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Jan. 17,2015
In normally functioning brain cells, mitochondria,
or the ''powerhouses'' of cells, generate the energy needed to keep cells
alive. When mitochondria become damaged and are no longer capable of making
energy, they are sent to a portion of the cell called a lysosome to be
repaired; however, in the brains of Parkinson's disease patients, mitochondria
fail to move to lysosomes, causing accumulations of damaged mitochondria that
kill brain cells.
Now, a University of Missouri (MU) researcher has
found a molecule that could aid mitochondrial recycling and keep brain cells
alive. The molecule could be key to developing drugs that will keep brain cells
healthy in individuals with Parkinson's disease.
''Mitochondria eventually become damaged and no
longer function properly, so the cell has a mechanism to recycle them, keeping
them strong,'' says Mark Hannink, a professor in the Department of Biochemistry
and an investigator at the Bond Life Sciences Center at MU.
He explains, ''In early onset Parkinson's, mutated
proteins 'forget' to recycle mitochondria, resulting in a build-up of toxic
waste and early onset of the disease. In our study, we found a peptide, or
molecule, responsible for an alternative pathway that bypasses the mutant
Parkinson's proteins and allows mitochondrial recycling. We feel that this
peptide could prove useful in fighting diseases in the brain.''
This alternative pathway for mitochondrial
recycling uses a protein called phosphoglycerate mutase family member 5
(PGAM5). In Hannink's study, he discovered a peptide which acts as a ''switch''
to cause the protein to create an alternate pathway. By regulating the protein
with the peptide he discovered, it may be possible to restore mitochondrial
recycling in neurons of patients with Parkinson's, lessening the severity of
the disease.
''Peptides behave like drug molecules,'' Hannink
says. ''Any time you can identify a biological process that is regulated by a
peptide, that peptide becomes a leading candidate in the search for small,
drug-like molecules that will act the same way.''
For Parkinson's disease, the goal is to find ways
to repair the mitochondria recycling process. The next step of his research is
to produce a drug molecule that can regulate the PGAM5 protein in cells, just
as the peptide did in his experiments, Hannink said.
The early-stage results of this research are
promising. If additional studies are successful within the next few years, MU
officials will request authority from the federal government to begin human
drug development (this is commonly referred to as the ''investigative new
drug'' status). After this status has been granted, researchers may conduct
human clinical trials with the hope of developing new treatments for
Parkinson's and other diseases.
Hannink's study, A conserved motif mediates both
multimer formulation and allosteric activation of phosphoglycerate mutase 5,
recently was published in the Journal of Biological Chemistry. Peter
Tipton, professor of biochemistry, and graduate students Jordan M. Wilkins and
Cyrus McConnell contributed to the research.
- See more at: http://www.domain-b.com/technology/Health_Medicine/20150117_parkinson.html#sthash.M6Hdr4dK.dpuf
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