Folic acid could suppress Parkinson’s – new study

Posted by er134 at Jan 21, 2014 01:35 PM |
Research in laboratory setting uses common vitamin to improve cell signaling and rescue problems associated with neurodegenerative disease

Issued by University of Leicester Press Office on 21 January 2014

Contact pressoffice@le.ac.uk to request images

Medical Research Council scientists based at the University of Leicester have described an ‘amazing new advance’ in the battle against neurodegenerative diseases such as Parkinson’s.

The team at the MRC Toxicology Unit at Leicester was investigating chemical pathways in the cells of flies which are used as a model organism to study neurodegenerative diseases such as Parkinson’s. They uncovered an unexpected pathway that, through the manipulation of a particular gene, led to the creation of a ‘super-fly’ - thereby combatting the effects of Parkinson’s features in the insects.

Their results have been published in the journal Nature Cell Biology.

“What we found is pretty simple, really, but amazing,” said lead researcher Dr L. Miguel Martins. “When we enhance this pathway in flies by manipulating a specific gene, we create super flies. They move faster, have more energy and are resistant to mitochondrial poisons.”

Dr Martins, MRC Programme Leader and Reader with the University of Leicester Cell Death Regulation Laboratory,  said their work was relevant to tackling a wide range of diseases where mitochondria are defective, such as Parkinson’s. Mitochondria are the ‘powerhouses’ of cells and when they fail to produce energy, the lack of energy contributes to diseases such as neurodegenerative diseases and to the ageing process in general.

He said: “For cells to function properly they need to have signaling networks. These networks can be defined as software mechanisms that control the response to stress in the environment or genes. We are interested in the role of mitochondria in influencing this ‘software’ so that it works as a SOS signal for these energy powerhouses.

“Defects in mitochondrial signaling are thought to be linked to age-associated human diseases like Parkinson’s disease, which is caused by the death of specific neurons.

“Defective mitochondria in Parkinson's models send SOS signals to the cell nucleus. This involves a demand to increasing the synthesis of their own genetic material. They use a major pathway the so-called ‘salvage pathway for DNA synthesis’ to do this.”

The Leicester team discovered that by providing cells with a key product that improves their signaling, it stimulated mitochondria function and, most interestingly, rescues the problems in Parkinson’s disease, both in fly models as well as cultured human cells.

“It turns-out that folic acid a common vitamin, is one of the chemicals we found to suppress Parkinson’s features by increasing mitochondrial health. This indicates that folic acid enhances the generation of new mitochondria and this protects the neurons that die in Parkinson's disease models,” said Dr Martins.

“This opens up the exciting possibility that diets rich in this vitamin or supplements such as the ones given to pregnant women to prevent birth defects could play a role in protecting mitochondria and therefore prevent or delay neurodegenerative diseases associated with mitochondrial problems such as Parkinson’s disease.”

“Our data support the therapeutic potential of folic acid to enhance nucleotide pools, promoting mitochondrial biogenesis and improving mitochondrial function in neurons in neurodegenerative disease and confirm a mechanism by which this acts. Based on our findings, we propose that a high folic acid diet might be beneficial to modulate the pathogenesis of Parkinson’s disease by repressing mitochondrial dysfunction, opening a promising avenue towards exploring the role of folic acid in the prevention and therapy for neurodegenerative diseases such as Parkinson’s as well as other neurodegenerative diseases associated with defective mitochondrial function.”

Professor Patrick Chinnery, from the MRC’s Neurosciences and Mental Health Board, said:

“Although these findings are a long way from developing a treatment, the identification of this new mechanism is certainly exciting and could have  broader significance for mitochondrial diseases as well as opening up new possibilities in other areas of neurodegeneration. The MRC believes that research such as this, which looks at the fundamental mechanisms of these devastating diseases, is absolutely vital.”

The work was funded by the Medical Research Council and the team is based at the University of Leicester.

  • Papers published online before they have been allocated to a print issue will be citable via a digital object identifier (DOI) number. The DOI for this paper will be 10.1038/ncb2901. Once the paper is published electronically, the DOI can be used to retrieve the abstract and full text by adding it to the following url: http://dx.doi.org/

Ends

NOTES TO EDITORS:

For more information contact:

Dr. L. M. Martins
Cell Death Regulation Laboratory
MRC Toxicology Unit

University of Leicester

Email: martins.lmiguel@gmail.com
Work: 0116-2525533
Mobile: 07905857446

Please cite the Medical Research Council and University of Leicester in any report.

About the Medical Research Council

For almost 100 years the Medical Research Council has improved the health of people in the UK and around the world by supporting the highest quality science. The MRC invests in world-class scientists. It has produced 29 Nobel Prize winners and sustains a flourishing environment for internationally recognised research. The MRC focuses on making an impact and provides the financial muscle and scientific expertise behind medical breakthroughs, including the first antibiotic penicillin, the structure of DNA and the lethal link between smoking and cancer. Today MRC funded scientists tackle research into the major health challenges of the 21st century. www.mrc.ac.uk<http://www.mrc.ac.uk/>

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