Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer’s Disease
Mast cell activation plays an important role in stress-mediated disease pathogenesis. Chronic stress cause or exacerbate aging and age-dependent neurodegenerative diseases. The severity of inflammatory diseases is worsened by the stress. Mast cell activation-dependent inflammatory mediators augment...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2019-02-01
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| Series: | Frontiers in Cellular Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/article/10.3389/fncel.2019.00054/full |
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| author | Duraisamy Kempuraj Duraisamy Kempuraj Shireen Mentor Ramasamy Thangavel Ramasamy Thangavel Mohammad E. Ahmed Mohammad E. Ahmed Govindhasamy Pushpavathi Selvakumar Govindhasamy Pushpavathi Selvakumar Sudhanshu P. Raikwar Sudhanshu P. Raikwar Iuliia Dubova Iuliia Dubova Smita Zaheer Shankar S. Iyer Shankar S. Iyer Asgar Zaheer Asgar Zaheer |
| author_facet | Duraisamy Kempuraj Duraisamy Kempuraj Shireen Mentor Ramasamy Thangavel Ramasamy Thangavel Mohammad E. Ahmed Mohammad E. Ahmed Govindhasamy Pushpavathi Selvakumar Govindhasamy Pushpavathi Selvakumar Sudhanshu P. Raikwar Sudhanshu P. Raikwar Iuliia Dubova Iuliia Dubova Smita Zaheer Shankar S. Iyer Shankar S. Iyer Asgar Zaheer Asgar Zaheer |
| author_sort | Duraisamy Kempuraj |
| collection | DOAJ |
| description | Mast cell activation plays an important role in stress-mediated disease pathogenesis. Chronic stress cause or exacerbate aging and age-dependent neurodegenerative diseases. The severity of inflammatory diseases is worsened by the stress. Mast cell activation-dependent inflammatory mediators augment stress associated pain and neuroinflammation. Stress is the second most common trigger of headache due to mast cell activation. Alzheimer’s disease (AD) is a progressive irreversible neurodegenerative disease that affects more women than men and woman’s increased susceptibility to chronic stress could increase the risk for AD. Modern life-related stress, social stress, isolation stress, restraint stress, early life stress are associated with an increased level of neurotoxic beta amyloid (Aβ) peptide. Stress increases cognitive dysfunction, generates amyloid precursor protein (APP), hyperphosphorylated tau, neurofibrillary tangles (NFTs), and amyloid plaques (APs) in the brain. Stress-induced Aβ persists for years and generates APs even several years after the stress exposure. Stress activates hypothalamic-pituitary adrenal (HPA) axis and releases corticotropin-releasing hormone (CRH) from hypothalamus and in peripheral system, which increases the formation of Aβ, tau hyperphosphorylation, and blood-brain barrier (BBB) disruption in the brain. Mast cells are implicated in nociception and pain. Mast cells are the source and target of CRH and other neuropeptides that mediate neuroinflammation. Microglia express receptor for CRH that mediate neurodegeneration in AD. However, the exact mechanisms of how stress-mediated mast cell activation contribute to the pathogenesis of AD remains elusive. This mini-review highlights the possible role of stress and mast cell activation in neuroinflammation, BBB, and tight junction disruption and AD pathogenesis. |
| first_indexed | 2024-12-21T19:05:25Z |
| format | Article |
| id | doaj.art-47a3aa91d7b045919e13565e7aaaa4ab |
| institution | Directory Open Access Journal |
| issn | 1662-5102 |
| language | English |
| last_indexed | 2024-12-21T19:05:25Z |
| publishDate | 2019-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cellular Neuroscience |
| spelling | doaj.art-47a3aa91d7b045919e13565e7aaaa4ab2022-12-21T18:53:21ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022019-02-011310.3389/fncel.2019.00054448252Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer’s DiseaseDuraisamy Kempuraj0Duraisamy Kempuraj1Shireen Mentor2Ramasamy Thangavel3Ramasamy Thangavel4Mohammad E. Ahmed5Mohammad E. Ahmed6Govindhasamy Pushpavathi Selvakumar7Govindhasamy Pushpavathi Selvakumar8Sudhanshu P. Raikwar9Sudhanshu P. Raikwar10Iuliia Dubova11Iuliia Dubova12Smita Zaheer13Shankar S. Iyer14Shankar S. Iyer15Asgar Zaheer16Asgar Zaheer17Harry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesHarry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesHarry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesHarry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesHarry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesHarry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesHarry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesHarry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs, Columbia, MO, United StatesDepartment of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United StatesMast cell activation plays an important role in stress-mediated disease pathogenesis. Chronic stress cause or exacerbate aging and age-dependent neurodegenerative diseases. The severity of inflammatory diseases is worsened by the stress. Mast cell activation-dependent inflammatory mediators augment stress associated pain and neuroinflammation. Stress is the second most common trigger of headache due to mast cell activation. Alzheimer’s disease (AD) is a progressive irreversible neurodegenerative disease that affects more women than men and woman’s increased susceptibility to chronic stress could increase the risk for AD. Modern life-related stress, social stress, isolation stress, restraint stress, early life stress are associated with an increased level of neurotoxic beta amyloid (Aβ) peptide. Stress increases cognitive dysfunction, generates amyloid precursor protein (APP), hyperphosphorylated tau, neurofibrillary tangles (NFTs), and amyloid plaques (APs) in the brain. Stress-induced Aβ persists for years and generates APs even several years after the stress exposure. Stress activates hypothalamic-pituitary adrenal (HPA) axis and releases corticotropin-releasing hormone (CRH) from hypothalamus and in peripheral system, which increases the formation of Aβ, tau hyperphosphorylation, and blood-brain barrier (BBB) disruption in the brain. Mast cells are implicated in nociception and pain. Mast cells are the source and target of CRH and other neuropeptides that mediate neuroinflammation. Microglia express receptor for CRH that mediate neurodegeneration in AD. However, the exact mechanisms of how stress-mediated mast cell activation contribute to the pathogenesis of AD remains elusive. This mini-review highlights the possible role of stress and mast cell activation in neuroinflammation, BBB, and tight junction disruption and AD pathogenesis.https://www.frontiersin.org/article/10.3389/fncel.2019.00054/fullAlzheimer’s diseaseamyloid plaqueschronic stresscorticotropin releasing hormonemast cellsneurodegenerative disease |
| spellingShingle | Duraisamy Kempuraj Duraisamy Kempuraj Shireen Mentor Ramasamy Thangavel Ramasamy Thangavel Mohammad E. Ahmed Mohammad E. Ahmed Govindhasamy Pushpavathi Selvakumar Govindhasamy Pushpavathi Selvakumar Sudhanshu P. Raikwar Sudhanshu P. Raikwar Iuliia Dubova Iuliia Dubova Smita Zaheer Shankar S. Iyer Shankar S. Iyer Asgar Zaheer Asgar Zaheer Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer’s Disease Frontiers in Cellular Neuroscience Alzheimer’s disease amyloid plaques chronic stress corticotropin releasing hormone mast cells neurodegenerative disease |
| title | Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer’s Disease |
| title_full | Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer’s Disease |
| title_fullStr | Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer’s Disease |
| title_full_unstemmed | Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer’s Disease |
| title_short | Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer’s Disease |
| title_sort | mast cells in stress pain blood brain barrier neuroinflammation and alzheimer s disease |
| topic | Alzheimer’s disease amyloid plaques chronic stress corticotropin releasing hormone mast cells neurodegenerative disease |
| url | https://www.frontiersin.org/article/10.3389/fncel.2019.00054/full |
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