Skip to main content

Research Repository

Advanced Search

The contribution of an imbalanced redox signalling to neurological and neurodegenerative conditions

Steinert, Joern R.; Amal, Haitham


Haitham Amal


Nitric oxide and other redox active molecules such as oxygen free radicals provide essential signalling in diverse neuronal functions, but their excess production and insufficient scavenging induces cytotoxic redox stress which is associated with numerous neurodegenerative and neurological conditions. A further component of redox signalling is mediated by a homeostatic regulation of divalent metal ions, the imbalance of which contributes to neuronal dysfunction. Additional antioxidant molecules such as glutathione and enzymes such as super oxide dismutase are involved in maintaining a physiological redox status within neurons. When cellular processes are perturbed and generation of free radicals overwhelms the antioxidants capacity of the neurons, a resulting redox damage leads to neuronal dysfunction and cell death. Cellular sources for production of redox-active molecules may include NADPH oxidases, mitochondria, cytochrome P450 and nitric oxide (NO)-generating enzymes, such as endothelial, neuronal and inducible NO synthases. Several neurodegenerative and developmental neurological conditions are associated with an imbalanced redox state as a result of neuroinflammatory processes leading to nitrosative and oxidative stress. Ongoing research aims at understanding the causes and consequences of such imbalanced redox homeostasis and its role in neuronal dysfunction.


Steinert, J. R., & Amal, H. (2023). The contribution of an imbalanced redox signalling to neurological and neurodegenerative conditions. Free Radical Biology and Medicine, 194, 71-83.

Journal Article Type Review
Acceptance Date Nov 22, 2022
Online Publication Date Nov 24, 2022
Publication Date 2023-01
Deposit Date Nov 25, 2022
Publicly Available Date Nov 25, 2023
Journal Free Radical Biology and Medicine
Print ISSN 0891-5849
Electronic ISSN 1873-4596
Publisher Elsevier
Peer Reviewed Peer Reviewed
Volume 194
Pages 71-83
Keywords Physiology (medical); Biochemistry
Public URL
Publisher URL