Do glia drive synaptic and cognitive impairment in disease?
Synaptic dysfunction is a hallmark of many neurodegenerative and psychiatric brain disorders, yet we know little about the mechanisms that underlie synaptic vulnerability. Although neuroinflammation and reactive gliosis are prominent in virtually every CNS disease, glia are largely viewed as passive responders to neuronal damage rather than drivers of synaptic dysfunction. This perspective is changing with the growing realization that glia actively signal with neurons and influence synaptic development, transmission and plasticity through an array of secreted and contact-dependent signals. We propose that disruptions in neuron-glia signaling contribute to synaptic and cognitive impairment in disease. Illuminating the mechanisms by which glia influence synapse function may lead to the development of new therapies and biomarkers for synaptic dysfunction.
Department of Neurobiology, Stanford University School of Medicine, Palo Alto, California 94305, USA.
Won-Suk
WS
Chung
Department of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Christina A
CA
Welsh
Department of Neurobiology, Stanford University School of Medicine, Palo Alto, California 94305, USA.
Ben A
BA
Barres
Department of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Beth
B
Stevens
D000818:Animals; D001253:Astrocytes / Q000502:physiology*; D003072:Cognition Disorders / Q000503:physiopathology*; D006801:Humans; D009457:Neuroglia / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*