Role of fungal mould in Parkinson's investigated
“Can damp, mouldy rooms increase risk of Parkinson’s? Study shows fungi can affect how brain chemicals function,” the Mail Online reports. But before you start frantically cleaning your home, the study in question involved flies, not humans.
In Parkinson’s disease the neurotransmitter dopamine is reduced, causing problems with initiating movement, tremor at rest and muscle stiffness.
In this study, the researchers exposed flies to one of the molecules produced by fungi that gives them the characteristic musty smell found in mouldy environments: 1-octen-3-ol. Flies exposed to the molecules had difficulty with movement, loss of dopamine neurons, reduced levels of dopamine and died earlier than flies not exposed.
Exposure to the molecules also caused difficulty in the dopamine system on human embryo kidney cells in the laboratory.
This is an interesting study but it cannot prove that living in a mouldy home causes Parkinson’s disease. Further large epidemiological studies in humans would be required to show a clear association between exposure and risk of developing Parkinson’s disease.
However, prolonged exposure to damp mouldy environments is not recommended as this could increase the risk of you developing asthma, allergic rhinitis and chest infections.
Where did the story come from?
The study was carried out by researchers from The State University of New Jersey, New Brunswick and Emory University, Atlanta and was funded by the Rutgers University Research Fund and the National Institutes of Health (NIH).
The study was published in the peer-reviewed medical journal Proceedings of the National Academy of Sciences (PNAS).
The Mail Online’s reporting of the study was accurate and included an important note of caution from Claire Bale, Research Communications Manager at Parkinson’s UK. Bale is quoted as saying: “It is important to remember this study was conducted using tiny fruit flies, so before we can really be confident about this new connection we need to see evidence from studies in people.
“Whilst exposure to chemicals produced by fungi - and possibly other chemicals - may play a role in Parkinson’s in some people, it’s likely just a small part of a much bigger puzzle and we wouldn’t want people to worry unnecessarily about developing the condition if they found mould or fungi in their homes.”
What kind of research was this?
This was a laboratory study of Drosophila fruit flies exposed to molecules emitted by fungi. It aimed to see if exposure to mouldy air conditions had an effect on dopamine, a neurotransmitter which is reduced in people with Parkinson’s disease.
Parkinson’s disease is caused by a loss of nerve cells in part of the brain, causing the level of dopamine in the brain to reduce over time. This causes symptoms including difficulty in initiating movement such as walking, a tremor in the hands when the person is at rest, and muscle stiffness. People can also experience other symptoms such as depression and difficulty swallowing.
There is currently no cure for the disease, but treatment involves increasing the level of dopamine with medication. It is not known what causes Parkinson’s disease, but current theories suggest it is a combination of genetic and environmental factors. Pesticides have been implicated in playing a role in causing it, as have many other artificial chemicals.
However, there are reports of Parkinson’s disease from before the industrial revolution which would suggest other environmental factors may also be involved. So the researchers’ wanted to see if exposure to naturally occurring conditions could have an effect, such as mouldy air.
This follows recent epidemiological studies that have shown an association between neuropsychological impairment (problems with thinking, mood and behaviour) and movement disorders and exposure to mouldy and water-damaged buildings.
A laboratory study of Drosophila flies such as this can contribute to the knowledge base of how fungi may affect the dopamine system, but it cannot prove that fungi cause Parkinson’s disease in humans.
Direct studies on humans would be required to establish whether a similar effect was happening in people as was seen in flies.
A randomised control trial in humans would be the gold standard proof, however, it would be unethical.
What did the research involve?
Initially the researchers tested different molecules that fungi release into the air to see how toxic they were. They did this by exposing Drosophila flies to five different molecules. The most toxic was called 1-octen-3-ol.
At high levels it caused damage to the dopamine system in the Drosophila flies’ brains.
They then took two groups of healthy flies and exposed one group to low dose 1-octen-3-ol, similar to that found in mouldy environments. The other group was the control group and were left in normal air conditions. They measured any changes in movement of the flies and how long it took for them to die.
They then exposed more flies to 1-octen-3-ol and dissected their brains after 24 hours to look for any effect on the dopamine system.
In order to produce some applicability to humans, they also measured the effect of exposure to different strengths of 1-octen-3-ol on the dopamine system in human embryonic kidney cells in the laboratory.
Furthermore, the researchers looked at different genetic types of neurotransporters in the flies’ brains to see if this changed the effects of the fungi chemical exposure on dopamine transport.
Neurotransporters are specialised proteins involved in the transportation of neurotransmitters through the brain and nervous system.
This was done because some people also have the same genetically different dopamine transporters as found in some flies.
What were the basic results?
Exposing wild Drosophila flies to low dose 1-octen-3-ol caused movement problems within the first 24 hours and 50% to die by 16.9 days. The control group all survived for at least 27 days, by which time the entire 1-octen-3-ol group had died.
In the second part of the study, exposure to 1-octen-3-ol reduced the number of all types of dopamine nerves except for one. This caused a reduction in dopamine levels of 28% compared to flies that were not exposed. It also increased the level of the waste product of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) by 40%.
In the human embryonic kidney cells, very low levels of 1-octen-3-ol did not have an effect, whereas low and higher levels caused a difficulty in transporting dopamine into the cells.
They found that overexpression (higher amount of gene activity) of a different genetic neurotransporter cell in flies’ brains was protective against the effects of 1-octen-3-ol.
How did the researchers interpret the results?
The researchers’ concluded they had “demonstrated that the fungal volatile 1-octen-3-ol damages the dopamine system and that its toxicity is exacerbated by mutations in genes involved in dopamine synthesis and packaging, suggesting it may contribute to the aetiology of Parkinson’s disease”.
This research furthers the knowledge of how one of the molecules produced by fungi can affect the dopamine system in flies. There appeared to be a similar effect seen in laboratory grown human cells.
However, as the researchers point out, it is difficult to know what level of exposure would be required for there to be an effect on humans in a real life scenario. Reported concentrations of 1-octen-3-ol in mouldy buildings and classrooms are around that used in the initial fly study, but much lower than that used in the direct exposure of human embryonic kidney cells to 1-octen-3-ol.
The researchers also point out that 1-octen-3-ol is also present in human sweat. It is produced as a breakdown product from the essential fatty acid, linoleic acid.
They suggest that excessive production of sweat may contribute to the risk of developing Parkinson’s disease.
This intriguing hypothesis would require further investigation before any firm conclusions can be drawn.
Overall, this laboratory study furthers our understanding of the potential toxic effects of exposure to 1-octen-3-ol on the dopamine system. However, it does not directly link this chemical to a higher risk of Parkinson’s disease in humans; the cause of which remains likely to be a combination of genetic susceptibility and a number of environmental factors.