By H. Kettenmann (auth.), H. Kettenmann, G. A. Burton, U. J. Moenning (eds.)
Recent paintings has implicated inflammatory approaches within the pathophysiology of quite a few neurodegenerative illnesses equivalent to Alzheimer's ailment, stroke and a number of sclerosis. during this booklet top specialists within the box talk about molecular, in vivo and scientific features of neuroinflammation. it's was hoping, with the wealth of analysis being conductied during this quarter, that novel healing pursuits might be pointed out to be able to let winning healing intervention in numerous neurodegenerative diseases.
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Additional resources for Neuroinflammation — From Bench to Bedside
1998). In addition to receptor mechanisms, several other factors are likely to contribute to the activation and migration of microglia toward A~ deposits, particularly soluble mediators secreted by A~-activated microglia. , in press (a)] and neurons (Yan et ai. 1999) to A~, induces microglial chemotaxis, proliferation, increased MSR expression, and enhanced microglial survival (Giulian and Baker 1986; Tomozawa et ai. 1996). A~-stimulated secretion of M-CSF could therefore contribute substantially to the accumulation of activated microglia in and around A~ plaques.
Exp Neurol 124:289-98 Cotter RL, Burke WJ, Thomas VS, Potter IF, Zheng J, Gendelman HE (1999) Insights into the neurodegenerative process of Alzheimer's disease: a role for mononuclear phagocyte-associated inflanunation an d neurotoxicity. J Leukoc Bioi 65:416-427 40 J. Rogers et al. B, McMurray HF, Schubert D (1992) The amyloid beta-protein of Alzheimer's disease is chemotactic for mononuclear phagocytes. Biochem Biophys Res Commun 189:1096-1100 DeGroot CIA, Montagne L, lanssen I, Ravid R, Van Der Valk P, Veerhuis R (2000) Isolation and characterization of adult microglial cells and oligodendrocytes Derived from postmortem human brain tissue.
In addition, there may be overproduction of AB such that microglia are being overwhelmed by a greater-than-normal amyloid burden. This may compromise not only the cells' AB-clearing ability, but could also impact other cell functions, such as neuroprotection and trophic functions to aid in the survival of neurons weakened by old age or otherwise. If dysfunctional microglia are neglecting their normal duties related to sustaining neuronal wellbeing, this could ultimately result in the development of neurodegenerative changes, such as neurofibrillary tangle formation.