Neuro-inflammation in Neuronal Death and Repair: Volume 82
Thus, MMP-3 has been shown to induce the release of pro-inflammatory cytokines from microglia via activation of ERK and NF-kB-dependent pathways. Increasing evidence highlights the importance of a balanced cross-talk between neurons and non-neuronal cells and indicates that the presence of reactive astrocytes, the activation of microglia and the release of inflammatory mediators may contribute to the progression of many central nervous system disorders, independently of the nature of the primary pathogenic event. However, many aspects still remain controversial and much more effort is needed to understand the role of neuroinflammatory mediators and processes in these conditions.
This volume brings together renowned, international scientists to discuss current knowledge and views on the mechanisms of neuroinflammation, on its role in the context of different neurodegenerative diseases (i.e. Alzheimer's, prion disease, HIV-associated dementia, multiple sclerosis, pain) and on the potential approaches for future therapeutic strategies.
- Hardback | 504 pages
- 157.48 x 231.14 x 25.4mm | 839.14g
- 16 Oct 2007
- Elsevier Science Publishing Co Inc
- Academic Press Inc
- San Diego, United States
- 82nd edition
- Illustrated; Illustrations, unspecified
Other books in this series
28 Aug 2017
29 Aug 2017
06 Aug 2014
24 Sep 2010
07 Oct 2003
31 Aug 2017
25 Nov 2013
15 Nov 2013
16 Oct 2007
09 Sep 2014
08 Dec 2009
02 Aug 2011
05 Apr 2011
10 Jan 1997
Table of contents
BASIC MECHANISMS OF NEUROINFLAMMATION.
Innate immunity and inflammation in the brain.
Microglia, astrocyte signaling and neuroinflammation.
New insights into the roles of metalloproteinases in
neurodegeneration and neuroprotection.
The role of astrocytes and the complement system in neural plasticity.
NFkB and neuroinflamation.
Glia re-sealed particles freshly prepared from adult rat brain are competent for exocytotic release of glutamate.
New Approaches to the Control of Chronic Inflammatory and Neuropathic Pain.
NEW TARGETS TO TREAT NEUROINFLAMMATORY DISEASES.
Early synaptic dysfunction in experimental multiple sclerosis.
Chemokines and multiple sclerosis.
Neuroinflammation mediators in AD.
Complement and Alzheimer disease.
New drugs to target neuroinflammation in AD.
COX-2, PGE2 and microglial activation in prion diseases.
Endocannabinoids and Neuroinflammation.
Microglia in HIV and Alzheimer disease.