Burnham Institute
Member
Oxidative stress in Alzheimer's disease: implications for prevention and therapy.
Behl C.
Institute for Physiological Chemistry & Pathobiochemistry, Faculty of Medicine, Johannes Gutenberg University, Mainz, D-55099 Mainz, Germany.
Oxidative stress is a marker of neurodegeneration and has been recently shown to be also involved in the early stages of the pathogenesis of various neurodegenerative disorders. In general, all biomolecules of the cell can be oxidized and thereby damaged. Consequently, the concept of neuroprotection by antioxidants has been developed. In many cases the direct scavanging of free radicals have been used as a strategy to prevent oxidative stress damage and a variety of physiological and synthetic antioxidant molecules have been identified and synthesized including the female sex homone estrogen. In Alzheimer's Disease amyloid-beta protein on its way to brain deposition can also induce oxidative changes rendering nerve cells more vulnerable to additional insults. In addition, inflammatory mediators are attracted by amyloid deposits that can further speed up the generation of an oxidative micro-environment. Based on recent clinical data the use of a combination of various antioxidants might indeed be effective in preventing Alzheimer's Disease. Nevertheless, the exact molecular mechanisms and the real impact of oxidative stress on the development and progression of Alzheimer's Disease as well as of other neurodegenerative disorders still needs to be further investigated.
Behl C.
Institute for Physiological Chemistry & Pathobiochemistry, Faculty of Medicine, Johannes Gutenberg University, Mainz, D-55099 Mainz, Germany.
Oxidative stress is a marker of neurodegeneration and has been recently shown to be also involved in the early stages of the pathogenesis of various neurodegenerative disorders. In general, all biomolecules of the cell can be oxidized and thereby damaged. Consequently, the concept of neuroprotection by antioxidants has been developed. In many cases the direct scavanging of free radicals have been used as a strategy to prevent oxidative stress damage and a variety of physiological and synthetic antioxidant molecules have been identified and synthesized including the female sex homone estrogen. In Alzheimer's Disease amyloid-beta protein on its way to brain deposition can also induce oxidative changes rendering nerve cells more vulnerable to additional insults. In addition, inflammatory mediators are attracted by amyloid deposits that can further speed up the generation of an oxidative micro-environment. Based on recent clinical data the use of a combination of various antioxidants might indeed be effective in preventing Alzheimer's Disease. Nevertheless, the exact molecular mechanisms and the real impact of oxidative stress on the development and progression of Alzheimer's Disease as well as of other neurodegenerative disorders still needs to be further investigated.