An estimated 10 million people are currently affected by Parkinson's
disease worldwide. A small percentage gets confronted with the disease
before the age of 40.
While the causes of the affected are not yet known, scientists believe that they consist of both genetic and environmental
factors. In genetic Parkinson's disease, a mutation in the PINK1 gene
causes changes in neurons' mitochondria, leading to the degeneration of
‘Reducing the effects of the protein FASN influences the mitochondria, leading to increased cardiolipin levels and reduced Parkinson's symptoms.’
A team of researchers led by Patrik Verstreken (VIB-KU Leuven) have
identified an underlying mechanism in early onset Parkinson's. Using
flies, mice and patient cells, the team focused on cardiolipin, a fat
unique to cells' mitochondria, organelles that produce energy.
demonstrated that reducing the effects of the protein FASN influences
the mitochondria, leading to increased cardiolipin levels and reduced
Parkinson's symptoms. These results could pave the way to therapies for
Parkinson's disease that target lipids. The team's research was
published in the scientific magazine Journal of Cell Biology
Existing oncological applications
In this study, prof. Verstreken and his team, consisting of
collaborators in Belgium, Germany and Portugal, observed that a protein
responsible for lipid creation in cells, FASN, bypasses the genetic
defect in mitochondria.
Prof. Patrik Verstreken (VIB-KU Leuven): "Several drugs that block
FASN already exist, as this protein is also important to cancer research
and treatment. Many of them have already been used in clinical trials.
Thanks to this research, we can now test them in the context of
Unexpected effects of FASN protein
In the course of their research, the researchers encountered a
surprising observation. Using fly, mouse and human cell models, they saw
that FASN has a direct effect on mitochondria, which have their own
separate genomes and operate as energy producing entities within their
Prof. Patrik Verstreken (VIB-KU Leuven): "The PINK1 gene encodes the
PINK1 protein, and mutations in it lead to lower levels of cardiolipin
in mitochondria. It was unexpected to see that blocking FASN - which is
not localized to the mitochondria - actually sidesteps the mitochondrial
effects of the PINK1 mutation. As a result, blocking FASN increases the
amounts of a specific type of lipids in mitochondria, reducing the
degradation of neurons."
Translating insights into therapies
Prof. Verstreken has already identified several targets for
future research projects seeking greater insights into the link between
the amounts of specific lipids in neurons and Parkinson's disease.
Prof. Patrik Verstreken (VIB-KU Leuven): "Some questions need to be
answered before new therapies can be developed, such as 'is there a link
between early onset Parkinson's prevalence and progression with lipid
content?' And while we successfully demonstrated that cardiolipin can
improve the function of mitochondria in flies, mouse models and in human
cells, we need to explore its effects in actual patients."