When I was considering reasons why the ‘flu jab was recommended for Parkinsonians, and before I came across the prevalent suggestion that we’re more likely to catch the ‘flu, to get it bad, and to suffer complications, it occurred to me that influenza might possibly make Parkinson’s – and other neurological conditions – worse.
I wondered if there was a link to inflammation (of the brain) – thought by some to be a cause of Parkinson’s – and there certainly seemed to be a suggestion that the inflammation caused by influenza may encroach upon the brain. Indeed, there is a well known example of this; the 1918 ‘flu pandemic (caused by the H1N1 virus) was followed by an outbreak of encephalitis and subsequent Parkinsonism, as described by Oliver Sacks in his book, Awakenings. More recent evidence was reported in a Telegraph article from 2009:
A team led by Prof Richard Smeyne, a neurobiologist at St Jude Children’s Research Hospital in Memphis, found that the bird flu virus that can enter the brain and cause damaging changes.
The study provides evidence for the long-held suspicion that viruses can increase the risk of developing certain severe conditions that appear unrelated to the original infection – even decades later.
The brief article goes on to describe how the virus – they were looking at the H5N1 strain – can “activate” the immune system, and that this can lead to the “build-up of proteins in the brain that characterise diseases such as Parkinson’s”. I suspect that they are referring to Lewy bodies; certainly, the abstract for the relevant academic paper cites alpha-synuclein, which is a major constituent of Lewy bodies. It mentions a “‘hit and run’ theory which states that a viral infection quickly cleared from the body may leave the immune system activated and the brain vulnerable”.
I could be reading too much into this latter idea, but the fact that the first time I had ‘flu I recovered with what appeared to be extreme alacrity (I was better after 3 days; my colleagues were all taking a week, or even two, to return to work) now seems highly suspicious. Was that the incident (circa 1996/7, a dozen years prior to my diagnosis with Parkinson’s) that sowed the seed of my current neurological condition? I doubt that I will ever know (nor will I know which virus sub-type I contracted, although several sources suggest that the prevalent sub-type in Europe at that time was H1N1), but it does seem plausible.
The press release for Smeyne et al‘s research findings can be found here (it is very similar to the Telegraph article). You may need to scroll down to find it.
A more in-depth article from The Scientist (“Magazine of the Life Sciences”) can be found here. Smeyne is quoted in this article saying that “this virus was mimicking the pattern of progression of Parkinson’s disease.”
According to the generally accepted system of staging the disease’s progression, Parkinson’s starts in peripheral neurons and slowly makes its way into the CNS, much like the progression of viral infection. “It is interesting to me,” said [Malu] Tansey [from Emory University School of Medicine, who was not involved in the research], that the virus “clearly infects the areas that are the most sensitive to chronic inflammation,” such as the midbrain, where much of the neuronal death seen in Parkinson’s disease occurs.
The biggest risk factor for Parkinson’s disease, said Smeyne, is age. “We think what is happening with the influenza is that it’s shifting the curve” to speed the onset of the disease.
the study doesn’t indicate the virus necessarily causes Parkinson’s, nor does it suggest that more common strains of influenza may predispose people to the disease. It would be interesting to test whether the flu-infected mice would be more likely to develop full-blown Parkinson’s disease if they were allowed to age, [Tansey] said, and to repeat the study in non-human primates.
We have three major aims that we are exploring. First, in research supported by the Michael J. Fox Foundation for Parkinson’s Research we are examining, in detail, the pattern, timing and transport of H5N1 virus from the enteric route as well as the olfactory route. Second, we are examining the profile of cytokine expression in the brain at different times following infection with H5N1, ranging from short term infection (days post infection 1-21) as well as longer term studies (says post infection, 30, 60, 90 and 120). Third, we are exploring the mechanism by which infection with H5N1 virus kills cells. We have shown in our recent paper that regions infected with H5N1 express activated caspase-3. What we don’t know at this time is if the cells that are dying are those infected by H5N1 or are bystanders.