title: Neurological diseases as primary gliopathies: a reassessment of neurocentrism.
abstract: Diseases of the human brain are almost universally attributed to malfunction or loss of nerve cells. However, a considerable amount of work has, during the last decade, expanded our view on the role of astrocytes in CNS (central nervous system), and this analysis suggests that astrocytes contribute to both initiation and propagation of many (if not all) neurological diseases. Astrocytes provide metabolic and trophic support to neurons and oligodendrocytes. Here, we shall endeavour a broad overviewing of the progress in the field and forward the idea that loss of homoeostatic astroglial function leads to an acute loss of neurons in the setting of acute insults such as ischaemia, whereas more subtle dysfunction of astrocytes over periods of months to years contributes to epilepsy and to progressive loss of neurons in neurodegenerative diseases. The majority of therapeutic drugs currently in clinical use target neuronal receptors, channels or transporters. Future therapeutic efforts may benefit by a stronger focus on the supportive homoeostatic functions of astrocytes.
authors.affiliation: Faculty of Life Sciences, The University of Manchester, Manchester, UK. Alexej.Verkhratsky@manchester.ac.uk
authors.forename: Alexei
authors.initials: A
authors.lastname: Verkhratsky
authors.forename: Michael V
authors.initials: MV
authors.lastname: Sofroniew
authors.forename: Albee
authors.initials: A
authors.lastname: Messing
authors.forename: Nihal C
authors.initials: NC
authors.lastname: deLanerolle
authors.forename: David
authors.initials: D
authors.lastname: Rempe
authors.forename: José Julio
authors.initials: JJ
authors.lastname: Rodríguez
authors.forename: Maiken
authors.initials: M
authors.lastname: Nedergaard
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D005911:Gliosis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D019636:Neurodegenerative Diseases / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*