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Trends Mol Med. 2017 Jun;23(6):486-500. doi: 10.1016/j.molmed.2017.04.005. Epub 2017 May 9.

Should We Stop Saying 'Glia' and 'Neuroinflammation'?

Author information

1
Institut de Neurociències and Departament de Bioquímica i Biologia Molecular, Unitat de Bioquímica de Medicina, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
2
Neuroimmunology Group, Functional and Systems Neurobiology Department, Instituto Cajal, Agencia Estatal del Consejo Superior de Investigaciones Científicas, Madrid, España; Spanish Network of Multiple Sclerosis, RETICS, Instituto de Salud Carlos III, Madrid, España.
3
Biogen, Cambridge, MA, USA.
4
Institut de Neurociències and Departament de Bioquímica i Biologia Molecular, Unitat de Bioquímica de Medicina, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain; ICREA, Pg. Lluís Companys 23, 08010 Barcelona, Spain. Electronic address: galea.inc@gmail.com.

Abstract

Central nervous system (CNS) therapeutics based on the theoretical framework of neuroinflammation have only barely succeeded. We argue that a problem may be the wrong use of the term 'neuroinflammation' as a distinct nosological entity when, based on recent evidence, it may not explain CNS disease pathology. Indeed, the terms 'neuroinflammation' and 'glia' could be obsolete. First, unbiased molecular profiling of CNS cell populations and individual cells reveals striking phenotypic heterogeneity in health and disease. Second, astrocytes, microglia, oligodendrocytes, and NG2 cells may contribute to higher-brain functions by performing actions beyond housekeeping. We propose that CNS diseases be viewed as failed circuits caused in part by disease-specific dysfunction of cells traditionally called 'glia', and hence, favor therapies promoting their functional recovery.

KEYWORDS:

cell replacement; central nervous system circuits; central nervous system repair; computation; induced pluripotent stem cell; single-cell RNA sequencing

PMID:
28499701
DOI:
10.1016/j.molmed.2017.04.005
[Indexed for MEDLINE]

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