The Migraine Attack as a Homeostatic, Neuroprotective Response to Brain Oxidative Stress: Preliminary Evidence for a Theory
| Autor: | Jonathan M. Borkum |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Migraine Disorders medicine.disease_cause Neuroprotection 03 medical and health sciences 0302 clinical medicine Neurotrophic factors medicine Animals Homeostasis Humans Platelet activation Neurogenic inflammation business.industry Cortical Spreading Depression Brain Platelet Activation medicine.disease Oxidative Stress Neuroprotective Agents 030104 developmental biology Neurology Migraine Mitochondrial biogenesis Cortical spreading depression Neurology (clinical) business Neuroscience 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Headache: The Journal of Head and Face Pain. 58:118-135 |
| ISSN: | 0017-8748 |
| DOI: | 10.1111/head.13214 |
| Popis: | Background Previous research has suggested that migraineurs show higher levels of oxidative stress (lipid peroxides) between migraine attacks and that migraine triggers may further increase brain oxidative stress. Oxidative stress is transduced into a neural signal by the TRPA1 ion channel on meningeal pain receptors, eliciting neurogenic inflammation, a key event in migraine. Thus, migraines may be a response to brain oxidative stress. Results In this article, a number of migraine components are considered: cortical spreading depression, platelet activation, plasma protein extravasation, endothelial nitric oxide synthesis, and the release of serotonin, substance P, calcitonin gene-related peptide, and brain-derived neurotrophic factor. Evidence is presented from in vitro research and animal and human studies of ischemia suggesting that each component has neuroprotective functions, decreasing oxidant production, upregulating antioxidant enzymes, stimulating neurogenesis, preventing apoptosis, facilitating mitochondrial biogenesis, and/or releasing growth factors in the brain. Feedback loops between these components are described. Limitations and challenges to the model are discussed. Conclusions The theory is presented that migraines are an integrated defensive, neuroprotective response to brain oxidative stress. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text