TY - CHAP
T1 - Protective effects of adaptation to hypoxia in experimental Alzheimer's disease
AU - Manukhina, Eugenia B.
AU - Goryacheva, Anna V.
AU - Pshennikova, Maya G.
AU - Malyshev, Igor Yu
AU - Mallet, Robert T.
AU - Downey, H. Fred
PY - 2014/5/1
Y1 - 2014/5/1
N2 - Alzheimer's disease (AD) is characterized by formation of amyloid plaques, intracellular neurofibrillary tangles, and cell death in the brain, resulting in progressive loss of memory and cognitive ability. Efficacy of drugs currently used for prevention and treatment of AD is limited by the fact that each drug influences only a single step of the pathogenesis in AD, and the drugs affect both damaged and normal cells. This is why major attention is now paid to nonpharmacological means that may enhance the adaptive capacity and mobilize the self-defense systems of the body. This chapter focuses on protective effects of adaptation to intermittent hypobaric hypoxia on the memory, brain neurons, and cerebral blood vessels in rats with experimental AD induced by intracerebral injections of beta-amyloid (Aß) and mechanisms of these protective effects. Special attention is paid to intermittent hypobaric hypoxia's ability to limit early stages in AD pathogenesis, such as nitrosative and oxidative stress in brain tissue. Presented data show that adaptation to hypoxia may be a promising approach to prevention and treatment of AD.
AB - Alzheimer's disease (AD) is characterized by formation of amyloid plaques, intracellular neurofibrillary tangles, and cell death in the brain, resulting in progressive loss of memory and cognitive ability. Efficacy of drugs currently used for prevention and treatment of AD is limited by the fact that each drug influences only a single step of the pathogenesis in AD, and the drugs affect both damaged and normal cells. This is why major attention is now paid to nonpharmacological means that may enhance the adaptive capacity and mobilize the self-defense systems of the body. This chapter focuses on protective effects of adaptation to intermittent hypobaric hypoxia on the memory, brain neurons, and cerebral blood vessels in rats with experimental AD induced by intracerebral injections of beta-amyloid (Aß) and mechanisms of these protective effects. Special attention is paid to intermittent hypobaric hypoxia's ability to limit early stages in AD pathogenesis, such as nitrosative and oxidative stress in brain tissue. Presented data show that adaptation to hypoxia may be a promising approach to prevention and treatment of AD.
UR - http://www.scopus.com/inward/record.url?scp=84899668689&partnerID=8YFLogxK
U2 - 10.1007/978-1-4471-2906-6_13
DO - 10.1007/978-1-4471-2906-6_13
M3 - Chapter
AN - SCOPUS:84899668689
SN - 1447129059
SN - 9781447129059
SP - 155
EP - 171
BT - Intermittent Hypoxia and Human Diseases
PB - Springer-Verlag London Ltd
ER -