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[DOI] [PMC free article] [PubMed] [Google Scholar] 90.Er H

High concentrations of ROS can oxidize mitochondrial proteins, lipids, and nucleic acids, cause cell dysfunction, damage the ability of cells to maintain energy levels, cause energy exhaustion, damage and death of neurons, and change the excitability of neurons, thus reducing the threshold of seizures (6, 7)

Cell surface phenotypes of acute leukemias at Memorial Hospital

Since mitochondrial defects have been broadly observed in many different diseases in which TDP-43 pathology is commonly detected, and because mitochondria are crucially important for maintaining metabolomic homeostasis, one of the key questions that remains unanswered is: What are the metabolomic changes that occur with respect to TDP-43 pathology? We investigated the metabolomic perturbations that occur in the motor cortex of prp-TDP-43 A315T mice, a mouse model which recapitulates many aspects of TDP-43 pathology observed in ALS and ALS/FTLD patients 19

Deshane et al., 2003