Parkinson’s Disease

On Wednesday 22nd January, I attended a talk by Samuel Deutsch entitled ‘Predicting Parkinson’s in our Sleep’.

He began by talking generally about the field of neurology – the study and treatment of disorders of the Central and Peripheral Nervous system. It therefore includes a wide range of disorders including psychological, and psychiatric disorders. But it is a complicated field as often the disorders’ causes aren’t clear cut. For example phantom limb syndrome, with 80-100% incidence, has no clear cause. Some people believe that it is due to a cortical re-organisation, while others believe that it is due to nervous pathways being hijacked. Furthermore, neurological diseases rarely have a cure – it is more about management symptoms; there is no ‘one pill treats all approach’. So, in the case of phantom limb syndrome, therapies include mirror therapy, stimulation therapy, and virtual/augmented reality. Furthermore, with our now ageing population, ‘the brain is dying before the body does’, and neurological diseases are therefore on the rise.

Image result for mirror therapy for phantom limb pain"Image result for virtual reality for phantom limb pain"

He then went on to speak about Parkinson’s, a motor-system disorder which includes cognitive, homeostatic and psychological issues. It is usually diagnosed in the 60s, and in 2018, 145 000 people were diagnosed; but this is expected to rise by 20%, by 2025. It is caused by a build up of alpha-synuclein in the synapses, which results in the death of neurones in the basal ganglia of the brain.

Parkinson’s has many symptoms, the main four being a tremor, rigidity (how well limbs move), bradykinesia (global slowness of movement), and postural instability. Alone, any one of these symptoms doesn’t mean Parkinson’s, for example, tremors could just be an essential tremor, which is very common. Other results of this disorder include psychiatric symptoms, dementia, cognitive impairment, and other motor problems. However it is extremely difficult to diagnose as it doesn’t occur the same in everyone; it could be cognitive first and motor later, or vice versa.

The treatments of Parkinson’s are wide-ranging. There are some drugs which can be used, such as: levodopa (produces more dopamine), DA agonists, MAO-B inhibitor and COMT inhibitor. All of these aim to increase the amount of dopamine in the nervous system, and therefore cocaine can have the same effect – however this isn’t recommended. Dopamine disregulation can occur as a side-effect to any of these drugs. This results in an inability to control urges, such as gambling. Therapies can also help, such as exercise, diet, SALT (speech and language therapy) and occupational therapy. We even discussed the possible future of stem cells in the treatment of Parkinson’s, helping to regrow cells in the basal ganglia. Although this wouldn’t cure the disease as the build up of alpha-synuclein in the synapses, would continue to kill cells in the basal ganglia.

He then went on to talk about RBD, which is a REM sleeping disorder when you act out your dreams while you are asleep. Usually you are paralysed during REM sleep, but with this disorder you aren’t. This can be extremely dangerous as, in 2010, an man who lived in Oregan with RBD beat up his wife while he was asleep, but he had no idea what he was doing. He was then sentenced to prison. RBD is usually diagnosed in your 50s.

The link between these two diseases is that on autopsy, 98% of people with RBD had a build up of alpha-synuclein. Furthermore, roughly 50% of patients with RBD have Parkinson’s. So, Mr Deutsch and his team at the John Radcliffe are trying to draw links between the two diseases. Since RBD develops 10 years earlier, they are trying to use this as a predictor of Parkinson’s, as one of the most important parts to treatment of Parkinson’s is catching it early.

Mr Deutsch currently has a cohort of 1 000 patients with Parkinson’s, 300 healthy patients, 150 relatives of people with Parkinson’s, and 300 RBD patients. His work is attempting to find whether there are cognitive phenotypes in prodromal Parkinson’s Disease – this is easy, and cheap to screen. This shows heterozygous profiles, and can be compared to RBD results for the same test.

If a link is found, anti-inflammatory or anti-oxidant promoting diets have been found to reduce microgial activation in rats (whether this is reliable is questionable, as it has only currently been tested on rats). Furthermore, exenatide, a glucagon-like peptide-1 receptor agonist that is used for treatment of diabetes, has been found to slow Parkinson’s Disease.

Another research project that occurred earlier this year (2020) across vast expanses of the population of China has found that the genes: LRRK2, PARKN, SNCA, PARK7, PINK1 and GBA have a link to Parkinson’s. Therefore, you can tell people at birth that they are at risk to developing Parkinson’s, and ensure that they have a good diet, and exercise regime to reduce the chances of getting it in the future. Specific genes being affected also points towards the future of treatments of Parkinson’s, in changing the expression of genes – however this isn’t currently possible.

He concluded by reinstating the fact that there is currently no cure to Parkinson’s, and that his work, and the work of doctor’s generally isn’t always about curing diseases – it is about making lives better by alleviating pain.

 

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