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Stress-induced oxidative changes in brain
José L M Madrigal1, Borja García-Bueno, Javier R Caso
1Department of Anesthesiology. University of Illinois, Chicago, Illinois 60657, USA. josem@uic.edu
CNS & Neurological Disorders Drug Targets
|November 1, 2006
Summary
Chronic stress damages the brain, causing hippocampal atrophy. This occurs via glucocorticoid release, excitotoxicity, and inflammatory responses involving TNFalpha and NFkappaB.
Area of Science:
- Neuroscience
- Stress Research
- Cellular Biology
Background:
- Stress impacts numerous bodily systems, with significant effects on the brain.
- The central nervous system (CNS) undergoes various processes under stress before irreversible damage occurs.
Purpose of the Study:
- To review the neurological effects of stress, focusing on the brain.
- To elucidate the molecular mechanisms linking stress to brain damage.
Main Methods:
- Review of existing literature on stress and brain function.
- Focus on the cascade of molecular events following stress exposure.
Main Results:
- Severe or chronic stress leads to hippocampal dendrite atrophy and reduced hippocampal size.
- Glucocorticoid release initiates neurotoxic pathways, including altered energy metabolism and increased extracellular glutamate.
- Stress activates TNFalpha convertase (TACE) and TNFalpha release, leading to NFkappaB activation.
- NFkappaB activation induces iNOS and COX2, contributing significantly to stress-induced neurological damage.
Conclusions:
- Stress triggers a cascade of molecular events in the brain, starting with glucocorticoid release.
- This cascade involves excitotoxicity and inflammatory mediators like TNFalpha and NFkappaB.
- The induction of iNOS and COX2 by NFkappaB is a key mechanism underlying stress-induced brain damage.
