Week in review: 24 – 30 Jan 2022


1. Both genes and the environment play a role in Parkinson’s disease.

Parkinson’s disease is a neurodegenerative disorder which affects the central nervous system and leads to motor symptoms, but also cognitive and behavioural ones. It is the second most common neurodegenerative disorder after Alzheimer’s disease. As for many other neurological disorders, it’s currently unknown what exactly causes it.

However, in recent years, there has been a shift from the idea that it’s exclusively caused by environmental factors to the idea that genetic components also play a role. Furthermore, genetic analyses have begun to shed light on the fact that Parkinson’s disease isn’t a unitary disorder, but a heterogeneous one. As such, about 5-10% of the cases can be directly linked to a genetic mutation. For the rest, it seems that mutations either increase the risk to various environmental toxins or several mutations that would be harmless on their own happen to be present in the same person, thus significantly increasing their risk.

2. No, smoking doesn’t actually protect you from Parkinson’s disease.

For decades, scientists have observed a strong link between smoking and Parkinson’s disease (PD): people who smoked more were less likely to develop Parkinson’s disease. At first, they assumed this was a typical case of a spurious correlation. After all, given all other adverse effects of smoking, it seems counterintuitive that it would magically protect you against Parkinson’s.

But even after controlling for other factors that might lead to this curious correlation, the relationship still remained there. So scientists actually began to entertain the idea of causality. In other words, that smoking, or more specifically nicotine, might have some “protective” effect against Parkinson’s disease. As nicotinic receptors are quite easy to target with artificial substitutes, this was exciting news. It meant the hunt for a Parkinson’s treatment would soon become easy-peasy lemon-squeezy.

Still, clinical trials in which patients with Parkinson’s were given nicotine showed controversial results. At the same time, a healthy dose of skepticism also remained in the scientific community. In particular, the hypothesis that perhaps Parkinson’s patients simply find it easier to quit smoking gained some traction. And a 2014 study found evidence towards exactly that.

The authors investigated 1808 Parkinson’s patients together with 1876 matched controls. They found two things. One, fewer Parkinson’s patients started smoking compared to healthy controls. Two, among those who had quit smoking, those who found it more difficult were less likely to end up developing Parkinson’s. But why is that?

The most likely explanation for these findings is that Parkinson’s disease leads to loss of nicotinic receptors even before symptoms set it. What this means is that people who will end up developing Parkinson’s don’t get the same feeling of reward from cigarettes as most of us do. In other words, they are less likely to get addicted to cigarettes. In this context, smoking behavior isn’t protective against, but predictive of Parkinson’s.

However, we need to mention that these results are far from final. The causal relationship between smoking and Parkinson’s has been observed across many studies. And until we find the molecular mechanisms through which smoking and Parkinson’s disease are interacting, it’s difficult to draw a definitive conclusion.

Still, if you were thinking that being a heavy smoker will at least ward of Parkinson’s, think again. As the evidence stands, it’s only a strong “maybe” at best for PD, but there are so many other confirmed negative effects associated with it.

3. Deep brain stimulation improves Parkinson’s disease motor symptoms.

Parkinson’s disease (PD) is characterized by a progressive loss of dopaminergic neurons in the brain. This leads to a wide array of symptoms, including cognitive and affective ones. However, the main clinical symptoms by which this disease is recognised are the motor ones: characteristic tremor, as well as walking, balance, and coordination problems.

Typically, to compensate for the loss of dopaminergic neurons, patients are treated with a dopamine replacement medication called levodopa. But, as the disease progresses, many patients either become less responsive to this medication, develop severe side effects or both. Therefore, alternative therapies are required.

One such therapy is deep brain stimulation or DBS, in short. This method relies on the implantation of electrodes deep into the brain tissue. To make sure that they are not affecting essential functions, surgeons will repeatedly turn the electrodes on and off during surgery. Sometimes, patients need to be woken up, if cognitive functions are the ones being tested. These electrodes are then connected to a small electrical generator implanted under the collarbone (for ease of access later on).

Interestingly, it’s not actually clear if DBS inhibits or stimulates the neurons on which it acts. Initially, scientists believed that the effect was an inhibitory one. This was because, normally, the role of those neurons which are lost in Parkinson’s is to inhibit the basal ganglia. Therefore, loss of neurons translates into abnormal excitation of the basal ganglia and into the tremor and uncoordinated movements observed in these patients. Since DBS reduces symptoms, the logical assumption was thus that it acts through inhibition.

But other studies directly measuring neuronal responses to DBS showed it had an excitatory effect, at least through indirect pathways. More recent evidence points towards a combined excitation-inhibition effect, which finally leads to the disruption of the abnormal flow of information caused by the loss of the dopaminergic neurons.

Regardless, DBS remains a really cool technique which provides a lot of relief to some Parkinson’s patients. Still, it’s important to note that not all patients qualify for this treatment. For example, if they also suffer from depression or dementia, DBS might do more harm than good. Additionally, both electrode implantation, as well as post-operative maintenance remain complicated and very expensive. Fortunately, scientists are trying to further develop DBS in order to make it more scalable.

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Further reading

Chiken, S., & Nambu, A. (2016). Mechanism of deep brain stimulation: inhibition, excitation, or disruption?. The neuroscientist, 22(3), 313-322.

Corti, O., Lesage, S., & Brice, A. (2011). What genetics tells us about the causes and mechanisms of Parkinson’s disease. Physiological reviews.

Hartmann, C. J., Fliegen, S., Groiss, S. J., Wojtecki, L., & Schnitzler, A. (2019). An update on best practice of deep brain stimulation in Parkinson’s disease. Therapeutic advances in neurological disorders, 12.

Kalia, L.V., Lang, & Lang, A. E. (2015). Parkinson’s disease. The Lancet.

Ritz, B., Lee, P. C., Lassen, C. F., & Arah, O. A. (2014). Parkinson disease and smoking revisited: ease of quitting is an early sign of the disease. Neurology, 83(16), 1396-1402.

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