Delinda A. Johnson

TL;DR: It is shown that Nrf2 overexpression can reengineer neurons to express this glial pathway and enhance antioxidant gene expression and protect fully cocultured naive neurons from oxidative glutamate toxicity associated with glutathione (GSH) depletion.

TL;DR: This work hypothesizes that Nrf2–ARE activation is a novel neuroprotective pathway that confers resistance to a variety of oxidative, stress‐related, neurodegenerative insults and transplanted NRF2‐overexpressing astrocytes into the mouse striatum prior to lesioning with malonate to lead to dramatic protection against malonated neurotoxicity.

TL;DR: Stark results indicate that Nrf2 expression restricted to astrocytes is sufficient to protect against MPTP andAstrocytic modulation of the NRF2-ARE pathway is a promising target for therapeutics aimed at reducing or preventing neuronal death in PD.

TL;DR: Strikingly, the change in neuronal gene expression after tBHQ treatment was dependent on Nrf2 activity in the astrocytes, suggesting that NRF2-dependent genetic changes alter neuron–glia interactions resulting in neuroprotection.

TL;DR: The widespread nature of NRF2 may have an important therapeutic potential, allowing prevention of carcinogenesis and neurodegenerative diseases, and is supported by microarray data indicating the protective role of Nrf2 is conveyed through both known ARE‐driven genes and novel cell type‐specific genes.