Fig. 2

Therapeutic Targets in X-ALD Linked to ABCD1 Mutations. The mutation disrupts normal ABCD1 functioning, leading to decreased β-oxidation of very-long-chain fatty acids (VLCFAs). This reduction leads to the accumulation of VLCFA-CoAs and thus an increase in concentrations of free VLCFAs. The accumulation of VLCFAs triggers oxidative stress and cellular damage. The figure indicates intervention points that must be addressed when developing treatments to target the underlying biochemical abnormalities in X-ALD. ROS = reactive oxygen species. The figure is created with BioRender.com