雌激素对淀粉样β蛋白代谢的调节和毒性缓解

Estrogen: Regulation of Amyloid-beta Protein Metabolism and Attenuation of Amyloid-beta Protein Neurotoxicity

以淀粉样 β蛋白为主的老年斑胞外沉积和神经元内神经原纤维缠结 ,是阿尔采末病 (AD)特征性的病理学改变。近来 ,人们逐渐认可淀粉样蛋白假说 ,即认为淀粉样蛋白沉积是AD最初起因。研究人员正在寻找针对淀粉样 β蛋白沉积的药物 ,雌激素是其中之一。初步的工作证明 ,雌激素能够调节淀粉样 β蛋白前体代谢 ,减少淀粉样 β蛋白生成 ,也能够减轻淀粉样 β蛋白引起的免疫炎症反应、氧应激对细胞造成的损伤 。

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 (Aβ) 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 Aβ, 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.