits persist long after the onset of the illness – that is to say, they are not affected by the disease.
Now it should be NOTED that this area of research remains controversial, and simply having some of these personality traits does not immediately mean that you will go on to develop Parkinson’s disease.
The most interesting results have come from studies comparing twins, in which one twin has developed Parkinson’s disease and the other has not. The first of this type of study was a retrospective analysis (Ward et al, 1984) in which 20 monozygotic twins (that is identical twins; they came from the same egg) were interviewed (Editor’s comment: isn’t it interesting to note that two individuals who are genetically identical can be affected differently by this disease). Personality-related questions were asked of the subjects at 8 and 16 years of age and then again 10 years after diagnosis of Parkinson’s disease. During all three periods the twin with Parkinson’s was more self-controlled than the non-affected twin.
Monozygotic Twins. Source: National Geographic
A similar study (Heberlein et al, 1998) which investigated 15 twins in which one of the pair was affected by Parkinson’s disease (6 monozygotic and 9 dizygotic/fraternal twins) found that affected twins showed higher inhibition and emotionality, and lower on extraversion than a set of control subjects (interestingly, they did not differ from their unaffected twin).
One very interesting study that has stemmed from this personality related research, focused on the idea that if people with Parkinson’s disease are more ‘inflexibility’ or ‘inhibited’, they may have trouble deceiving people. Taken another way: people with Parkinson’s may be more honest!
Here is the study I am referring to:
Title: Do parkinsonian patients have trouble telling lies? The neurobiological basis of deceptive behaviour.
Authors: Abe N, Fujii T, Hirayama K, Takeda A, Hosokai Y, Ishioka T, Nishio Y, Suzuki K, Itoyama Y, Takahashi S, Fukuda H, Mori E.
Journal: Brain. 2009 May;132(Pt 5):1386-95.
Using a novel cognitive task, the authors studied 32 patients with mild Parkinson’s disease of short duration and found that they had difficulty making deceptive responses when compared to healthy controls. That is to say, when the subject with Parkinson’s were commanded to lie, they had more trouble than healthy controls.
Parkinson’s subjects had trouble lying. Source: Abe et al, 2009
The authors then analysed the brains of the participants, using brain imaging techniques and found that this difficulty was significantly correlated with reduced metabolism in the prefrontal cortex – an area at the front of the brain where a lot of the higher-order (or executive) functioning of the brain is occurring.
The blue area indicating reduced metabolism in the prefrontal cortex. Source: Abe et al, 2009
While the study is very interesting, it can not determine whether this inability to lie (and the reduced metabolism in the prefrontal cortex) is personality-based or as a result of the disease course. This will require further investigation.
In summary, while it is fair to say that while some personality traits may appear to be associated with Parkinson’s disease, the results are controversial. Most of the studies have been conducted after diagnosis, and thus one can not be sure if the personality traits in question are really associated with the disease or simply a result of the disease. In addition, it may be that certain traits are associated with the disease, but it must be emphasised that being in possession of these traits does not necessarily mean you will develop Parkinson’s disease.