Degenerative Diseases Of The Brain – New Therapies
Late onset diseases like Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) are degenerative as well as progressive and thereby diminish the quality of life of patients significantly. At present, therapies to treat or reverse degeneration of brain cells are limited and these diseases usually progress into disabilities. However, recent research seems to indicate that it may be possible to limit the damage caused by the onset of AD, PD and ALS by activating innate biological mechanisms.
A consequence of the natural respiration process that is always active in our cells is the production of harmful forms of oxygen, which are known as reactive oxygen species (ROS). Reactive oxygen species like hydroxyl ions and hydrogen peroxide are produced in mitochondria. During periods of wakefulness, our brain consumes 20% of the total oxygen used in the body and it therefore follows that the chances of generating reactive oxygen species in brain cells are very high. These highly destructive molecules are neutralized by two enzyme: heme oxidase-1 (HO-1) and superoxide dismutase (SOD). In the early stages of AD and PD, the activity of these enzymes is either normal or reduced. It is surmised that the capability of the brain to increase the activity of these antioxidants is diminished in the stages preceding the onset of these degenerative diseases. In the case of AD, the protein (beta-amyloid peptide) deposited on nerve cells actually causes an increase in the ROS within nerve cells.
Recent research suggests that inhalation of gases like hydrogen, hydrogen sulfide and carbon monoxide, in low and regulated doses, can actually help to reduce oxidative damage caused by ROS. Although hydrogen sulfide is toxic, small quantities of this gas can actually be therapeutic against ROS. A modified form of aspirin which can release hydrogen sulfide, termed as S-aspirin, is able to protect brain cells from damage caused by the beta-amyloid peptide. Similarly, hydrogen, when inhaled, can reach the brain within an hour and can help to reverse nerve cell damage evident in PD. Hydrogen can be also given to patients in the form of hydrogen water and is faster in action than when inhaled in gas form. In experimental animal models for Parkinson’s disease, treatment with hydrogen water helped to rescue neurons which respond to dopamine from damage caused by ROS.
Hydrogen is capable of reacting with hydroxyl radicals to form water. In addition to this short-term chemical neutralization of reactive oxygen species, exposure to low doses of hydrogen also causes enhanced expression of HO-1 and SOD enzymes. Similar effects are also seen when nerve cells are exposed to carbon monoxide and hydrogen sulfide. These medical gases boost innate protective responses against reactive oxygen species and provide long-term protection that goes beyond immediate and local chemistry in the brain. Exposure of brain cells to hydrogen sulfide also reduces the amount of beta-amyloid peptide in nerve cells thereby limiting the damage caused by this protein.
Since administration of medical gases is a pretty standard procedure in hospitals and clinics, these scientific advances may represent a chance of recovery to patients who have been diagnosed with debilitating diseases like AD, Parkinson’s disease and ALS, at least in the early stages. The efficiency of these treatments in patients suffering from advanced stages of these neurodegenerative diseases is not known yet.
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Liu YY, Sparatore A, Del Soldato P, & Bian JS (2011). H2S releasing aspirin protects amyloid beta induced cell toxicity in BV-2 microglial cells. Neuroscience, 193, 80-8 PMID: 21784135
Noda M, Fujita K, Lee CH, & Yoshioka T (2011). The principle and the potential approach to ROS-dependent cytotoxicity by non-pharmaceutical therapies: optimal use of medical gases with antioxidant properties. Current pharmaceutical design, 17 (22), 2253-63 PMID: 21736540
Tang XQ, Yang CT, Chen J, Yin WL, Tian SW, Hu B, Feng JQ, & Li YJ (2008). Effect of hydrogen sulphide on beta-amyloid-induced damage in PC12 cells. Clinical and experimental pharmacology & physiology, 35 (2), 180-6 PMID: 17892504
Zhang H, Gao Y, Zhao F, Dai Z, Meng T, Tu S, & Yan Y (2011). Hydrogen sulfide reduces mRNA and protein levels of ?-site amyloid precursor protein cleaving enzyme 1 in PC12 cells. Neurochemistry international, 58 (2), 169-75 PMID: 21095213
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