Titlebook: Microglia in the Regenerating and Degenerating Central Nervous System; Wolfgang J. Streit Book 2002 Springer Science+Business Media New Yo

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ous system and also reviews microglial cell function and physiology. Cellular neurobiologists will find that this is a valuable guide to the importance and role of microglia in the CNS.978-1-4419-2944-0978-1-4757-4139-1

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Microglia and Macrophage Responses in Cerebral Ischemia,ndary zone, apoptotic cell death is ongoing during the first week after focal ischemia (Li et al. (1995); Braun et al. (1996); Isenmann et al. (1998)). Accordingly, several studies using modem imaging techniques provided evidence for infarct growth during the first few days after cerebral ischemia (

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Role of Microglia and Macrophages in Secondary Injury of the Traumatized Spinal Cord: Troublemakersns, Blight postulated a role for macrophages in secondary injury (Blight (1985); Blight (1992)). Later independent studies in guinea pig, rabbit and rodent models of SCI supported this notion that inflammation in general, and macrophages in particular, contribute to delayed secondary injury (Giulian

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Influences of Activated Microglia/Brain Macrophages on Spinal Cord Injury and Regeneration, regarding the distinction and relation between microglia-derived brain macrophages and infiltrating peripheral macrophages, and their conflicting roles in creating a pro-regenerative environment. To this end, evidence is reviewed that suggests that microglia-derived brain macrophages are capable of

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Opportunities for Axon Repair in the CNS: Use of Microglia and Biopolymer Compositions,n et al. (1995), Reier et al. (1994); Bregman et al. (1989)). However, while fetal tissue transplantation may allow filling of a lesion cavity, host fibers in adult animals tend to terminate within fetal transplants, rather than grow across them (Reier et al. (1983)). The same problem may also arise

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Beta Amyloid Protein Clearance and Microglial Activation,ed amyloid formation. Other potential genetic risk factors for late-onset AD may also influence AD pathogenesis at levels beyond Aβ production, including alpha-2 macroglobulin (Liao et al. 1998), alpha-1 antichymotrypsin (Thome et al. (1995)), interleukin 1 (Nicoll et al. (2000)), and transforming g

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