[Estrogen: regulation of amyloid-beta protein metabolism and attenuation of amyloid-beta protein neurotoxicity].
Alzheimer's disease(AD) is characterized by two pathological lesions: intracellular neurofibrillary tangles and extracellular amyloid deposits. Recently researchers accept the amyloid hypothesis which states that accumulation of amyloid-beta protein (A beta) in the brain is the primary causal factor driving AD pathogenesis. Since estrogen has been demonstrated to be able to modulate the metabolism of amyloid-beta precursor protein, reduce the generation of A beta, ameliorate the injury caused by inflammation and oxidative stress, and exhibit an antiapoptotic effect, it is considered that estrogen is of benefit to the prevention of AD.
Zhang
Sun
S
Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032.
Yao
Tai
T
D000544:Alzheimer Disease / Q000378:metabolism*; D000682:Amyloid / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism; D004967:Estrogens / Q000494:pharmacology / Q000502:physiology*; D006801:Humans; D016874:Neurofibrillary Tangles / Q000378:metabolism; D018696:Neuroprotective Agents / Q000378:metabolism
D000682:Amyloid; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D004967:Estrogens; D018696:Neuroprotective Agents