Parkinson’s disease is a neurological condition resulting from an imbalance of dopamine and acetylcholine, two chemical messengers (“neurotransmitters”) in the brain that help control movement. Too little dopamine leads to problems with gross and fine motor coordination. It is thought to be caused by a combination of genetic and environmental factors, in conjunction with increasing age. More recently an immunological cause has been under investigation. Below we examine the possibility of a connection between Parkinson’s and autoimmune disease.
What are the signs and symptoms of Parkinson’s disease?
The three most prominent and well-known Parkinson’s symptoms all involve movement dysfunction resulting from damage to certain motor fibers and centers within the brain. Of the three, tremor, or involuntary shaking, is probably the one most people recognize and associate with Parkinson’s. A classic example in Parkinson’s is a “pill-rolling” tremor, featuring back and forth rubbing movements of the thumb and forefinger (as if rolling a pill between the two). Another common finding in those with Parkinson’s is rigidity, or muscle stiffness, which yields a resistance to both passive and active movement, and may be defined by the specific type of resistance on examination. The third typical Parkinson’s symptom is called bradykinesia, which literally means “slow movement”. Patients experience difficulty ambulating – especially initiating movement – and often walk with a “shuffling gait” where they take very little steps without lifting their feet from the ground.
Aside from those above, Parkinson’s patients may present with a fairly wide range of other signs and symptoms, which are alternately present or absent depending on the individual. They may experience psychological issues such as depression or anxiety, which is likely the result of biochemical changes within the brain, coupled with the considerable burden of living with Parkinson’s. And some patients will exhibit varying degrees of “autonomic dysfunction”, where the automatic/involuntary functions of the body, such as urination or sweating, are disrupted. Still others have trouble maintaining their balance during normal activities.
Have there been studies linking Parkinson’s to an autoimmune trigger?
Yes. The past couple of decades have seen quite a bit of activity in this area, with gradual progress being made over the years towards finding a definitive link. While the exact nature of the interaction is still unclear, it does seem that at least in part, an autoimmune process drives Parkinson’s. Whether this apparent autoimmune response is in turn triggered by another process, such as infection or other source of inflammation, remains to be discovered as well. But a thorough chronological review of the literature shows clear evidence of continual progress in these efforts, with successive studies adding new pieces to the emerging puzzle.
That said, these investigations have still varied in their findings and conclusions. Some research has shown promising links to specific genes, while other studies have found little to no correlation between autoimmune disease and Parkinson’s; and there are competing theories on the exact pathology taking place during the neurodegenerative process, e.g., this study published in Medical Hypotheses and this manuscript published in Nature Precedings.
Does the research indicate that, similar to hypothyroidism, Parkinson’s has an autoimmune and non-autoimmune root cause?
Yes and no. There is not much specific research at this point on actually separating the distinct causative mechanisms, but there is a general consensus that – as is the case with so many human diseases – Parkinson’s is likely the result of a combination of genetic, immune and environmental factors. The obvious next step is to figure out how these variables come together and affect one another, and whether one or more has greater influence than the others in the development of Parkinson’s. But in short, it does appear that an autoimmune process may be part of (if not totally) the reason certain people develop Parkinson’s. Interestingly, considering the question, one study that examined whether Parkinson’s patients have a higher incidence of autoimmune thyroid problems found no significant correlation.
Is it known what percent of those with Parkinson’s also have other autoimmune diseases?
Not in those exact terms, though there have been a few large studies conducted that looked at the reverse association, i.e. how many autoimmune patients later developed Parkinson’s, which generally found somewhat of an increased risk.
And there does seem to be a higher-than-normal correlation between Parkinson’s and certain autoimmune disease, as well as shared regulatory proteins as outlined in this article about Parkinson’s and Inflammatory Bowel Disease.
In contrast, another study found no clear risk of future Parkinson’s based on the existence of one or more autoimmune disease at the start of the investigation. It’s difficult to make any sort of confident determination as to the nature of these relationships, especially based on one or a handful of studies, but researchers seem to be convinced that a link exists, even if they are as of yet uncertain what it is.
Questions for your doctor:
- Do you believe there is a link between autoimmune disease and Parkinson’s? What is the evidence for and against this theory?
- Does knowing whether my Parkinson’s is autoimmune-based affect or determine my treatment in any way?
- If I have the inherited form of Parkinson’s, does that mean that it’s not autoimmune?
- Is it possible that some of the medications used to combat autoimmune conditions might be useful in slowing or stopping Parkinson’s? What about taking NSAIDs to reduce overall inflammation
- Are there any foods or supplements known to be neuroprotective with regard to Parkinson’s?
About the Author
Dr. Rothbard is a professional medical writer and consultant based in New York City, specializing in medical education articles targeted at a variety of audiences, from children through clinicians. After leaving medicine, he worked as a biology and medical science educator for several years, before deciding to pursue writing full-time. He may be reached at firstname.lastname@example.org.