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Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence

Journal of neuroinflammation, 2013-12, Vol.10 (1), p.142-142, Article 906 [Peer Reviewed Journal]

COPYRIGHT 2013 BioMed Central Ltd. ;2013 Najjar et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ;Copyright © 2013 Najjar et al.; licensee BioMed Central Ltd. 2013 Najjar et al.; licensee BioMed Central Ltd. ;ISSN: 1742-2094 ;EISSN: 1742-2094 ;DOI: 10.1186/1742-2094-10-142 ;PMID: 24289502

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Title:
Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence
Author: Najjar, Souhel ; Pearlman, Daniel M ; Devinsky, Orrin ; Najjar, Amanda ; Zagzag, David
Subjects: Animals ; Aquaporins ; Biomarkers ; Blood-brain barrier ; Blood-Brain Barrier - physiopathology ; Brain - blood supply ; Brain - physiopathology ; Brain research ; Capillary Permeability - physiology ; Comorbidity ; Depressive Disorder, Major - etiology ; Depressive Disorder, Major - physiopathology ; Dyes ; Endothelium ; Enzymes ; Epilepsy ; Health aspects ; Humans ; Inflammation ; Major depressive disorder ; Medical imaging ; Medicine ; Multiple sclerosis ; Neuroimmunomodulation - physiology ; Neuropathology ; Neurophysiology ; Neurosciences ; Nitric oxide ; NMR ; Nuclear magnetic resonance ; Oxidative stress ; Oxidative Stress - physiology ; Physiological aspects ; Review ; Risk factors ; Rodents ; Studies ; Tomography
Is Part Of: Journal of neuroinflammation, 2013-12, Vol.10 (1), p.142-142, Article 906
Description: About one-third of people with major depressive disorder (MDD) fail at least two antidepressant drug trials at 1 year. Together with clinical and experimental evidence indicating that the pathophysiology of MDD is multifactorial, this observation underscores the importance of elucidating mechanisms beyond monoaminergic dysregulation that can contribute to the genesis and persistence of MDD. Oxidative stress and neuroinflammation are mechanistically linked to the presence of neurovascular dysfunction with blood-brain barrier (BBB) hyperpermeability in selected neurological disorders, such as stroke, epilepsy, multiple sclerosis, traumatic brain injury, and Alzheimer's disease. In contrast to other major psychiatric disorders, MDD is frequently comorbid with such neurological disorders and constitutes an independent risk factor for morbidity and mortality in disorders characterized by vascular endothelial dysfunction (cardiovascular disease and diabetes mellitus). Oxidative stress and neuroinflammation are implicated in the neurobiology of MDD. More recent evidence links neurovascular dysfunction with BBB hyperpermeability to MDD without neurological comorbidity. We review this emerging literature and present a theoretical integration between these abnormalities to those involving oxidative stress and neuroinflammation in MDD. We discuss our hypothesis that alterations in endothelial nitric oxide levels and endothelial nitric oxide synthase uncoupling are central mechanistic links in this regard. Understanding the contribution of neurovascular dysfunction with BBB hyperpermeability to the pathophysiology of MDD may help to identify novel therapeutic and preventative approaches.
Publisher: England: BioMed Central Ltd
Language: English
Identifier: ISSN: 1742-2094
EISSN: 1742-2094
DOI: 10.1186/1742-2094-10-142
PMID: 24289502
Source: GFMER Free Medical Journals
MEDLINE
PubMed Central
Springer Nature OA/Free Journals
ROAD: Directory of Open Access Scholarly Resources
ProQuest Central
DOAJ Directory of Open Access Journals

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Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence

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