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      Inflammation in CNS neurodegenerative diseases

      1 , 2 , 2 , 2 , 1 , 2

      Immunology

      Wiley

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          Abstract

          <p id="d293304e238">Neurodegenerative diseases, the leading cause of morbidity and disability, are gaining increased attention as they impose a considerable socioeconomic impact, due in part to the ageing community. Neuronal damage is a pathological hallmark of Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, Huntington's disease, spinocerebellar ataxia and multiple sclerosis, although such damage is also observed following neurotropic viral infections, stroke, genetic white matter diseases and paraneoplastic disorders. Despite the different aetiologies, for example, infections, genetic mutations, trauma and protein aggregations, neuronal damage is frequently associated with chronic activation of an innate immune response in the <span style="fixed-case">CNS</span>. The growing awareness that the immune system is inextricably involved in shaping the brain during development as well as mediating damage, but also regeneration and repair, has stimulated therapeutic approaches to modulate the immune system in neurodegenerative diseases. Here, we review the current understanding of how astrocytes and microglia, as well as neurons and oligodendrocytes, shape the neuroimmune response during development, and how aberrant responses that arise due to genetic or environmental triggers may predispose the <span style="fixed-case">CNS</span> to neurodegenerative diseases. We discuss the known interactions between the peripheral immune system and the brain, and review the current concepts on how immune cells enter and leave the <span style="fixed-case">CNS</span>. A better understanding of neuroimmune interactions during development and disease will be key to further manipulating these responses and the development of effective therapies to improve quality of life, and reduce the impact of neuroinflammatory and degenerative diseases. </p>

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          Psychotic syndromes can be understood as disorders of adaptation to social context. Although heritability is often emphasized, onset is associated with environmental factors such as early life adversity, growing up in an urban environment, minority group position and cannabis use, suggesting that exposure may have an impact on the developing 'social' brain during sensitive periods. Therefore heritability, as an index of genetic influence, may be of limited explanatory power unless viewed in the context of interaction with social effects. Longitudinal research is needed to uncover gene-environment interplay that determines how expression of vulnerability in the general population may give rise to more severe psychopathology.
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            Systemic infections and inflammation affect chronic neurodegeneration.

            It is well known that systemic infections cause flare-ups of disease in individuals with asthma and rheumatoid arthritis, and that relapses in multiple sclerosis can often be associated with upper respiratory-tract infections. Here we review evidence to support our hypothesis that in chronic neurodegenerative diseases such as Alzheimer's disease, with an ongoing innate immune response in the brain, systemic infections and inflammation can cause acute exacerbations of symptoms and drive the progression of neurodegeneration.
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              Global epidemiology of meningococcal disease.

              As reviewed in this paper, meningococcal disease epidemiology varies substantially by geographic area and time. The disease can occur as sporadic cases, outbreaks, and large epidemics. Surveillance is crucial for understanding meningococcal disease epidemiology, as well as the need for and impact of vaccination. Despite limited data from some regions of the world and constant change, current meningococcal disease epidemiology can be summarized by region. By far the highest incidence of meningococcal disease occurs in the meningitis belt of sub-Saharan Africa. During epidemics, the incidence can approach 1000 per 100,000, or 1% of the population. Serogroup A has been the most important serogroup in this region. However, serogroup C disease has also occurred, as has serogroup X disease and, most recently, serogroup W-135 disease. In the Americas, the reported incidence of disease, in the range of 0.3-4 cases per 100,000 population, is much lower than in the meningitis belt. In addition, in some countries such as the United States, the incidence is at an historical low. The bulk of the disease in the Americas is caused by serogroups C and B, although serogroup Y causes a substantial proportion of infections in some countries and W-135 is becoming increasingly problematic as well. The majority of meningococcal disease in European countries, which ranges in incidence from 0.2 to 14 cases per 100,000, is caused by serogroup B strains, particularly in countries that have introduced serogroup C meningococcal conjugate vaccines. Serogroup B also predominates in Australia and New Zealand, in Australia because of the control of serogroup C disease through vaccination and in New Zealand because of a serogroup B epidemic. Based on limited data, most disease in Asia is caused by serogroup A and C strains. Although this review summarizes the current status of meningococcal disease epidemiology, the dynamic nature of this disease requires ongoing surveillance both to provide data for vaccine formulation and vaccine policy and to monitor the impact of vaccines following introduction.
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                Author and article information

                Journal
                Immunology
                Immunology
                Wiley
                00192805
                April 17 2018
                Affiliations
                [1 ]Centre for Neuroscience and Trauma; Barts and the Blizard Institute, London; School of Medicine and Dentistry; Queen Mary University of London; London UK
                [2 ]Department of Pathology; VU University Medical Centre; Amsterdam the Netherlands
                Article
                10.1111/imm.12922
                5980185
                29513402
                © 2018

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