老年痴呆症,脑细胞的退化原因,被称为进行性神经退行性疾病,并且似乎具有异质性病因,主要侧重于淀粉样蛋白级联和高磷酸化tau级联假说,直接与称为酶的大分子相连,如β-和γ-分泌酶,胆碱酯酶,转谷氨酰胺酶,和糖原合成酶激酶(GSK-3),细胞周期蛋白依赖性激酶(cdk-5),微管亲和调节激酶(MARK)。上述酶的催化活性是认知缺陷的结果,记忆障碍和突触功能障碍和丧失,最终神经元死亡。然而,其他一些酶在大脑中降低到正常活动和水平时也会导致这些功能失调的事件,如α-分泌酶,蛋白激酶C,磷酸酶等;代谢成神经递质,酶,如单胺氧化酶(MAO),儿茶酚-O-甲基转移酶(COMT)等。或当酶通过其他机制如磷酸二酯酶降低脑核苷酸(cGMP和cAMP)水平时,这些异常可能发生,磷脂酶A2:PLA2与活性氧(ROS)产生等有关。在治疗方面,几项重要的临床试验正在进行中,通过针对不同的酶来开发治疗阿尔茨海默病的新疗法,如β-分泌酶抑制剂,GSK-3,MAO,磷酸二酯酶,PLA2、胆碱酯酶等,α-和γ-分泌酶活性调节剂和蛋白激酶C的激活剂,sirtuins等.在过去的几十年中,人们越来越关注阿尔茨海默病的发现和寻找新的推定和新的酶靶标。这里,我们审查功能,病理角色,和价值几乎所有的阿尔茨海默氏症相关的酶,解决治疗策略和预防方法治疗阿尔茨海默氏症。
Alzheimer\'s, a degenerative cause of the brain cells, is called as a progressive neurodegenerative disease and appears to have a heterogeneous etiology with main emphasis on amyloid-cascade and hyperphosphorylated tau-cascade hypotheses, that are directly linked with macromolecules called enzymes such as β- & γ-secretases, colinesterases, transglutaminases, and glycogen synthase kinase (GSK-3), cyclin-dependent kinase (cdk-5), microtubule affinity-regulating kinase (MARK). The catalytic activity of the above enzymes is the result of cognitive deficits, memory impairment and synaptic dysfunction and loss, and ultimately neuronal death. However, some other enzymes also lead to these dysfunctional events when reduced to their normal activities and levels in the brain, such as α- secretase, protein kinase C, phosphatases etc; metabolized to neurotransmitters, enzymes like monoamine oxidase (MAO), catechol-O-methyltransferase (COMT) etc. or these abnormalities can occur when enzymes act by other mechanisms such as phosphodiesterase reduces brain nucleotides (cGMP and cAMP) levels, phospholipase A2: PLA2 is associated with reactive oxygen species (ROS) production etc. On therapeutic fronts, several significant clinical trials are underway by targeting different enzymes for development of new therapeutics to treat Alzheimer\'s, such as inhibitors for β-secretase, GSK-3, MAO, phosphodiesterase, PLA2, cholinesterases etc, modulators of α- & γ-secretase activities and activators for protein kinase C, sirtuins etc. The last decades have perceived an increasing focus on findings and search for new putative and novel enzymatic targets for Alzheimer\'s. Here, we
review the functions, pathological roles, and worth of almost all the Alzheimer\'s associated enzymes that address to therapeutic strategies and preventive approaches for treatment of Alzheimer\'s.