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Related Experiment Video

Updated: May 10, 2026

Real Time Monitoring of Intracellular Bile Acid Dynamics Using a Genetically Encoded FRET-based Bile Acid Sensor

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Published on: January 4, 2016

Developing BACE-1 inhibitors for FXS.

Cara J Westmark¹, Elizabeth M Berry-Kravis, Chrysanthy Ikonomidou

¹Department of Neurology, University of Wisconsin Madison, WI, USA.

Frontiers in Cellular Neuroscience

|June 12, 2013

Summary

This summary is machine-generated.

Fragile X syndrome (FXS) may benefit from Alzheimer's disease (AD) drugs. Targeting amyloid precursor protein (APP) and BACE-1 may restore synaptic balance in FXS patients.

Keywords:

Alzheimer’s disease BACE-1 amyloid-beta fragile X syndrome mGluR5

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Published on: December 21, 2019

Area of Science:

Neuroscience
Genetics
Pharmacology

Background:

Fragile X syndrome (FXS) is a genetic disorder with limited treatment options.
FXS involves overactive metabotropic glutamate receptor 5 signaling, leading to synaptic protein overexpression.
Amyloid precursor protein (APP) and amyloid-beta are overexpressed in FXS, similar to Alzheimer's disease (AD).

Purpose of the Study:

To explore the potential of AD therapeutics for FXS treatment.
To investigate if modulating APP and its metabolites can be a viable strategy for FXS.

Main Methods:

Reviewing existing research on FXS and AD.
Identifying potential drug targets common to both diseases, specifically APP and BACE-1.
Considering the use of acetyltransferase inhibitors to reduce BACE-1 activity.

Main Results:

Excessive APP and amyloid-beta are implicated in FXS pathophysiology.
Pharmaceuticals targeting APP and BACE-1 in AD research show promise for FXS.

Conclusions:

Modulating APP catabolites via BACE-1 inhibition is a potential therapeutic avenue for FXS.
Repurposing AD drugs could offer new hope for treating FXS.