Get Started for FREE
Sign up with Facebook Sign up with X
I don't have a Facebook or a X account
 Your new post is loading...
Your new post is loading...
Scoop.it!
Dysregulation of the complement system is evident in many CNS diseases but mechanisms regulating complement activation in the CNS remain unclear. Via Krishan Maggon 
Scoop.it!
Via Krishan Maggon
Krishan Maggon 's curator insight,
January 11, 2015 4:37 AM
Neurobiology of Disease Volume 73, January 2015, Pages 137–149 Review Eph receptors: New players in Alzheimer's disease pathogenesisMoustapha Cissé, , Frédéric Checler, doi:10.1016/j.nbd.2014.08.028
Scoop.it!
Cell death and differentiation is a monthly research journal focused on the exciting field of programmed cell death and apoptosis. Via Krishan Maggon
Krishan Maggon 's curator insight,
November 25, 2014 3:42 AM
Cell Research advance online publication 21 November 2014; doi: 10.1038/cr.2014.154 STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation Wanqiang Sheng1,2, Fan Yang1, Yi Zhou3, Henry Yang1, Pey Yng Low4, David Michael Kemeny4, Patrick Tan1,5, Akira Moh7, Mark H Kaplan7,8, Yongliang Zhang4 and Xin-Yuan Fu1,3,6,8 1Cancer Science Institute of Singapore, YLL School of Medicine, National University of Singapore, Singapore2Department of Biological Sciences, Faculty of Science, National University of Singapore, Singapore3Department of Biochemistry, YLL School of Medicine, National University of Singapore, Singapore4Immunology Programme and Department of Microbiology, YLL School of Medicine, National University of Singapore, Singapore5Cancer and Stem Cell Biology, Duke-NUS Graduate Medical School, Singapore6Neurobiology Programme, Life Sciences Institute, National University of Singapore, Singapore7Departments of Pediatrics and Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA8Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA Correspondence: Yongliang Zhang, E-mail: miczy@nus.edu.sg; Xin-Yuan Fu, E-mail: xin-yuan_fu@nuhs.edu.sg Received 22 September 2014; Revised 29 September 2014; Accepted 9 October 2014 |
Scoop.it!
Abstract Alzheimer's disease (AD) is the world's most common dementing illness, affecting over 150 million patients. Classically AD has been viewed as a neurodegenerative disease of the elderly, characterized by the extracellular deposition of misfolded amyloid-β (Aβ) peptide and the intracellular formation of neurofibrillary tangles. Only recently has neuroinflammation emerged as an important component of AD pathology. Experimental, genetic and epidemiological data now indicate a crucial role for activation of the innate immune system as a disease-promoting factor. The sustained formation and deposition of Aβ aggregates causes chronic activation of the immune system and disturbance of microglial clearance functions. Here we review advances in the molecular understanding of the inflammatory response in AD that point to novel therapeutic approaches for the treatment of this devastating disease. Via Krishan Maggon
Krishan Maggon 's curator insight,
March 2, 2015 2:10 AM
NATURE IMMUNOLOGY | REVIEW Innate immunity in Alzheimer's diseaseMichael T Heneka,Douglas T Golenbock& Eicke LatzAffiliationsCorresponding authorNature Immunology 16, 229–236 (2015) doi:10.1038/ni.3102Received 03 December 2014 Accepted 13 January 2015 Published online 17 February 2015
Scoop.it!
Cell death and differentiation is a monthly research journal focused on the exciting field of programmed cell death and apoptosis. Via Krishan Maggon
Krishan Maggon 's curator insight,
November 25, 2014 3:42 AM
Cell Research advance online publication 21 November 2014; doi: 10.1038/cr.2014.154 STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation Wanqiang Sheng1,2, Fan Yang1, Yi Zhou3, Henry Yang1, Pey Yng Low4, David Michael Kemeny4, Patrick Tan1,5, Akira Moh7, Mark H Kaplan7,8, Yongliang Zhang4 and Xin-Yuan Fu1,3,6,8 1Cancer Science Institute of Singapore, YLL School of Medicine, National University of Singapore, Singapore2Department of Biological Sciences, Faculty of Science, National University of Singapore, Singapore3Department of Biochemistry, YLL School of Medicine, National University of Singapore, Singapore4Immunology Programme and Department of Microbiology, YLL School of Medicine, National University of Singapore, Singapore5Cancer and Stem Cell Biology, Duke-NUS Graduate Medical School, Singapore6Neurobiology Programme, Life Sciences Institute, National University of Singapore, Singapore7Departments of Pediatrics and Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA8Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA Correspondence: Yongliang Zhang, E-mail: miczy@nus.edu.sg; Xin-Yuan Fu, E-mail: xin-yuan_fu@nuhs.edu.sg Received 22 September 2014; Revised 29 September 2014; Accepted 9 October 2014
Scoop.it!
Alzheimer's disease: Making Aβ better Nature.com Microglia express a number of genes that have been implicated in the pathology of Alzheimer's disease (AD), which is characterized by extracellular accumulation of amyloid-β peptide (Aβ) peptides and... Via Krishan Maggon
Krishan Maggon 's curator insight,
October 20, 2014 12:43 PM
A small molecule binding HMGB1 and HMGB2inhibits microglia-mediated neuroinflammationSanghee Lee,Youngpyo Nam,Ja Young Koo,Donghyun Lim,Jongmin Park,Jiyeon Ock,Jaehong Kim,Kyoungho Suk& Seung Bum ParkAffiliationsContributionsCorresponding authorsNature Chemical Biology (2014) doi:10.1038/nchembio.1669Received 19 March 2014 Accepted 18 September 2014 Published online 12 October 2014
|
Citation: Aeinehband S, Lindblom RPF, Al Nimer F, Vijayaraghavan S, Sandholm K, et al. (2015) Complement Component C3 and Butyrylcholinesterase Activity Are Associated with Neurodegeneration and Clinical Disability in Multiple Sclerosis. PLoS ONE 10(4): e0122048. doi:10.1371/journal.pone.0122048