Part 2
Alzheimer's Disease and Glutathione
Free radicals and oxidative damage in neurons is known to be a primary cause of degenerative diseases like Alzheimer's disease.
Amyloid-ß peptide (Aß) accumulation in senile plaques, a pathological hallmark of Alzheimer's disease (AD), has been implicated in neuronal degeneration.
Amyloid plaques encroaching on the brain increase the production of free radicals, or oxidative stress. Antioxidants, such as vitamin C and E "mop up" the damaging free radicals.
Glutathione (GSH) precursors can prevent death of brain cells induced by amyloid plaques in Alzhiemer's disease, while substances that deplete GSH increase cell death.
Evidence has been piling up over the link between the amount of an amino acid called homocysteine in the blood and the chance of developing Alzheimer's.
For people not genetically predisposed to developing Alzheimer's, cholesterol and homocysteine, largely caused by an unhealthy lifestyle, are the core causal factors.
Welsh GP, Andrew McCaddon, showed that the more homocysteine that patients with Alzheimer's had, the worse their mental performance, and the worse their "cognitive impairment," the less they had of the antioxidant glutathione.
Glutathione and Mood Disorders
Studies have found that the mood stabilizing drug, valproate, used to treat epilepsy and bi-polar disorder, regulates expression of the genes that make glutathione-S-transferase (GST).
In addition, chronic treatment with lithium, another commonly prescribed mood stabilizer used in treating manic-depression, also increased levels of GST.
These findings led researchers to conclude that glutathione S-transferase may be a novel target for mood stabilizing drugs.
by Priya F Shah