Nrf2/ARE Signaling Pathway: Key Mediator in Oxidative Stress and Potential Therapeutic Target in ALS.
Source: Department of Neurology, Hannover Medical School, Hannover, Germany.
Nrf2 (pronounced “Nerf2) (nuclear erythroid 2-related factor 2) is a basic region leucine-zipper transcription factor. It binds to the antioxidant response element (ARE) and thereby regulates the expression of a large battery of genes involved in the cellular antioxidant and anti-inflammatory defence as well as mitochondrial protection.
(Translation: Nrf2 regulates the expression of genes, including antioxidant and anti-inflammatory ones.)
As oxidative stress, inflammation and mitochondrial dysfunctions have been identified as important pathomechanisms in amyotrophic lateral sclerosis (ALS), this signaling cascade has gained interest both with respect to ALS pathogenesis and therapy.
(Translation: Oxidative stress and inflammation are key factors in the pathology of ALS.)
Nrf2 and Keap1 expressions are reduced in motor neurons in postmortem ALS tissue.
Nrf2-activating compounds have shown therapeutic efficacy in the ALS mouse model and other neurodegenerative disease models.
Alterations in Nrf2 and Keap1 expression and dysregulation of the Nrf2/ARE signalling program could contribute to the chronic motor neuron degeneration in ALS and other neurodegenerative diseases.
Therefore, Nrf2 emerges as a key neuroprotective molecule in neurodegenerative diseases.
Our recent studies strongly support that the Nrf2/ARE signaling pathway is an important mediator of neuroprotection and therefore represents a promising target for development of novel therapies against ALS, Parkinson’s disease (PD), Huntington’s disease (HD), and Alzheimer’s disease (AD).
(Note from: Rebecca R. Riales, M.Ed., Ph.D., LPC-LPCC-NCC) It’s a “connect the dots” situation.
This article says that patients with neurodegenerative diseases including ALS are in great need of Nrf2 activation to protect and treat their nerves.
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