Abstract
Studies in animals showed that stress is associated with changes in hippocampal function and structure, an effect mediated through decreased neurogenesis, increased glucocorticoids, and/or decreased brain derived neurotrophic factor. Antidepressants and some anticonvulsants block the effects of stress and/or promote neurogenesis in animal studies. Patients with posttraumatic stress disorder (PTSD) have been shown to have smaller hippocampal volume on magnetic resonance imaging and deficits in hippocampal-based memory. Symptom activation is associated with decreased anterior cingulate and medial prefrontal function, which is proposed as the neural correlate of a failure of extinction seen in these patients. Treatment with antidepressants and phenytoin reverse hippocampal volume reduction and memory deficits in PTSD patients, suggesting that these agents may promote neurogenesis in humans.
Keywords: Corticotropin-releasing factor (CRF), MRI, neuroimaging, memory research, benzodiazepine
CNS & Neurological Disorders - Drug Targets
Title: Stress and Brain Atrophy
Volume: 5 Issue: 5
Author(s): J. Douglas Bremner
Affiliation:
Keywords: Corticotropin-releasing factor (CRF), MRI, neuroimaging, memory research, benzodiazepine
Abstract: Studies in animals showed that stress is associated with changes in hippocampal function and structure, an effect mediated through decreased neurogenesis, increased glucocorticoids, and/or decreased brain derived neurotrophic factor. Antidepressants and some anticonvulsants block the effects of stress and/or promote neurogenesis in animal studies. Patients with posttraumatic stress disorder (PTSD) have been shown to have smaller hippocampal volume on magnetic resonance imaging and deficits in hippocampal-based memory. Symptom activation is associated with decreased anterior cingulate and medial prefrontal function, which is proposed as the neural correlate of a failure of extinction seen in these patients. Treatment with antidepressants and phenytoin reverse hippocampal volume reduction and memory deficits in PTSD patients, suggesting that these agents may promote neurogenesis in humans.
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Cite this article as:
Douglas Bremner J., Stress and Brain Atrophy, CNS & Neurological Disorders - Drug Targets 2006; 5 (5) . https://dx.doi.org/10.2174/187152706778559309
DOI https://dx.doi.org/10.2174/187152706778559309 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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