Unraveling the regulatory nexus of aggrephagy in ALS: identification of novel candidate biomarkers and molecular triggers

Bioinformatics analysis of the alterations in neuregulin 1/4 and their correlation with ferroptosis-related genes in amyotrophic lateral sclerosis

Background & Objective: Dysregulation of the ErbB4 signaling pathway has been implicated as a significant factor in the pathogenesis of amyotrophic lateral sclerosis （ALS）, with neuregulin 1 (NRG1) and NRG4 serving as key regulatory ligands of ErbB4. This study mainly employs bioinformatics approaches to investigate...

In silico evaluation of deleterious nsSNPs in SOD1 and TARDBP genes associated with amyotrophic lateral sclerosis

Network and pathway analyses highlighted SOD1 and TARDBP as key nodes in ALS-related mechanisms, such as oxidative stress, RNA metabolism, proteostasis, and mitochondrial impairment, and network-based functions were combined.

Cuproptosis-associated genes DLD, ULK2, CCL8, and CCS link metabolic and immunological dysfunction in Parkinson’s disease: a multi-omics study

It is suggested that dysregulation of cuproptosis-associated hub genes is associated with cell-type-specific pathological alterations in PD, rather than demonstrating a direct causal or synergistic regulatory mechanism.

Transcriptomic profiling and structural characterization reveal UQCRC1 and COX4I1 as key mitochondrial regulators associated with oxidative stress in multiple sclerosis.

It is demonstrated that mitochondrial respiratory chain-related pathways, particularly those involving complexes III and IV, are consistently associated with the transcriptomic alterations observed in multiple sclerosis, providing evidence that mitochondrial bioenergetics and redox homeostasis may contribute to MS path...

Dysregulation of mitochondrial bioenergetics, RNA processing, and cellular stress responses in FUS-ALS: a multi-dataset transcriptomic perspective

Integrating Target Prediction and Transcriptomic Analysis Identifies the AKR1C2-KRT8 Axis in Rotenone-Induced Dopaminergic Neuron Injury.

KRT8 re‑expression reversed the protective effects of AKR1C2 knockdown, while KRT8 knockdown reversed AKR1C2 overexpression‑induced impairments, collectively confirming the causal role of the AKR1C2-KRT8 axis.