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      The complexity of neuroinflammation consequent to traumatic brain injury: from research evidence to potential treatments

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          Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football.

          Players of American football may be at increased risk of long-term neurological conditions, particularly chronic traumatic encephalopathy (CTE).
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            Dystrophic microglia in the aging human brain.

            We have studied microglial morphology in the human cerebral cortex of two nondemented subjects using high-resolution LN-3 immunohistochemistry. Several abnormalities in microglial cytoplasmic structure, including deramification, spheroid formation, gnarling, and fragmentation of processes, were identified. These changes were determined to be different from the morphological changes that occur during microglial activation and they were designated collectively as microglial dystrophy. Quantitative evaluation of dystrophic changes in microglia revealed that these were much more prevalent in the older subject (68-year-old) than in the younger one (38-year-old). Thus, we conclude that microglial dystrophy is a sign of microglial cell senescence. We hypothesize that microglial senescence could be important for understanding age-related declines in cognitive function. Copyright 2003 Wiley-Liss, Inc.
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              Inflammation-associated depression: from serotonin to kynurenine.

              In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptophan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms. Copyright © 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Acta Neuropathologica
                Acta Neuropathol
                Springer Science and Business Media LLC
                0001-6322
                1432-0533
                May 2019
                December 7 2018
                May 2019
                : 137
                : 5
                : 731-755
                Article
                10.1007/s00401-018-1944-6
                30535946
                2ec0a62e-5d84-49ec-bc57-91ca304c40a6
                © 2019

                http://www.springer.com/tdm

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