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      The Role of Immunosenescence in Neurodegenerative Diseases

      review-article
      Author(s): , ,
      Publication date (Electronic):
      Journal: Mediators of Inflammation
      Publisher: Hindawi

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          Abstract

          Aging is characterized by the progressive decline of physiological function and tissue homeostasis leading to increased vulnerability, degeneration, and death. Aging-related changes of the innate and adaptive immune system include decline in the preservation and enhancement of many immune functions, such as changes in the number of circulating monocytic and dendritic cells, thymic involution, T cell polyfunctionality, or production of proinflammatory cytokines, and are defined as immunosenescence. Inflammatory functions are increased with age, causing the chronic low-grade inflammation, referred to as inflamm-aging, that contribute, together with immunosenescence, to neurodegenerative diseases. In this review, we discuss the link between the immune and nervous systems and how the immunosenescence and inflamm-aging can contribute to neurodegenerative diseases.

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          Development of monocytes, macrophages, and dendritic cells.

          Frederic Geissmann, Markus Manz, Steffen Jung … (2010)
          Monocytes and macrophages are critical effectors and regulators of inflammation and the innate immune response, the immediate arm of the immune system. Dendritic cells initiate and regulate the highly pathogen-specific adaptive immune responses and are central to the development of immunologic memory and tolerance. Recent in vivo experimental approaches in the mouse have unveiled new aspects of the developmental and lineage relationships among these cell populations. Despite this, the origin and differentiation cues for many tissue macrophages, monocytes, and dendritic cell subsets in mice, and the corresponding cell populations in humans, remain to be elucidated.
          Article 0 comments Cited 891 times – based on 0 reviews     Review now
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            Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

            Tony Wyss-Coray (2006)
            Alzheimer disease is a progressive dementia with unknown etiology that affects a growing number of the aging population. Increased expression of inflammatory mediators in postmortem brains of people with Alzheimer disease has been reported, and epidemiological studies link the use of anti-inflammatory drugs with reduced risk for the disorder. On the initial basis of this kind of evidence, inflammation has been proposed as a possible cause or driving force of Alzheimer disease. If true, this could have important implications for the development of new treatments. Alternatively, inflammation could simply be a byproduct of the disease process and may not substantially alter its course. Or components of the inflammatory response might even be beneficial and slow the disease. To address these possibilities, we need to determine whether inflammation in Alzheimer disease is an early event, whether it is genetically linked with the disease and whether manipulation of inflammatory pathways changes the course of the pathology. Although there is still little evidence that inflammation triggers or promotes Alzheimer disease, increasing evidence from mouse models suggests that certain inflammatory mediators are potent drivers of the disease. Related factors, on the other hand, elicit beneficial responses and can reduce disease.
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              Aging of the innate immune system.

              Albert Shaw, Samit R. Joshi, Hannah Greenwood … (2010)
              The innate immune system is composed of a network of cells including neutrophils, NK and NKT cells, monocytes/macrophages, and dendritic cells that mediate the earliest interactions with pathogens. Age-associated defects are observed in the activation of all of these cell types, linked to compromised signal transduction pathways including the Toll-like Receptors. However, aging is also characterized by a constitutive pro-inflammatory environment (inflamm-aging) with persistent low-grade innate immune activation that may augment tissue damage caused by infections in elderly individuals. Thus, immunosenescence in the innate immune system appears to reflect dysregulation, rather than exclusively impaired function. Copyright 2010. Published by Elsevier Ltd.
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                Author and article information

                Contributors
                Marcella Reale:
                ORCID: http://orcid.org/0000-0002-4164-8781
                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (iso-abbrev): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date Collection: 2018
                Publication date (Electronic): 8 March 2018
                Volume: 2018
                Electronic Location Identifier: 6039171
                Affiliations
                Unit of Immunodiagnostic and Molecular Pathology, Department of Medical, Oral and Biotechnological Sciences, “G. d'Annunzio” University of Chieti-Pescara, 66100 Chieti, Italy
                Author notes

                Academic Editor: Francesco Prattichizzo

                Author information
                http://orcid.org/0000-0003-2175-4226
                http://orcid.org/0000-0002-4164-8781
                Article
                DOI: 10.1155/2018/6039171
                PMC ID: 5863336
                PubMed ID: 29706800
                SO-VID: 1098156f-15ac-412b-87ca-89a41a483a48
                Copyright © Copyright © 2018 Erica Costantini et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 29 September 2017
                Date revision received : 15 December 2017
                Date accepted : 17 January 2018
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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