Abstract
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and is associated with increased risk for ASD, anxiety, ADHD, and epilepsy. Although our understanding of FXS pathophysiology has improved, a lack of validated blood-based biomarkers of disease continues to impede bench-to-bedside efforts. As a biomarker target in FXS, amyloid-β (Aβ) precursor protein (APP) is best understood in the context of Alzheimer disease; there is a growing body of evidence suggesting that the molecule and its derivatives play a broader role in neuronal hyperexcitability, a characteristic of FXS.
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