Date:
November 5, 2014
Source:
University of Plymouth
Summary:
The inhibition of a particular
mitochondrial fission protein could hold the key to potential treatment for
Parkinson's disease (PD), a new study has concluded. PD is a progressive
neurological condition that affects movement. At present there is no cure and
little understanding of why some people get the condition.
The findings of the research are
published today, 5th November 2014, in Nature Communications.
PD is a progressive neurological
condition that affects movement. At present there is no cure and little
understanding of why some people get the condition. In the UK one on 500
people, around 127,000, have PD.
The debilitating movement
symptoms of the disease are primarily caused by the death of a type of brain
cell that produces a chemical called dopamine. This brain chemical (also known
as a neurotransmitter) helps nerve cells to send signals to other nerve cells.
A reduction in dopamine from cell death results in a lack of communication
between nerve cells, which in turn leads to difficulty in movement control.
Understanding why these nerve cells die or do not work properly could lead to
new therapies for PD.
Mitochondria are small structures
within nerve cells that help keep the cells healthy and working properly --
they are, in effect, the power generators of the cell. Mitochondria undergo
frequent changes in shape, size, number and location either through
mitochondrial fission (which leads to multiple, smaller mitochondria) or
mitochondrial fusion (resulting in larger mitochondria). These processes are
controlled mainly by their respective mitochondrial fission and fusion
proteins. A balance of mitochondrial fission/fusion is critical to cell
function and viability.
The research team found that when
a particular mitochondrial fission protein (GTPase dynamin-related protein-1 --
Drp1) was blocked using either gene-therapy or a chemical approach in
experimental models of PD in mice, it reduced both cell death and the deficits
in dopamine release -- effectively reversing the PD process. The results
suggest that finding a strategy to inhibit Drp1 could be a potential treatment
for PD.
The research team is led by Dr.
Kim Tieu from the Institute of Translational and Stratified Medicine, Plymouth
University Peninsula Schools of Medicine and Dentistry. Dr. Tieu is a respected
researcher in the field of PD. He initiated this research when he was a
principal investigator at the University of Rochester School of Medicine and
continued it on his move to Plymouth University in the UK.
He said: "Our findings show
exciting potential for an effective treatment for PD and pave the way for
future in-depth studies in this field. It's worth noting that other researchers
are also targeting this mitochondrial fission/fusion pathway as potential
treatments for other neurological diseases such as Alzheimer's disease,
Huntington's disease and Amyotrophic Lateral Sclerosis."
Claire Bale, Research
Communications Manager at Parkinson's UK, said: "We've known for decades
that problems with mitochondria -- the batteries of the cell -- play a key role
in the death of nerve cells in Parkinson's, but the research in this area
hasn't yet led to new treatments.
"This study, which reveals a
potential new drug target to protect mitochondria, is a promising step towards
slowing down or stopping the progression of Parkinson's."
end text
Story Source:
The above story is based on materials
provided by University of Plymouth.
The original article was written by Andrew Gould. Note: Materials may be
edited for content and length.
end story_source
Journal Reference:
1
Phillip M. Rappold, Mei Cui,
Jonathan C. Grima, Rebecca Z. Fan, Karen L. de Mesy-Bentley, Linan Chen, Xiaoxi
Zhuang, William J. Bowers, Kim Tieu. Drp1 inhibition attenuates
neurotoxicity and dopamine release deficits in vivo. Nature
Communications, 2014; 5: 5244 DOI: 10.1038/ncomms6244
end journal_references
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University of Plymouth.
"Blocking mitochondrial fission: Effective treatment for Parkinson's disease?."
ScienceDaily. ScienceDaily, 5 November 2014.
<www.sciencedaily.com/releases/2014/11/141105093500.htm>.
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