The Scientist : NewsBlog Print: Avian flu promotes Parkinson's?
The Scientist: NewsBlog:
Avian flu promotes Parkinson's?
Posted by Edyta Zielinska
[Entry posted at 10th August 2009 07:41 PM GMT]

Avian influenza can cause a predisposition to Parkinson's disease, according to research published this week in the Proceedings of the National Academy of Sciences.

"It's an exciting finding," said Malu Tansey from Emory University School of Medicine, who was not involved in the research.

Influenza A virus
Image: Wikimedia Commons,
CDC, Erskine Palmer
Epidemiological studies done in the 1980s showed that survivors of the 1918 Spanish influenza, a pandemic that killed more than 50 million people worldwide, had a greater incidence of Parkinson's disease later in life than the general population. Recent studies have suggested that the currently circulating strain of avian influenza has similar pathology to the 1918 flu. Though the subtypes of the viruses are different (Spanish flu shares the H1N1 subtype with the current H1N1 swine flu, whereas avian influenza has an H5N1 subtype), both viruses appear to enter the central nervous system (CNS) and can cause encephalitis, or inflammation of the brain.

Richard Smeyne at St. Jude's Hospital in Memphis, Tennessee, and colleagues infected mice with avian flu and tracked how the infection progressed to the nervous system. "We thought [the virus] would get in [to the CNS] via the blood stream," through the blood brain barrier, said Smeyne. Instead, the virus entered "in a backdoor way," infecting the axon terminals of peripheral neurons first, specifically those of the gut and lung. The virus then traveled from the axon to the neuron cell body, where the researchers think it may be able to infect other neurons.

Strikingly, said Smeyne, "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 Tansey, 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.

Smeyne observed a loss of about 17% of dopamine-producing neurons -- a clinical indicator of Parkinson's disease -- in the infected mice. Parkinson's patients normally lose between 50-80% of their dopamine-producing neurons, and the loss in Smeyne's mice suggests a predisposition to the disease, he said. Although all traces of the virus were cleared from the brain after about 20 days, the virus appeared to have caused a prolonged activation of microglial cells, the immune cells that mediate inflammation in the brain. That effect -- observed 90 days post-infection -- suggests that these cells had become much more sensitive to subsequent neural insults, said Smeyne.

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. Tansey cautioned, however, that 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, she said, and to repeat the study in non-human primates.


Related stories:
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    [11th May 2009]
  • A Parkinson disease gene discovered, an oncogene remembered
    [14th March 2005]
  • Twin disorders
    [November 2008]


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    In regard to rheumatic fever & latency comments
    by anonymous poster

    [Comment posted 2010-01-24 18:35:15]
    My mother, aunt and their parents (my maternal grandparents) were all in German labor camps. My aunt had rheumatic fever and developed parkinsons in her early 70's that progressed very rapidly. My grandfather(born 1902), had parkinsons in his late 80's that did not progress rapidly at all and did not get worse until his 90's. Both my mother and grandmother never developed parkinsons at all. In fact, my mother and grandmother never got sick, never had the flu and were never in the hospital.


    Correlation is not causation
    by Steven Anderson

    [Comment posted 2009-08-15 14:01:47]
    If there is a correlation in humans vis-a-vis influenza and Parkinson's, should we look at the possibility that causality works the other way 'round? Is it possible that genetic factors that predispose one to Parkinson's, usually with a post-reproductive onset, may have been selected because they offer protection from mortality hazards of influenza viruses that attack younger people? Selection might have been most effective before there was any medical intervention in treating infected victims.


    The author did not say it was big news
    by Gar Hildenbrand

    [Comment posted 2009-08-12 14:57:17]
    This article has a headline that ends with a question mark. It makes no sensational claims, and the researchers are appropriately circumspect. Nevertheless, this is a very cool finding and it clearly merits further investigation.


    This headline is far ahead of the science
    by anonymous poster

    [Comment posted 2009-08-12 10:05:32]
    it is unclear why this is big news. Lower vertebrate models of PD have been useful heuristically, but have not translated etiologically. Moveover, as the summary notes, the damage to DA systems was small and there is no evidence it was progressive. Indeed, the hypothesis that PD begins with peripheral nerves is just that, hypothesis. This type of story leads to public perceptions as shown in the first comment, and ultimately to more hysteria about public health issues. The Scientist should provide the appropriate skepticism (sketicism being the heart of the scientific method) when covering such stories.


    Any research into those that had rheumatic fever?
    by anonymous poster

    [Comment posted 2009-08-11 13:26:45]
    This is a great finding. Both my mother and aunt were in German labor camps as young children. My aunt contracted rheumatic fever and my mother did not. My aunt is suffering from Alzheimer disease in a very bad way that is progressing quickly and she is only in her mid-70's. My mother never did. Just wondering if anyone has heard of the relationship between Alzheimer disease and rheumatic fever.


    Wondering about latency
    by anonymous poster

    [Comment posted 2009-08-11 13:23:15]
    The information in this post makes me wonder whether avian flu similar to the 1918 variety could be latent within the post-pandemic population. My grandfather, who was born in 1903 and exposed to the 1918 influenza, suffered from Parkinson's when he was in his late 70s but did not show severe symptoms until he was in his early 90s. But his son (my father) born in 1936 developed Parkinsons some time between the age of 54 and 58 (at the time of his diagnosis, the disease had already progressed substantially). Although the treatment he was given stabilized it for a time, after about three years the disease suddenly began to progress rapidly. Most notably, my father went from being able to shuffle under his own power to being virtually wheelchair bound within a five-week span of deterioration, and he died of heart failure shortly afterward. Is it possible that latent influenza was at work in his precipitous decline?


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