Developing BACE-1 inhibitors for FXS

doi:10.3389/fncel.2013.00077

Developing BACE-1 inhibitors for FXS

2013-01-01

8

OA

AI

C

Cara J. Westmark *

E

Elizabeth Berry‐Kravis

C

Chrysanthy Ikonomidou

DOI：10.3389/fncel.2013.00077

原文链接

查看原文

摘要

En 中文

Fragile X syndrome (FXS) is a debilitating genetic disorder with no cure and few therapeutic options. Excessive signaling through metabotropic glutamate receptor 5 in FXS leads to increased translation of numerous synaptic proteins and exaggerated long-term depression. Two of the overexpressed proteins are amyloid-beta protein precursor (APP) and its metabolite amyloid-beta, which have been well-studied in Alzheimer's disease (AD). Here we discus the possibility that pharmaceuticals under study for the modulation of these proteins in AD might be viable therapeutic strategies for FXS. Specifically, a recently identified acetyltransferase inhibitor that reduces the levels and activity of beta-site APP cleaving enzyme (BACE-1) has strong potential to attenuate BACE-1 activity and maintain homeostatic levels APP catabolites in FXS.

Keyword:

fragile X syndrome

BACE-1

Alzheimer's disease

amyloid-beta

mGluR(5)

Developing BACE-1 inhibitors for FXS

摘要

AI总结

期刊

机构

引用论文