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01 August 2005

Possible use of adaptation to hypoxia in Alzheimer's disease: a hypothesis.

Igor Malyshev, Frederik Wiegant, Svetlana Mashina, Vladimir Torshin, Anna Goryacheva, Inna Khomenko, Sergey Kruglov, Dmitry Pokidyshev, Elena Popkova, Maya Pshennikova, Mariya Vlasova, Olga Zelenina, Eugenia Manukhina

Med Sci Monit 2005; 11(8): HY36-38 :: ID: 199662

Abstract

Disorders in memory and other cognitive functions in Alzheimer's disease(AD) may result from an exhaustion of adaptive reserves in the brain. Therefore it is a challenge tofind methods to increase the adaptive reserve of the organism to combat AD. Excitotoxicity, Ca2(+) homeostasisdisruptions, oxidative stress, disturbed synthesis of NO, and impaired cerebral circulation are suggestedas key pathogenic factors of AD. At present it appears that stimulation of the self-defense systems inneural cells is a promising strategy in restricting the progression of AD. These systems include thoseof antioxidants, heat shock proteins (HSPs), NO, and other so-called stress-limiting systems. Non-drugactivation of these systems can be achieved most efficiently by adaptation of the organism to environmentalchallenges, such as hypoxia. In this paper the potential of methods used in adaptive medicine is explored.The protective mechanisms of adaptation to hypoxia may be related to restriction of oxidative stressin the hippocampus, the limitation of a decrease in NO production induced by b-amyloid, and increaseddensity of the vascular network in the brain. In this review we selectively present data that supportthe idea that adaptation to hypoxia is a possible non-drug means in the prevention of AD. In our opinionthis strategy may provide a break-through in the clinical approach of this disease.

Keywords: Alzheimer Disease - metabolism, Anoxia - metabolism, Adaptation, Physiological, Alzheimer Disease - therapy, Anoxia - metabolism, Cerebrovascular Circulation, Environment, Free Radicals - metabolism, HSP70 Heat-Shock Proteins - metabolism, Models, Biological, Nitric Oxide - metabolism, Oxidation-Reduction

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Medical Science Monitor Basic Research eISSN: 2325-4416
Medical Science Monitor Basic Research eISSN: 2325-4416