000			03898nam a22004695i 4500
001			978-1-4614-8313-7
003			DE-He213
005			20140220082831.0
007			cr nn 008mamaa
008			130913s2013 xxu| s |||| 0|eng d
020			_a9781461483137 _9978-1-4614-8313-7
024	7		_a10.1007/978-1-4614-8313-7 _2doi
050		4	_aRC321-580
072		7	_aPSAN _2bicssc
072		7	_aMED057000 _2bisacsh
082	0	4	_a612.8 _223
100	1		_aSuzumura, Akio. _eeditor.
245	1	0	_aNeuron-Glia Interaction in Neuroinflammation _h[electronic resource] / _cedited by Akio Suzumura, Kazuhiro Ikenaka.
264		1	_aNew York, NY : _bSpringer New York : _bImprint: Springer, _c2013.
300			_aX, 187 p. 25 illus., 24 illus. in color. _bonline resource.
336			_atext _btxt _2rdacontent
337			_acomputer _bc _2rdamedia
338			_aonline resource _bcr _2rdacarrier
347			_atext file _bPDF _2rda
490	1		_aAdvances in Neurobiology, _x2190-5215 ; _v7
505	0		_aAcute, Chronic, and Non-classical Neuroinflammation: Definitions in a Changing Scientific Environment -- Neuroinflammation in Neurological Disorders -- Factors from Intact and Damaged Neurons -- Interactions between Neurons and Microglia During Neuroinflammation -- Neuron-Astrocyte Interactions in Neuroinflammation -- Neuron-oligodendrocyte Interactions in Neuroinflammation -- Neuron-glia Interaction via Neurotrophins -- Glial Communication via Gap Junction in Neuroinflammation -- Toll-Like Receptors and Neuroinflammation -- The Blood-Brain-Barrier in Neuroinflammation.
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		0	_aMedicine.
650		0	_aNeurosciences.
650		0	_aNeurology.
650	1	4	_aBiomedicine.
650	2	4	_aNeurosciences.
650	2	4	_aNeurology.
700	1		_aIkenaka, Kazuhiro. _eeditor.
710	2		_aSpringerLink (Online service)
773	0		_tSpringer eBooks
776	0	8	_iPrinted edition: _z9781461483120
830		0	_aAdvances in Neurobiology, _x2190-5215 ; _v7
856	4	0	_uhttp://dx.doi.org/10.1007/978-1-4614-8313-7
912			_aZDB-2-SBL
999			_c96046 _d96046