Kelby M. Killoy

TL;DR: Several pathogenic mechanisms that have been proposed to explain astrocyte-mediated motor neuron death in ALS are discussed and examples of strategies that revert astroCyte- mediated motor neuron toxicity are reviewed to illustrate the therapeutic potential of astroicytes in ALS.

TL;DR: A growing body of evidence suggests the beneficial role of enhancing NAD+ availability in models of neurodegeneration and age-related diseases.

TL;DR: Results indicate that boosting NAD+ levels with the use of bioavailable precursors would be the preferred therapeutic strategy for ALS, and find altered expression of enzymes involved in NAD+ synthesis and decreased SIRT6 expression in the spinal cord of ALS patients, suggesting deficits of this neuroprotective pathway in the human pathology.

TL;DR: It is shown that increasing total NAD+ content in astrocytes leads to the activation of the transcription factor nuclear factor, erythroid‐derived 2, like 2 (Nfe212 or Nrf2) and up‐regulation of the antioxidant proteins heme oxygenase 1 (HO‐1) and sulfiredoxin 1 (SRXN1).

TL;DR: The data show that FABP7 overexpression directly promotes an NF‐κB‐driven pro‐inflammatory response in nontransgenic astrocytes that ultimately is detrimental for motor neuron survival and identifies FABp7 as a potential therapeutic target to preventAstrocyte‐mediated motor neuron toxicity in ALS.