en de ziekte van Alzheimer en Parkinson.*
een studie met muizen blijkt dat Glutathion de ziekte van Alzheimer en Parkinson
zou kunnen voorkomen en bestrijden. Bij deze ziektes doet een bepaald eiwit
(EAAC1 bij muizen en EAAT3 bij mensen) niet goed functioneren waardoor de opname
van cyste´ne in de hersenneuronen geblokkeerd wordt. Door deze blokkade wordt
wordt er minder glutathion aangemaakt en dientengevolge hebben de neuronen
lagere waarden aan glutathion waardoor er meer oxidatieschade in de hersenen
ontstaat. In de test werden de muizen met dit gebrek gesupplementeerd met NAC (N-acetylcysteine,
een vorm van cyste´ne) waardoor de glutathionwaarden en de weerstand tegen
oxidatie in de neuronen weer normaal werden. Inmiddels zijn de onderzoekers aan
het bestuderen of deze resultaten ook bij de mens het geval zijn.
Brain Antioxidant Linked To Alzheimer's And Parkinson's
study conducted at the San Francisco VA
study, led by Raymond Swanson, MD, chief of neurology and
had been thought previously that the main function of the protein was to remove
excess glutamate, a neurotransmitter, from brain cells.
known that neurons don't take up cysteine directly, and it's never been clear
exactly how it gets there," says Swanson, who is also professor and vice
chair of neurology at the University of California, San Francisco. "This
study provides the first evidence that EAAC1 is the mechanism by which cysteine
gets into neurons -- and that transporting cysteine is probably its chief
findings are currently available in the Advance Online Publication section of
such as glutathione provide protection from oxidative stress, which kills cells
through the "uncontrolled reaction of lipids in the cells with oxygen--basically,
burning them out," says Swanson. Since the brain uses a lot of oxygen and
is "chock full of lipids," it is particularly vulnerable to oxidative
stress, he notes.
the first part of the study, Swanson and his co-authors observed a colony of
mice deficient in the gene responsible for the production of EAAC1 and compared
their behavior with that of a colony of normal, or "wild type," mice.
They noticed that around the age of 11 months -- old age for a mouse -- the
gene-deficient mice began to act listlessly, not groom themselves properly, and
exhibit other signs of senility. In contrast, the wild type mice "looked
and acted totally normal," according to Swanson.
in postmortem examination, the researchers found that the brains of the
EACC1-deficient mice had abnormally enlarged ventricles -- openings within the
brain that provide a path for cerebrospinal fluid -- while the ventricles of the
wild type mice were normal. Enlarged ventricles "also occur in Alzheimer's
patients," Swanson notes.
addition, it was found that the EAAC1-deficient brains had fewer neurons in the
hippocampus, and that all neurons in the hippocampus and cortex showed evidence
of oxidative stress, unlike in the wild type mice.
researchers then compared brain slices from younger mice in both groups. They
found that it took ten times less hydrogen peroxide -- a powerful oxidant -- to
kill slices from the EAAC1-deficient mice than it took to kill slices from the
normal mice. This demonstrated that brains of mice unable to produce EAAC1 were
ten times as vulnerable to oxidative stress as mice with the ability to produce
researchers also found that the neurons of the EAAC1-deficient mice contained
lower levels of the antioxidant glutathione compared to those of the normal mice.
together, these results "support the idea that oxidative stress contributes
to aging" in the brain, a well-known concept that Swanson calls "appealing,"
but difficult to prove or disprove. "This certainly adds credence to the
idea," he says.
the final part of the study, Swanson and his team investigated whether oxidative
stress in EAAC1-deficient mice might be reversible.
several days, a group of gene-deficient mice were fed N-acetylcysteine, an oral
form of cysteine that is readily taken up by neurons. When their neuron slices
were compared with slices from untreated gene-deficient mice, it was found that
N-acetylcysteine "had completely corrected the biochemical defect" in
their neurons, recounts Swanson. "Their glutathione levels were normal,
their ability to withstand hydrogen peroxide toxicity was normal, and the
oxidants we saw in the neurons in response to oxidative challenges were normal."
Based on the results of the current study, Swanson and his group are working to determine whether EAAC1 expression is altered in neurodegenerative illnesses such as Alzheimer's and Parkinson's diseases. Should this prove to be the case, says Swanson, then manipulation of EAAC1 levels "might provide a novel approach" to the treatment of these diseases in the future. ( Januari 2006) (Opm. NAC is een precursor voor Glutathion, meer over Glutathion en een nog betere precursor kijk hier.)