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This is not such a complicated disease afterall
Lane Simonian
Posted: Saturday, April 18, 2015 12:24 AM
Joined: 12/12/2011
Posts: 4863


The following researcher touches upon the key to preventing and treating Alzheimer's disease. Modern day diets, stress, and pollutants (among other factors) have increased oxidation and reduced levels of the brain's master antioxidant: glutathione. The key is to either supplement the body's own antioxidant systems (which for a variety of reasons is not easy) or to add the most effective outside antioxidants to reduce the damage done to the brain by oxidants.

“A long-standing theory of aging called the free-radical theory explains that oxidative stress plays a key role in aging, aging-associated neurodegenerative diseases such as Alzheimer’s disease,” says lead study author In-Young Choi, an associate professor of neurology at the University of Kansas Medical Center. “Glutathione is a major antioxidant in our brains and is known to fight against oxidative stress and protect our nerve cells. Therefore, increasing glutathione concentrations could be an important strategy to promote brain health.”

Throughout our lives, the liver produces glutathione from a combination of amino acids. That glutathione is integral to scavenging free radicals to prevent their harmful effects throughout the body. “In a perfect world, our body should be able to recycle its own glutathione for use,” says registered dietitian Jaime Mass. However, pollution, lack of exercise, junk food and mental stress can all cause your body’s levels of circulating glutathione to drop. “Glutathione is a perfect example of how modern-day living could be playing a role in increased disease states and illness,” she says.

Unfortunately, the brain is particularly vulnerable to oxidative stress. So when glutathione levels get too low, so too can your cognitive health, says Dr. Richard Isaacson, director of the Alzheimer’s Prevention Clinic at Weill Cornell Medical College/NewYork-Presbyterian Hospital and co-author of "The Alzheimer’s Diet." Hence why, according to research published in The Journal of Nutrition, consuming foods that help the body produce more glutathione is critical to preventing Alzheimer’s disease.

You can’t just eat more glutathione. You have to consume precursors of the molecule to help your body increase its levels naturally, Mass says. “That’s why dairy products may have a potential connection to glutathione levels. They are rich in cysteine, one of the building blocks of glutathione.”

http://health.usnews.com/health-news/health-wellness/articles/2015/04/17/can-drinking-milk-prevent-alzheimers-disease

And from a more technical standpoint:

1996;18(5-6):391-6.

Glutathione protects astrocytes from peroxynitrite-mediated mitochondrial damage: implications for neuronal/astrocytic trafficking and neurodegeneration.

Abstract

In this study we have examined the susceptibility of the mitochondrial respiratory chain of astrocytes and astrocytes depleted of glutathione to peroxynitrite exposure. Astrocytes, as reported previously by us, appeared resistant to the actions of peroxynitrite. In contrast, depletion (-94%) of astrocytic glutathione rendered the cells susceptible with mitochondrial complexes I and II/III being decreased in activity by 80 and 64%, respectively, after peroxynitrite exposure. Furthermore, cell death, as judged by lactate dehydrogenase release, was significantly increased (+81%) in the glutathione-depleted astrocytes exposed to peroxynitrite. Glutathione depletion alone had no effect on any of the measured parameters. It is concluded that glutathione is an important intracellular defence against peroxynitrite and that when glutathione levels are compromised the mitochondrial respiratory chain is a vulnerable target and cell death ensues. In view of the relative paucity of neuronal glutathione, it is possible that astrocyte-derived peroxynitrite may, in certain pathological conditions, be released and diffuse into neighboring neurones where mitochondrial damage may occur.


Whether intentionally or not, some people make this disease more complicated than it is and this is delaying the more widespread use of effective treatments.


Lane Simonian
Posted: Saturday, April 18, 2015 1:43 PM
Joined: 12/12/2011
Posts: 4863


I am being lazy today cutting and pasting from comments that I have made elsewhere (this time from the Alzheimer's Reading Room) but sometimes I am able to present things clearer the second time through.

A fairly careful reading of this article will provide all the clues you need to understand and treat Alzheimer's disease. I will highlight a few presented here and from another source on the same study:

Oxidative stress is known to be associated with a number of different diseases and conditions, including Alzheimer's disease, Parkinson's disease and many other conditions, said Dr. Choi.

Throughout our lives, the liver produces glutathione from a combination of amino acids. That glutathione is integral to scavenging free radicals to prevent their harmful effects throughout the body. “In a perfect world, our body should be able to recycle its own glutathione for use,” says registered dietitian Jaime Mass. However, pollution, lack of exercise, junk food and mental stress can all cause your body’s levels of circulating glutathione to drop. “Glutathione is a perfect example of how modern-day living could be playing a role in increased disease states and illness,” she says.

"If we can find a way to fight this by instituting lifestyle changes including diet and exercise, it could have major implications for brain health," Choi said.

And from a technical standpoint this is what happens when glutahione levels are depleted by oxidative stress in Alzheimer's disease:

Dev Neurosci. 1996;18(5-6):391-6.

Glutathione protects astrocytes from peroxynitrite-mediated mitochondrial damage: implications for neuronal/astrocytic trafficking and neurodegeneration.

Barker JE1, Bolaños JP, Land JM, Clark JB, Heales SJ.

Abstract

In this study we have examined the susceptibility of the mitochondrial respiratory chain of astrocytes and astrocytes depleted of glutathione to peroxynitrite exposure. Astrocytes, as reported previously by us, appeared resistant to the actions of peroxynitrite. In contrast, depletion (-94%) of astrocytic glutathione rendered the cells susceptible with mitochondrial complexes I and II/III being decreased in activity by 80 and 64%, respectively, after peroxynitrite exposure. Furthermore, cell death, as judged by lactate dehydrogenase release, was significantly increased (+81%) in the glutathione-depleted astrocytes exposed to peroxynitrite. Glutathione depletion alone had no effect on any of the measured parameters. It is concluded that glutathione is an important intracellular defence against peroxynitrite and that when glutathione levels are compromised the mitochondrial respiratory chain is a vulnerable target and cell death ensues. In view of the relative paucity of neuronal glutathione, it is possible that astrocyte-derived peroxynitrite may, in certain pathological conditions, be released and diffuse into neighboring neurones where mitochondrial damage may occur.

The problem as hinted at in this study is that glutathione supplements do not enter cells. You have to use their precursors and especially cysteine. But the transport of cysteine in disrupted in Alzheimer's disease so cysteine supplementation does not seem to help much.

However, in the larger picture, this study is very important because it acknowledges that oxidation is a key factor in Alzheimer's disease, spotlights how a junk food diet, lack of exercise, mental stress, and pollutants can increase oxidative stress (and thus the risk for Alzheimer's disease), and perhaps most importantly says if the brain's master antioxidant is nearly exhausted you have to find ways to increase glutathione levels (or for what I always argue find antioxidants that are as effective or nearly as effective as glutathione). After a month of misleading studies (Biogen amyloid antibodies, ultrasounds, arginase inhibitors), finally one that focuses on the real causes and treatments of Alzheimer's disease.