In early December, the medical headlines were screaming that Parkinson’s disease might start in the gut. A friend of mine, with the illness, emailed me to show me the news. I wrote back saying, old news…not realizing that another new article had just come out.
The connection between alterations in the microbiome and Parkinson’s is not new news. I’ve been reading about this for several years and I learned this morning, upon doing some more research, that actually, scientists have been looking at the connection for about a decade.
The first time I remember reading about a possible connection was in 2014, when I saw this headline on Medical News Today: “Study links Parkinson’s disease to gut bacteria.”[i] Finnish researchers examined the flora of 72 individuals with Parkinson’s and compared them to matched controls: “Our most important observation was that patients with Parkinson’s have much less bacteria from the Prevotellaceae family; unlike the control group, practically no one in the patient group had a large quantity of bacteria from this family.”[ii]
In preparation for writing about the research that has just come out, I did some reading this morning and came across a 2011 paper [iii] in the journal PLoS One, that was actually the original predecessor to the this month’s headline news. Five years ago, researchers had “…hypothesized that PD subjects might exhibit increased intestinal permeability to proinflammatory bacterial products in the intestine.” After testing a group with Parkinson’s disease versus control, they found that those with Parkinson’s exhibited “…significantly greater intestinal permeability (gut leakiness) than controls.”
According to this paper, the “…pathogenic hallmark of PD is neuronal inclusions termed Lewy bodies whose main component is alpha-synuclein protein.” (Upon further research, I learned that apparently alpha-synuclean is a protein normally found in the brain (and in other tissues a little bit), but in PD patients, it begins to clump together and forms toxic fibers in their brains. This team of researchers found these Lewy bodies in the nerves in the intestines, which led them to hypothesize that the intestines might indeed be an “early site of PD disease in response to an environmental toxin or pathogen [i.e. bad bacteria].”
The research[iv] that my friend emailed me about is actually confirmation of what this original team had already found.
These researchers had two separate groups of mice with genetic susceptibility to PD because they over-produced this alpha-synuclein: some were raised in normal, non-sterile cages and the 2nd group was raised in a sterile, germ-free environment. This latter group showed fewer motor deficits and less of these toxic fibers in their brains. Interestingly, antibiotic treatment was able to reduce symptoms in the non-sterile, more affected mice, which suggests that the bacterial microbiome was enhancing their symptoms.
The scientists also injected gut bacteria from human PD patients into the germ-free mice, who rapidly deteriorated.
They conclude, “These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for PD.”
In snooping around this morning, educating myself, I found a pretty great summary article (now a little dated, as it’s from 2015 and won’t include this latest paper) on the PD/gut connection on the National Parkinson Foundation’s website: “What’s Hot in PD? More Evidence Linking Gut Bacteria to Parkinson’s Disease: A Guide for Patients.”[v]
Actually, the human biome is what’s hot in pretty much ALL chronic inflammatory disease, as far as I’m concerned. As I have pointed out before, this blog is totally trending.
[ii] Gut microbiota are related to Parkinson’s disease and clinical phenotype, Filip Scheperjans, et al., Movement Disorders, doi:10.1002/mds.26069, published online 5 December 2014,
[iii] Forsyth CB, Shannon KM, Kordower JH, et al. Increased Intestinal Permeability Correlates with Sigmoid Mucosa alpha-Synuclein Staining and Endotoxin Exposure Markers in Early Parkinson’s Disease. Oreja-Guevara C, ed. PLoS ONE. 2011;6(12):e28032. doi:10.1371/journal.pone.0028032.
[iv] Sampson, TR, etc. al. Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkingon’s disease. Cell: volume 167, issue 6, p1469-1480, December 2016.