Articles on Neurodegenerative Diseases (Parkinson’s, Alzheimer’s, etc)
Glutathione plays a crucial role in mediating free radical damage & maintaining the oxidant/ anti oxidant balance. Since the Brain consumes about 20% of the oxygen utilized by the body, the potential for oxidative stress is high. When glutathione is depleted this tilts the balance in favor of the oxidants – resulting in oxidative stress.
Immunocal provides cells with the precursors, or building blocks, needed to produce glutathione. This helps scavenge the free radicals and may slow down the degenerative process in Alzheimer’s, Parkinson’s Disease, as well as other neurodegenerative disorders.
Immunocal and preservation of glutathione as a novel neuroprotective strategy for degenerative disorders of the nervous system.Ross EK, Gray JJ, Winter AN, Linseman DA.
Oxidative stress and glutathione (GSH) depletion are both recognized as significant contributors to the pathogenesis of many devastating neurodegenerative diseases. Strategies that increase or preserve the levels of intracellular GSH have been shown to act in a neuroprotective manner, suggesting that augmentation of the available GSH pool may be a promising therapeutic target for neurodegeneration.
This review discusses the capacity of a cystine-rich, whey protein supplement (Immunocal®) to enhance the de novo synthesis of GSH in neurons, and highlights its potential as a novel therapeutic approach to mitigate the oxidative damage that underlies the pathogenesis of various neurodegenerative diseases. Additionally, this review discusses various patents from 1993 to 2012 both with Immunocal® and other methods that modulate GSH in neurodegeneration. ->> Read More <<-
Glutathione, oxidative stress and neurodegeneration.Schulz JB, Lindenau J, Seyfried J, Dichgans J.
There is significant evidence that the pathogenesis of several neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, Friedreich’s ataxia and amyotrophic lateral sclerosis, may involve the generation of reactive oxygen species and mitochondrial dysfunction. Here, we review the evidence for a disturbance of glutathione homeostasis that may either lead to or result from oxidative stress in neurodegenerative disorders.
Glutathione is an important intracellular antioxidant that protects against a variety of different antioxidant species. An important role for glutathione was proposed for the pathogenesis of Parkinson’s disease, because a decrease in total glutathione concentrations in the substantia nigra has been observed in preclinical stages, at a time at which other biochemical changes are not yet detectable. Because glutathione does not cross the blood-brain barrier other treatment options to increase brain concentrations of glutathione including glutathione analogs, mimetics or precursors are discussed. ->> Read More <<-
Metabolism and functions of glutathione in brainRalf Dringen
Physiologisch-chemisches Institut der UniversitaÈt, Hoppe-Seyler-Str. 4, D-72076 TuÈbingen, Germany
The tripeptide glutathione is the thiol compound present in the highest concentration in cells of all organs. Glutathione has many physiological functions including its involvement in the defense against reactive oxygen species. The cells of the human brain consume about 20% of the oxygen utilized by the body but constitute only 2% of the body weight. Consequently, reactive oxygen species which are continuously generated during oxidative metabolism will be generated in high rates within the brain.
Therefore, the detoxification of reactive oxygen species is an essential task within the brain and the involvement of the antioxidant glutathione in such processes is very important. The main focus of this review article will be recent results on glutathione metabolism of different brain cell types in culture. The glutathione content of brain cells depends strongly on the availability of precursors for glutathione. Glutathione is involved in the disposal of peroxides by brain cells and in the protection against reactive oxygen species. ->> Read more <<-