Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2008 Nov 15;45(10):1375-83.
doi: 10.1016/j.freeradbiomed.2008.09.001. Epub 2008 Sep 13.

Nrf2-induced Antioxidant Protection: A Promising Target to Counteract ROS-mediated Damage in Neurodegenerative Disease?

Affiliations
Review

Nrf2-induced Antioxidant Protection: A Promising Target to Counteract ROS-mediated Damage in Neurodegenerative Disease?

Helga E de Vries et al. Free Radic Biol Med. .

Abstract

Neurodegenerative diseases share various pathological features, such as accumulation of aberrant protein aggregates, microglial activation, and mitochondrial dysfunction. These pathological processes are associated with generation of reactive oxygen species (ROS), which cause oxidative stress and subsequent damage to essential molecules, such as lipids, proteins, and DNA. Hence, enhanced ROS production and oxidative injury play a cardinal role in the onset and progression of neurodegenerative disorders. To maintain a proper redox balance, the central nervous system is endowed with an antioxidant defense mechanism consisting of endogenous antioxidant enzymes. Expression of most antioxidant enzymes is tightly controlled by the antioxidant response element (ARE) and is activated by nuclear factor E2-related factor 2 (Nrf2). In past years reports have highlighted the protective effects of Nrf2 activation in reducing oxidative stress in both in vitro and in vivo models of neurodegenerative disorders. Here we provide an overview of the involvement of ROS-induced oxidative damage in Alzheimer's disease, Parkinson's disease, and Huntington's disease and we discuss the potential therapeutic effects of antioxidant enzymes and compounds that activate the Nrf2-ARE pathway.

Similar articles

See all similar articles

Cited by 127 articles

See all "Cited by" articles

Publication types

MeSH terms

Feedback