000			04426cam a2200553 i 4500
999			_c58484 _d58484
001			17856518
005			20170913120551.0
008			130819s2013 nyua g b 001 0 eng c
010			_a 2013948228
016	7		_a101624940 _2DNLM
020			_a9781461483120 (alk. paper)
020			_a1461483123 (alk. paper)
020			_z9781461483137 (eBook)
035			_a(OCoLC)ocn847348501
041			_aeng
042			_apcc
050	0	0	_aQP363.2 _b.N53 2013
060	0	0	_a2014 B-075
060	1	0	_aWL 102
082	0	4	_a612.81045 _223 _bS N
100	1		_aSuzumura, Akio _91454
245	1	0	_aNeuron-glia interaction in neuroinflammation / _cAkio Suzumura, Kazuhiro Ikenaka, editors.
260			_anew york : _bspringer sience + business media ; _c2013 .
265			_aاقرأ للنشر و التوزيع
300			_ax, 187 pages : _billustrations (some color) ; _c24 cm.
490	1		_aAdvances in neurobiology, _x2190-5215 ; _vvolume 7
504			_aIncludes bibliographical references and index.
505	0	0	_tAcute, Chronic, and Nonclassical Neuroinflammation: Definitions in a Changing Scientific Environment / _rRobert P. Lisak, Joyce A. Benjamin -- _tNeuroinflammation in Neurological Disorders / _rJun-ichi Kira -- _tFactors from Intact and Damaged Neurons / _rTetsuya Mizuno -- _tInteractions Between Neurons and Microglia During Neuroinflammation / _rAkio Suzumura -- _tNeuron-Astrocyte Interactions in Neuroinflammation / _rJasna Kriz -- _tNeuron-Oligodendrocyte Interactions in Neuroinflammation / _rKazuhiro Ikenaka -- _tNeuron-Glia Interaction via Neurotrophins / _rCinthia Farina -- _tGlial Communication via Gap Junction in Neuroinflammation / _rHideyuki Takeuchi -- _tToll-Like Receptors and Neuroinflammation / _rSung Joong Lee -- _tThe Blood-Brain Barrier in Neuroinflammation / _rFumitaka Shimizu.
520			_aAccumulation of glia, gliosis, in various neurological disorders is not a static scar, but actively involved in pathogenesis of various neurological and psychiatric disorders, where glial cells produce both inflammatory and neurotrophic factors. These factors may play a role in neuronal damage, but also have a protective and reparative function by inducing neuroinflammation. However, definition as well as the mechanisms of neuroinflammation is not yet clear. We first define acute, chronic and non-classical neuroinflammation. Glial cells are activated by a variety of stimuli via receptors on glial cells. Toll like receptors (TLR) are one of these receptors. In response to harmful stimuli, neurons produce factors as either eat-me or help-me signals. These factors include cytokines, chemokines and damage-associated molecular pattern (DAMP). Some of them activate glial cells via TLR, and function to protect neurons or further induce neuroinflammation. Thus, the interaction between neuron-glia and glia-glia is a main feature of neuroinflammation. Glial cells communicate with other glial or neural cells via gap-junctions. The communication may also be important for the understanding of neuroinflammation. Oligodendrocytes-neurons communication may be critical in either myelination or demyelination. Damage of blood-brain barrier (BBB) is common feature of both inflammatory and degenerative neurological disorders. Thus, relation of BBB damage and functions of glial cell may also be important in the development of neuroinflammation. In this book, we focused on neuron-glia interaction of various aspects for understanding of pathophysiology of neuroinflammation in development of inflammatory as well as degenerative neurological disorders.
650	1	4	_aNeuroglia. _91456
650	1	4	_aNeural transmission. _91457
650		0	_aNervous system _xDegeneration. _91458
650		0	_aInflammation. _91459
650	1	2	_aNeuroglia _xphysiology.
650	2	2	_aInflammation _xphysiopathology.
650	2	2	_aNervous System Physiological Phenomena.
650	2	2	_aNeurodegenerative Diseases.
650	2	2	_aNeuroimmunomodulation.
650		7	_aInflammation. _2fast
650		7	_aNervous system _xDegeneration. _2fast
650		7	_aNeural transmission. _2fast
650		7	_aNeuroglia. _2fast
700	1		_aSuzumura, Akio, _eeditor.
700	1		_aIkenaka, Kazuhiro, _eeditor.
830		0	_aAdvances in neurobiology ; _vv. 7.
942			_2ddc _cBK _iFOE _6FOE
955			_brl09 2015-09-18 z-processor _irl09 2015-09-24 ; to Dewey
955			_apc17 2013-08-19 _arl00 2014-06-18 to SMA