Saturday 16 November 2013

Chemical produced by fungi produces Parkinson Disease-like neurodegeneration in flies

 

Researchers find that a chemical produced by fungi, called 1-octen-3-ol can produce the death of dopaminergic neurons and movement disorders in flies, hinting that this chemical may be capable of causing Parkinson's Disease in humans too.

This has raised concerns raised that moulds found in damp living conditions may contribute to PD in humans. This may even help explain the higher incidence of PD in rural areas, where more moulds and fungi can be found.


Could mould like this contribute to PD?

However, showing that these fungal compounds can cause neurodegeneration in flies most certainly does not prove that living in damp, mouldy conditions causes PD. In order to establish an association between damp living conditions and PD, 'epidemiological' evidence showing that poor quality housing increases risk of PD in humans will be required.

ResearchBlogging.org Inamdar AA, Hossain MM, Bernstein AI, Miller GW, Richardson JR, & Bennett JW (2013). Fungal-derived semiochemical 1-octen-3-ol disrupts dopamine packaging and causes neurodegeneration. Proceedings of the National Academy of Sciences of the United States of America PMID: 24218591


Abstract: Fungal-derived semiochemical 1-octen-3-ol disrupts dopamine packaging and causes neurodegeneration

Parkinson disease (PD) is the most common movement disorder and, although the exact causes are unknown, recent epidemiological and experimental studies indicate that several environmental agents may be significant risk factors. To date, these suspected environmental risk factors have been man-made chemicals. In this report, we demonstrate via genetic, biochemical, and immunological studies that the common volatile fungal semiochemical 1-octen-3-ol reduces dopamine levels and causes dopamine neuron degeneration in Drosophila melanogaster. Overexpression of the vesicular monoamine transporter (VMAT) rescued the dopamine toxicity and neurodegeneration, whereas mutations decreasing VMAT and tyrosine hydroxylase exacerbated toxicity. Furthermore, 1-octen-3-ol also inhibited uptake of dopamine in human cell lines expressing the human plasma membrane dopamine transporter (DAT) and human VMAT ortholog, VMAT2. These data demonstrate that 1-octen-3-ol exerts toxicity via disruption of dopamine homeostasis and may represent a naturally occurring environmental agent involved in parkinsonism. 

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