[Estrogen: regulation of amyloid-beta protein metabolism and attenuation of amyloid-beta protein neurotoxicity]

Abstract

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.