Scientists at the Buck Institute have shown that
mice suffering from a depletion of the antioxidant
glutathione in dopamine-producing neurons developed
nerve damage and symptoms associated with Parkinson’s
disease (PD) in humans.
Dopamine is a neurotransmitter produced in the mid-brain
which facilitates many critical functions, including
motor skills. Past studies have shown that depletion
of the naturally occurring antioxidant in the affected
area of the brain is one of the earliest signs of PD,
but this study shows that glutathione depletion may be
a causal factor in the disorder.
Results of the study, led by faculty member Julie
Andersen PhD, are to be published in the December,
2007 issue of The Journal of Neuroscience.
In the course of their research, Buck Institute
scientists created a new model for studying PD,
a progressive, incurable neurodegenerative disorder
that affects 1.5 million Americans and results in
tremor, slowness of movement and rigidity. They bred
mice that can be chemically induced to develop a
depletion of glutathione in the dopaminergic neurons
as adults (animals unable to create glutathione would
not survive in the womb). By inducing the depletion
at various stages of the adult life cycle
scientists researchers also highlighted the
connection between aging and PD. Mice induced to
have glutathione depletion as young adults did
not develop Parkinsonian-like nerve damage and
symptoms, while those who suffered from the
depletion in late middle age did develop a loss of
dopaminergic neurons specifically related to PD.
In addition, the study suggests that loss of
glutathione in the affected neurons may impact
on energy production in the mitochondria, the
“power plant” of the cells. This appears to
involve a particular co-factor complex called
mitochondrial complex I. Co-facter activity of
this complex has been found to be compromised in
PD patients, but to date it has not been clear
how this inhibition occurs.
Glutathione is recognized as a detoxifying
super antioxidant that helps the body repair
damage from stress, pollution, outfection and damage
due to dietary and metabolic acids. While available
in supplemental form, the antioxidant does not easily
cross the blood-brain barrier. A pilot study in 1996
in which a small group of untreated PD patients were
given daily intravenous infusions of glutathione
over the period of a month reportedly resulted in
a significant improvement in disability.
“Whether such treatment was effective in altering
brain levels of glutathione or in having lasting
effects is unclear,” said Andersen. “However, our
data suggests that maintaining glutathione levels
is critical for protecting neurons associated with
PD from neurodegeneration. This work also points
to glutathione replacement as a possible therapeutic
avenue for PD and other related disorders.”
“The novelty of this study is in finding a way to
decrease glutathione synthesis in neural tissue
by genetic manipulation and in demonstrating that
this appears to allow inactivation of a critical
component of mitochondrial function through the
same mechanism that could only be previously
demonstrated in a cell culture model,” said Henry
Jay Forman, PhD, Professor, School of Natural
Sciences, UC Merced. “The implications for the
role of glutathione depletion in the mechanism of
Parkinson’s disease are clear.”
To learn more about Glutathione as a powerful
antioxidant in buffering dietary and metabolic
acids in the prevention or reversal of Parkinson's
dis-ease, go to:
http://www.phmiracleliving.com/glutathione.htm
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