: how does Aβ affects our body?
In order to reduce the social and economic burden, therapeutic methods to ND, such as AD and PD, should be developed [1]. Since the presence and aggregation of amyloidogenic proteins, Aβ, tau, and α-Syn, could be major causes of the onset and progression of AD and PD [2], it is necessary to control the production, aggregation, and degrading process of the proteins to care the diseases. Based on the published reports we summarized above, regulating the activity/expression of ADE by short peptide and/or chemical agents could be a promising strategy to treat AD and PD; modulation of the expression and/or activity of NEP, IDE, AEP, and ADAM10 presented the clearance of amyloid deposits and improvement of cognitive deficits in vivo. The negative effect caused by inducing the activity of ADE could occur; however, the clearance of amyloidogenic proteins may result in a relatively good way to care AD and PD. In addition, it is essential to consider multiple risk factors due to the causes of the diseases that vary. Therefore, recently, various multifunctional (multitarget) small molecules have been invented to control the actions of those amyloidogenic proteins with other risk factors of AD and PD (i.e., metal ions and reactive oxygen species) [2], but most of them do not contain the capability to adjust the actions of ADE. A combination of previously developed molecules with the chemical agents which can upregulate the expression and/or activity of ADE could be the key to the success of treatment of ND, particularly AD and PD.
question: how does Aβ affects our body?
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