LEADER 03703nam  2200397z- 450 
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035   $a(CKB)3710000000631127
035   $a(oapen)https://directory.doabooks.org/handle/20.500.12854/52948
035   $a(EXLCZ)993710000000631127
100   $a20202102d2015      |y             0
101 0 $aeng
135   $aurmn|---annan
181   $ctxt$2rdacontent
182   $cc$2rdamedia
183   $acr$2rdacarrier
200 10$aMechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury
210   $cFrontiers Media SA$d2015
215   $a1 electronic resource (284 p.)
225 1 $aFrontiers Research Topics
311   $a2-88919-691-7 
330   $aMechanisms of brain-immune interactions became a cutting-edge topic in systemic neurosciences over the past years. Acute lesions of the brain parenchyma, particularly, induce a profound and highly complex neuroinflammatory reaction with similar mechanistic properties between differing disease paradigms like ischemic stroke, intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Resident microglial cells sense tissue damage and initiate inflammation, activation of the endothelial brain-immune interface promotes recruitment of systemic immune cells to the brain and systemic humoral immune mediators (e.g. complements and cytokines) enter the brain through the damaged blood-brain barrier. These cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute substantially to secondary brain damage and neurodegeneration. Diverse inflammatory cascades such as pro-inflammatory cytokine secretion of invading leukocytes and direct cell-cell-contact cytotoxicity between lymphocytes and neurons have been demonstrated to mediate the inflammatory ?collateral damage? in models of acute brain injury. Besides mediating neuronal cell loss and degeneration, secondary inflammatory mechanisms also contribute to functional modulation of neurons and the impact of post-lesional neuroinflammation can even be detected on the behavioral level. The contribution of several specific immune cell subpopulations to the complex orchestration of secondary neuroinflammation has been revealed just recently. However, the differential vulnerability of specific neuronal cell types and the molecular mechanisms of inflammatory neurodegeneration are still elusive. Furthermore, we are only on the verge of characterizing the control of long-term recovery and neuronal plasticity after brain damage by inflammatory pathways. Yet, a more detailed but also comprehensive understanding of the multifaceted interaction of these two supersystems is of direct translational relevance. Immunotherapeutic strategies currently shift to the center of translational research in acute CNS lesion since all clinical trials investigating direct neuroprotective therapies failed. To advance our knowledge on brain-immune communications after brain damage an interdisciplinary approach covered by cellular neuroscience as well as neuroimmunology, brain imaging and behavioral sciences is crucial to thoroughly depict the intricate mechanisms.
610   $aintracerebral hemorrhage
610   $aStroke
610   $aTraumatic Brain Injury
610   $aCytokines
610   $aneurodegeneration
610   $aNeuroinflammation
610   $aLeukocytes
610   $aImmunity
700   $aArthur Liesz$4auth$01278632
702   $aChristoph Kleinschnitz$4auth
906   $aBOOK
912   $a9910136799503321
996   $aMechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury$93013628
997   $aUNINA