Published online Nov 27, 2020. doi: 10.4331/wjbc.v11.i3.99
Peer-review started: June 4, 2020
First decision: July 4, 2020
Revised: July 10, 2020
Accepted: September 18, 2020
Article in press: September 18, 2020
Published online: November 27, 2020
Processing time: 160 Days and 2.3 Hours
X-linked adrenoleukodystrophy (X-ALD), an inborn error of peroxisomal β-oxidation, is caused by defects in the ATP Binding Cassette Subfamily D Member 1 (ABCD1) gene. X-ALD patients may be asymptomatic or present with several clinical phenotypes varying from severe to mild, severe cerebral adrenoleuko-dystrophy to mild adrenomyeloneuropathy (AMN). Although most female heterozygotes present with AMN-like symptoms after 60 years of age, occasional cases of females with the cerebral form have been reported. Phenotypic variability has been described within the same kindreds and even among monozygotic twins. There is no association between the nature of ABCD1 mutation and the clinical phenotypes, and the molecular basis of phenotypic variability in X-ALD is yet to be resolved. Various genetic, epigenetic, and environmental influences are speculated to modify the disease onset and severity. In this review, we summarize the observations made in various studies investigating the potential modifying factors regulating the clinical manifestation of X-ALD, which could help understand the pathogenesis of the disease and develop suitable therapeutic strategies.
Core Tip: The monogenic peroxisomal disorder, X-linked adrenoleukodystrophy (X-ALD), presents with different clinical phenotypes. The molecular basis for the phenotypic variation has yet to be resolved and is considered to be influenced by genetic, epigenetic, cellular, or environmental factors. We herein discuss the various modifying factors, which can potentially alter the phenotypic presentation of X-ALD.