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Loss of Mitochondria Linked to Parkinson's
If supported by additional studies, the results could warrant clinical trials of existing drugs (currently used to treat other diseases) that activate a key pathway able to repair and replace broken mitochondria, reports Nature.
In recent years, evidence has been mounting that damaged mitochondria contribute to the neurological damage wrought by the disease.
For the latest study, neurologist Clemens Scherzer of Harvard Medical School in Boston, Massachusetts - lead author on the current study - and an international consortium of researchers began by profiling patterns of gene expression in diseased versus healthy brains.
The team gathered data from roughly ten times more samples than had ever before been analysed in a single Parkinson's disease study, says Scherzer, allowing his team to conduct a more sensitive sweep of gene
expression changes.
The trawl through millions of data points yielded ten gene sets not previously associated with Parkinson's disease. All are involved in mitochondrial function and energy generation.
What's more, genes regulated by a single protein called PGC-1a were expressed at abnormally low levels in patients with Parkinson's disease. Increasing the expression of that protein in rat neurons grown in culture was enough to reduce the toxic effects of MPTP and rotenone.
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