For some time me and others like myself have been toying with the idea could it be possible that Parkinson’s is yet another autoimmune disease like diabetes or thyroid disease or even pernicious anemia? Or even an inflammatory disorders like ulcerative colitis? Perhaps some genetic subtypes can more easily fall into this category than others. For instance, it is interesting that the majority of Parkinson’s Disease (PD) patients have B12 deficiency as a co morbidity. Or that the type of Gaucher patients that are most likely to develop and have an increase risk of developing PD are type I patients – those without central nervous system involvement.
Patients who posses Gaucher and are carriers of a GBA gene mutation have increased risk of developing Parkinson’s disease and parkinsonism. Gaucher patients carry a deficiency of the enzyme glucocerobrosidase. This enzyme is typically acts on the glycolipid glucocerobroside. So, when the enzyme is defective, glucosylceramide aggregates and accumulates in white cells (which are responsible for mounting immune attack but particularly like to congregate in the macrophages. The macrophages are like “Pac Man” hungry white blood cells gobbling up invading bacteria. They are formed in response to an infection or accumulating damage or dead cells. Thus, they are unable to break down fatty acids and they have abnormal accumulation into the white cells and macrophages which are the ones responsible for being able to mount an appropriate immune response against a foreign attack like bacteria or virus. But, if these cells who are to destroy the offending viruses etc. are unable to take them up because already full with unwanted stored up material then more white cells, T cells and macrophages have to be created jamming up the system and thus indiscriminately attacking normal cells throughout the body and brain. Some evidence of this is present in the preliminary data in a study I am involved at the University Of Texas Houston Center. My friend and colleague has informed me that my blood levels of T cells and other inflammatory and immune markers have been measured and found to be elevated and have improved as my disease has been treated. Data hopefully will be released soon.(this is all preliminary and confidential).
The other subtype of PD which points to an inflammatory and autoimmune component is the LRRK2 gene phenotype. Many of these patients with this type of phenotype have a history of inflammatory bowel disease most often ulcerative colitis. Ulcerative colitis (UC) is another autoimmune disease characterized by T-cells infiltrating the colon. Although Crohn’s disease another inflammatory bowel disease which is much more extensive beyond the colon as compared to UC has also been seen in this group of PD patients, once again making a case for a possibility of our immune system going haywire and attacking the nervous system. In medicine, it is dogma to say that once a patient has one autoimmune disease they are at higher risk for contracting another and we frequently see this in our practices. But, until recently, no one had really dared to contradict the underlying notion that “neurons” were somehow protected from attacks from the immune system. Although, we have clear evidence of instances of where there is an autoimmune reaction in the central and peripheral nervous system after vaccine injections causing “Acute disseminated encephalomyelitis” and also MS but these have only targeted the connections not destroyed or actually damaged actual Neurons! Therefore, if it is true that Parkinson’s neuronal loss is a result of attack of the immune system itself it would revolutionize not only our thinking but our way of preventing and going after treatments for Parkinson’s.
So, recently researchers tested this hypothesis to see if indeed living neurons would display antigens (like bacteria or viruses) which then trigger an immune mediated response to neutralize this force. Drs. Sutzer and Cebrian from Columbia University used in vitro mouse and human neurons from embryonic stem cells. Their studies revealed that under certain circumstances- including those known to occur in PD. These neurons produced a special protein which presented an antigen which was recognized by the T cells and triggered an attack on these neurons. They prove an autoimmune process can happen and neurons can be attacked but is not known if this is the initial or final response or if all Parkinson’s is started this way or only those subtypes I alluded to previously. One thing is for sure future is bright and field is ripe for new and novel treatment options!
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Dr. M. De Leon is a movement disorder specialist on sabbatical, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at www.facebook.com/defeatparkinsons101 you can also learn more about Parkinson’s disease at www.pdf.org or at www.wemove.org; www.aan.org, www.defeatparkinsons.blogspot.com
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