November 11th, 2019
In the July 2019 edition of Nature, Diana Matheoud writes a riveting letter about Parkinson's disease. The article discusses the research in mice that are prone to the mouse version of Parkinson's like disease.
Parkinson's disease is a neuro-degenerative disorder affecting older Americans roughly 60,000 times a year. By 2020, 1,000,000 Americans will have this devastating disease. The disease is based on a diminishing volume of the neurotransmitter dopamine in a critical motor region of the brain called the substantia nigra. Over time, patients with Parkinson's disease lose motor function beginning with extremity tremors and ending with severe rigidity. (Parkinson's Foundation website)
The disease's etiology has long been unknown. Now we have another glimpse of the ever growing field of autoimmune disease based neurological attack with this new animal model based research. The common denominator to most if not all of these autoimmune diseases is a combination of inflammation, self protein attack and/or mitochondrial power center dysfunction in damaged cells. The other piece of the puzzle that keeps rearing it's ugly head is gut microbial damage.
The authors write: "An early-onset form of Parkinson's disease is associated with mutations in the PINK1 kinase and PRKN ubiquitin ligase genes. PINK1 and Parkin (encoded by PRKN) are involved in the clearance of damaged mitochondria in cultured cells, but recent evidence obtained using knockout and knockin mouse models have led to contradictory results regarding the contributions of PINK1 and Parkin to mitophagy in vivo. It has previously been shown that PINK1 and Parkin have a key role in adaptive immunity by repressing presentation of mitochondrial antigens, which suggests that autoimmune mechanisms participate in the aetiology of Parkinson's disease. Here we show that intestinal infection with Gram-negative bacteria in Pink1−/− mice engages mitochondrial antigen presentation and autoimmune mechanisms that elicit the establishment of cytotoxic mitochondria-specific CD8+ T cells in the periphery and in the brain." (Matheoud D. et. al. 2019)
Based on the animal model, what this complex paragraph says is as follows: If we extrapolate this data set to humans and you have certain genetic risk factors noted by mutations in susceptible enzyme pathways coupled with a disturbed gram negative rod centric intestinal microbiome, then you are at risk for the immune system to overreact to your brain cells that govern movement. The immune system can then unfortunately recognize these cell's power houses called the mitochondria in an auto reactive way targeting them for death. We then start to develop disease when enough of these cells die leading to symptoms that we call Parkinson's disease.
The development of autoimmune antibodies usually precedes clinical symptoms by 5-10 years. Thus, it behooves us to work against this process long before we develop our first symptoms.
The how to work against autoimmunity is listed below on the following link: