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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Published in | Frontiers in cellular neuroscience Vol. 13; p. 54 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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Frontiers Research Foundation
19.02.2019
Frontiers Media S.A |
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Abstract | 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. |
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AbstractList | 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. 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 after several years stress of 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. |
Author | Dubova, Iuliia Iyer, Shankar S Kempuraj, Duraisamy Thangavel, Ramasamy Mentor, Shireen Selvakumar, Govindhasamy Pushpavathi Ahmed, Mohammad E Zaheer, Smita Zaheer, Asgar Raikwar, Sudhanshu P |
AuthorAffiliation | 1 Harry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs , Columbia, MO , United States 2 Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri , Columbia, MO , United States |
AuthorAffiliation_xml | – name: 1 Harry S. Truman Memorial Veterans’ Hospital (VA), U.S. Department of Veterans Affairs , Columbia, MO , United States – name: 2 Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri , Columbia, MO , United States |
Author_xml | – sequence: 1 givenname: Duraisamy surname: Kempuraj fullname: Kempuraj, Duraisamy organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 2 givenname: Shireen surname: Mentor fullname: Mentor, Shireen organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 3 givenname: Ramasamy surname: Thangavel fullname: Thangavel, Ramasamy organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 4 givenname: Mohammad E surname: Ahmed fullname: Ahmed, Mohammad E organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 5 givenname: Govindhasamy Pushpavathi surname: Selvakumar fullname: Selvakumar, Govindhasamy Pushpavathi organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 6 givenname: Sudhanshu P surname: Raikwar fullname: Raikwar, Sudhanshu P organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 7 givenname: Iuliia surname: Dubova fullname: Dubova, Iuliia organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 8 givenname: Smita surname: Zaheer fullname: Zaheer, Smita organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 9 givenname: Shankar S surname: Iyer fullname: Iyer, Shankar S organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States – sequence: 10 givenname: Asgar surname: Zaheer fullname: Zaheer, Asgar organization: Department of Neurology and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, United States |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30837843$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Copyright © 2019 Kempuraj, Mentor, Thangavel, Ahmed, Selvakumar, Raikwar, Dubova, Zaheer, Iyer and Zaheer. 2019 Kempuraj, Mentor, Thangavel, Ahmed, Selvakumar, Raikwar, Dubova, Zaheer, Iyer and Zaheer |
Copyright_xml | – notice: 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: Copyright © 2019 Kempuraj, Mentor, Thangavel, Ahmed, Selvakumar, Raikwar, Dubova, Zaheer, Iyer and Zaheer. 2019 Kempuraj, Mentor, Thangavel, Ahmed, Selvakumar, Raikwar, Dubova, Zaheer, Iyer and Zaheer |
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Keywords | neurodegenerative disease Alzheimer’s disease neuroinflammation chronic stress mast cells amyloid plaques corticotropin releasing hormone |
Language | English |
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Notes | Edited by: Kalpna Gupta, University of Minnesota, United States Reviewed by: Pio Conti, Università degli Studi G. d’Annunzio Chieti e Pescara, Italy; Mihir Gupta, University of California, San Diego, United States |
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Title | Mast Cells in Stress, Pain, Blood-Brain Barrier, Neuroinflammation and Alzheimer's Disease |
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