This post is part I of a two part series on the question of PD transmission.
OK now don’t panic! The purpose of this post is not to scare anyone. Parkinson’s is not a virus that spreads from person to person. At least we haven’t observed anything like that in the hundreds of years that medicine has known about the disease. That said, with a 20 plus year incubation period it’s possible that some low level of transmission could be missed. But it is very unlikely.
So why the question? Why ask if Parkinson’s is contagious?
Well, because one of the current, favored hypotheses (that means "theory" in scientific language) for how Parkinson’s starts and spreads within the body is that PD is highly similar to an infection.
The idea is that something enters the body, possibly through the gut or the nose, and sets off a chain reaction that spreads from cell to cell, finally working its way to the brain where it destroys the dopaminergic neurons, among others. That "something" may be a virus, a pesticide, metal dust, or any number of environmental toxins. We just don’t know yet. Genetics plays a role in determining how easily and quickly that process happens.
The fact that this process appears to spread from cell to cell implies a contagion. Additionally, one of the proteins implicated in Parkinson’s disease, α-synuclein, appears to have many similarities to a prion.
What is a prion? A prion is a contagious, pathogenic protein. It is responsible for "Mad Cow" disease, and there are a number of related diseases that affect humans, including certain tribes in Papua New Guinea who contract the disease by eating the brains of their dead family members.
What appears to happen is that the prion protein is just a normal protein with a normal function within the body. But something changes the form of one of them, which then changes the form of another, and so on and so on, until these mass of "misfolded" proteins, or aggregations of those proteins, are doing damage and causing disease.
Prion diseases can be transmitted by eating infected animals, or injecting or implanting material derived from infected animals. Once in the body these prion proteins induce the abnormal folding of normal proteins, creating a chain reaction. The incubation time of human prion diseases can sometimes be more than 20 years.
While certain aspects of PD etiology are similar to that of prion diseases, it is still unclear whether this pathological protein is sufficient to cause PD in humans. Even if that were to be the case, that pathological protein would likely not be spread by saliva or by sex. Again, those that postulate an entry point into the body suggest either the gut or the nose, possibly via a virus or triggered by some environmental toxin which is either ingested or inhaled through the nose.
Evidence for the prion-like behavior of Parkinson’s disease includes:
- α-synuclein aggregates are toxic in living cells.
- Pathological human α-synuclein can be inoculated into the brains of animals, initiating a PD-like disease in those animals.
- Animals can even be infected by injecting the protein into their muscle tissue. This infection then appears to travel up the sciatic nerve on its way to the brain.
- Transplantation of fetal cells in PD subjects became "infected" 14 years after grafting.
- Origins of PD pathology appear to be in the gut or nasal area, then followed by migration to the brain.
- Some of the vaccines being created to stop PD progression aim to prevent the chain reaction and aggregation mentioned above. Success of these vaccines depends on the validity of the pathogenic protein hypothesis for PD.
There is also evidence arguing against a pathological protein model for PD etiology. Either way, there is still much to discover about the role of α-synuclein in Parkinson’s pathogenesis. Our Machine is busy calculating the optimal combinations of safe, natural substances most likely to stop PD progression. Currently it includes natural substances known to block α-synuclein misfolding and aggregation. We will be sharing these combinations with our mailing list.
No doubt you will hear more in the future about prions and PD. Assuming this turns out to be true, please keep in mind that any casual transmission is very unlikely. So if there were any fears about transmission to friends, family and coworkers of PD sufferers, this post has hopefully allayed them. However, there is still a potential danger of PD transmission through blood or organ donation. This will be the subject of part II of this series, which will be posted shortly.
Researcher at Stop Parkinson's
Dr. Steve is a biochemist, specializing in medical bioinformatics and nutrition. Dr. Steve directs a biomedical consulting laboratory, focusing primarily on biomedical investing and health policy.
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