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      Neuroinflammation, Pain and Depression: An Overview of the Main Findings

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          Abstract

          Chronic pain is a serious public health problem with a strong affective-motivational component that makes it difficult to treat. Most patients with chronic pain suffer from severe depression; hence, both conditions coexist and exacerbate one another. Brain inflammatory mediators are critical for maintaining depression-pain syndrome and could be substrates for it. The goal of our paper was to review clinical and preclinical findings to identify the neuroinflammatory profile associated with the cooccurrence of pain and depression. In addition, we aimed to explore the regulatory effect of neuronal reorganization on the inflammatory response in pain and depression. We conducted a quantitative review supplemented by manual screening. Our results revealed inflammatory signatures in different preclinical models and clinical articles regarding depression-pain syndrome. We also identified that improvements in depressive symptoms and amelioration of pain can be modulated through direct targeting of inflammatory mediators, such as cytokines and molecular inhibitors of the inflammatory cascade. Additionally, therapeutic targets that improve and regulate the synaptic environment and its neurotransmitters may act as anti-inflammatory compounds, reducing local damage-associated molecular patterns and inhibiting the activation of immune and glial cells. Taken together, our data will help to better elucidate the neuroinflammatory profile in pain and depression and may help to identify pharmacological targets for effective management of depression-pain syndrome.

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          Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.

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            Neuropathic pain in the general population: a systematic review of epidemiological studies.

            Most patients with neuropathic pain symptoms present and are managed in primary care, with only a minority being referred for specialist clinical assessment and diagnoses. Previous reviews have focused mainly on specific neuropathic pain conditions based in specialist settings. This is the first systematic review of epidemiological studies of neuropathic pain in the general population. Electronic databases were searched from January 1966 to December 2012, and studies were included where the main focus was on neuropathic pain prevalence and/or incidence, either as part of a specific neuropathic pain-related condition or as a global entity in the general population. We excluded studies in which data were extracted from pain or other specialist clinics or focusing on specific population subgroups. Twenty-one articles were identified and underwent quality assessment and data extraction. Included studies differed in 3 main ways: method of data retrieval, case ascertainment tool used, and presentation of prevalence/incidence rates. This heterogeneity precluded any meta-analysis. We categorised comparable incidence and prevalence rates into 2 main subgroups: (1) chronic pain with neuropathic characteristics (range 3-17%), and (2) neuropathic pain associated with a specific condition, including postherpetic neuralgia (3.9-42.0/100,000 person-years [PY]), trigeminal neuralgia (12.6-28.9/100,000 PY), painful diabetic peripheral neuropathy (15.3-72.3/100,000 PY), glossopharyngeal neuralgia (0.2-0.4/100,000 PY). These differences highlight the importance of a standardised approach for identifying neuropathic pain in future epidemiological studies. A best estimate of population prevalence of pain with neuropathic characteristics is likely to lie between 6.9% and 10%. Copyright © 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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              Pain regulation by non-neuronal cells and inflammation

              Acute pain is protective and a cardinal feature of inflammation. Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated with chronic neuroinflammation, a local inflammation in the peripheral or central nervous system. Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells play active roles in the pathogenesis and resolution of pain. We review how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain. Recent studies also suggest that bacterial infections regulate pain through direct actions on sensory neurons, and specific receptors are present in nociceptors to detect danger signals from infections. We also discuss new therapeutic strategies to control neuroinflammation for the prevention and treatment of chronic pain.
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                Author and article information

                Contributors
                URI : http://loop.frontiersin.org/people/1016160/overview
                URI : http://loop.frontiersin.org/people/1016178/overview
                URI : http://loop.frontiersin.org/people/323176/overview
                Journal
                Front Psychol
                Front Psychol
                Front. Psychol.
                Frontiers in Psychology
                Frontiers Media S.A.
                1664-1078
                31 July 2020
                2020
                : 11
                : 1825
                Affiliations
                [1] 1Division of Neuroscience, Hospital Sirio-Libanes , São Paulo, Brazil
                [2] 2Anesthesiology Medical Center, Hospital Sirio-Libanes , São Paulo, Brazil
                [3] 3LIM 23, Institute of Psychiatry, University of São Paulo School of Medicine , São Paulo, Brazil
                Author notes

                Edited by: Qing Zhao, Second Affiliated Hospital of Guangzhou Medical University, China

                Reviewed by: Ming Yi, Peking University, China; Jixin Liu, Xidian University, China; Patricia Barton Crane, East Carolina University, United States

                *Correspondence: Raquel Chacon Ruiz Martinez, quelmartinez@ 123456yahoo.com.br

                These authors have contributed equally to this work

                This article was submitted to Health Psychology, a section of the journal Frontiers in Psychology

                Article
                10.3389/fpsyg.2020.01825
                7412934
                32849076
                3bbd3cb1-efb3-49d6-9ee5-a38435c0ab40
                Copyright © 2020 Campos, Antunes, Matsumoto, Pagano and Martinez.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 27 February 2020
                : 02 July 2020
                Page count
                Figures: 4, Tables: 2, Equations: 0, References: 254, Pages: 30, Words: 0
                Categories
                Psychology
                Review

                Clinical Psychology & Psychiatry
                neuroinflammation,pain,depression,depression-pain syndrome,glial cells

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