This finding, published online in the journal Neurobiology of Aging, could have significant implications for identifying patients who may be at risk of developing Parkinson's disease and for the early treatment of the disease.
Parkinson's disease is a degenerative, progressive disorder characterised by the dramatic reduction of nerve cells, particularly dopamine neurons that are involved in movement initiation, in an area of the brain called the substantia nigra.
"This (study) potentially provides an opportunity to treat lipid changes early on in Parkinson's disease and protect nerve cells from dying, as well as the chance to use the lipid levels as biomarkers for patients at risk," said study lead author Penny Hallett from McLean Hospital, an affiliate of Harvard Medical School in the US.
For many years now, the loss of the nerve cells has been attributed to the toxic accumulation of the protein alpha-synuclein.
In the past 15 years, however, researchers have been studying an interesting relationship between the risk of developing the disease and mutations that lead to loss of function in the glucocerebrosidase (GBA) gene.
Scientists at the Neuroregeneration Research Institute at McLean Hospital had previously shown that there is an elevation of a class of lipids, called glycosphingolipids, in the substantia nigra of patients with Parkinson's disease.
Since ageing is the most significant risk factor for developing Parkinson's disease, the team measured the levels of glycosphingolipids in the ageing brain, using young and old mice.
They found that the same glycosphingolipids that are increased in the brains of Parkinson's disease patients are also elevated in the brains of ageing mice.
These findings showed that both genetics (GBA gene mutation) and ageing can cause the same lipid elevations in the brain that are demonstrated in Parkinson's disease pathology.
"These results lead to a new hypothesis that lipid alterations may create a number of problems inside nerve cells in degenerative ageing and Parkinson's disease, and that these changes may precede some of the more obvious hallmarks of Parkinson's disease, such as protein aggregates," Hallett said.
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