Energy cell clue to Parkinson’s

The body’s energy cells may play a key role in Parkinson’s disease, British scientists have revealed.

New research links a Parkinson gene to the mitochondria, cells which produce energy.

The findings could open the way to developing radical new treatments for Parkinson’s.

The researchers say mitochondria are especially important in the brain and nervous system, which require a great deal of energy.

According to the study, reported in Nature Neuroscience, the gene Fbxo7 interferes with the body’s ability to get rid of damaged mitochondria, a process known as mitophagy.

Other studies previously have linked two genes which cause an inherited form of Parkinson’s, PINK1 and Parkin, to the same process.

The researchers say the finding of strong links means they are "at the beginning" of the work.

The research has involved University College London, the University of Cambridge and the University of Sheffield.

Researcher Professor Nicholas Wood, of University College London, said: "It is very exciting to see how detailed biological work of this type can highlight a single pathway that contributes to Parkinson’s disease. This presents the opportunity of more rational drug design for many forms of parkinsonism."

Fellow researcher Dr Heike Laman, from Cambridge, said: "We are really only at the very beginning of this work, but perhaps we can use this information to enable earlier diagnosis for Parkinson’s disease patients or design therapies aimed at supporting mitochondrial health."

Professor Hugh Perry, of the UK Medical Research Council, which backed the study, said it raised "interesting questions" about how brain cells died in the disease.

He said: "The more we understand about the basic molecular events which contribute to the onset and progression of Parkinson’s disease, the better placed we will be to develop treatments to stop it in its tracks."

Plun-Favreau et al. The Parkinson’s disease-linked proteins Fbxo7 and Parkin interact to mediate mitophagy. Nature Neuroscience 11 August 2013

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