Ying-Hao Chen

1 Introduction Several cell death pathways contribute to the development and progression of both acute kidney injury and chronic kidney disease (1). Among these pathways, ferroptosis can be distinguished by its dependence on iron-driven lipid peroxidation that ultimately leads to oxidative damage to cell membranes, which then drives the pathogenesis of multiple disease states (2). Ferroptosis is a distinct form of regulated cell death and is different from apoptosis, autophagy, and necrosis.

Adrenoleukodystrophy (ALD) is a rare and progressive neurogenetic disease that may manifest disparate symptoms. The present study aims at investigating the role of ataxic variant of ALD (AVALD) in patients with adult-onset cerebellar ataxia, as well as characterizing their clinical features that distinguish AVALD from other cerebellar ataxias. Mutations in the ATP binding cassette subfamily D member 1 gene (ABCD1) were ascertained in 516 unrelated patients with ataxia.