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Autoimmune Diseases

Monday September 25, 2017

Full disclosure: I am not a doctor, nurse, therapist or any type of medical professional. I do, however, live with a chronic (it’s never going away) and progressive (it’s going to get worse) disease: Parkinson’s. What I am about to share comes from personal experience, medical research, media and other reference material.  Any errors of fact or conclusion are mine.

In general, autoimmune diseases are those in which the body, for some known or unknown reason, attacks itself—destroying the body’s own tissue. Examples include Celiac disease, Sjogren’s disease, Arthritis, Multiple Sclerosis and Lupus.  All together there are over a hundred such intrusions into our general well being. Some are relatively easy to treat like Celiac which simply (?) requires a gluten free diet. Others are much more complex—attacking multiple tissues and systems—like MS. In layman’s terms, the mechanism for this is our normally beneficial killer T-cells (a key part of our immune system) to identify our own body tissue as a foreign invader and attack.

Until recently, scientists suspected, but could not prove that Parkinson’s was one of these autoimmune diseases. Unfortunately, they still can’t, but they’re another step closer to an understanding of the mechanisms, causes and potentially better treatment. That’s how science usually works—incremental steps leading to reproducible results that validate (or invalidate) a hypothesis.

In last month’s column, I introduced Dr. Sulzer of Columbia University. In March, I had the privilege of participating in his autoimmune study for People with Parkinson’s—better known as PWP’s or Parkies. It is this study that provides evidence (not proof) that PD may be an autoimmune disease.

Scientific studies are generally published in a journal—available for peer review, criticism or validation. Before attempting to explain the results of this study, I thought it might be enlightening, and fun, to share the actual abstract of this study as published in Nature with Dr. Sulzer listed as lead author. Don’t be overwhelmed—it will all make sense in the following paragraphs.

Genetic studies have shown the association of Parkinson’s disease with alleles of the major histocompatibility complex. Here we show that a defined set of peptides that are derived from alpha-synuclein, a protein aggregated in Parkinson’s disease, act as antigenic epitopes displayed by these alleles and drive helper and cytotoxic T cell responses in patients with Parkinson’s disease. These responses may explain the association of Parkinson’s disease with specific major histocompatibility complex alleles. 

Did you get all that? I’ve read it a few dozen times and I’m still confused. Fortunately, other folks have explained it in terms that make sense and show how important this research is. Part of what makes science fascinating is how the various pieces come together as we learn more. Dr. Sulzer likens the process to completing a jigsaw puzzle—even if we don’t have the complete picture.

A few columns back, I wrote that researchers believe PD may start in the gut—a protein (alpha synuclein) begins to misfold and this is first observed in the gut. For some reason, these misfolded proteins in the brain may begin to clump and lead to brain cell death—the hallmark of Parkinson’s. However, scientists don’t know exactly how and why that happens. In the gut, killer T-cells (remember them?) go after the clumps of misfolded protein and eliminate them—with no apparent harm to our body. Unfortunately, in the brain, these T-cells appear to kill the brain cells while attempting to eliminate the protein clumps.

The million dollar question is, “So what?” IF Parkinson’s is an autoimmune disease, the potential for development of new treatments is obvious. There are numerous immune system drugs in existence that may be re-purposed.  It may be possible to develop new therapies that prevent brain cell death—thus preventing Parkinson’s.

And that brings us full circle to why I believe research is so important and why I have participated in more than a dozen studies. If researchers develop an effective means to prevent brain cell death due to these misfolded proteins, we still have a major problem. As of today, we do not have any way to tell who might get PD. We have no biomarker—no test or procedure to determine who might hear those chilling words, “You have PD.”  In other words, we may have a solution without a means to identify who may benefit.  Again, we’re left with an incomplete puzzle. I choose to be optimistic because more and more pieces of the puzzle are beginning to fit together.  Soon, we may have the complete picture and an end to Parkinson’s.

*This is an opinion blog written by A.C. Woolnough. 

A.C. WoolnoughA.C. Woolnough
NWPF Blogger

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