Glial connexin expression and function in the context of Alzheimer's disease.
A hallmark of neurodegenerative diseases is the reactive gliosis characterized by a phenotypic change in astrocytes and microglia. This glial response is associated with modifications in the expression and function of connexins (Cxs), the proteins forming gap junction channels and hemichannels. Increased Cx expression is detected in most reactive astrocytes located at amyloid plaques, the histopathological lesions typically present in the brain of Alzheimer's patients and animal models of the disease. The activity of Cx channels analyzed in vivo as well as in vitro after treatment with the amyloid β peptide is also modified and, in particular, hemichannel activation may contribute to neuronal damage. In this review, we summarize and discuss recent data that suggest glial Cx channels participate in the neurodegenerative process of Alzheimer's disease. This article is part of a Special Issue entitled: The Communicating junctions, composition, structure and characteristics.
Centre National de la Recherche Scientifique, Unité Mixte de Recherche, Paris Cedex 05, France.
Annette
A
Koulakoff
Xin
X
Mei
Juan A
JA
Orellana
Juan C
JC
Sáez
Christian
C
Giaume
D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D017630:Connexins / Q000378:metabolism*; D004195:Disease Models, Animal; D017629:Gap Junctions / Q000378:metabolism*; D005911:Gliosis / Q000378:metabolism; D006801:Humans; D051379:Mice; D017628:Microglia / Q000378:metabolism; D008954:Models, Biological; D009457:Neuroglia / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism; D010641:Phenotype
D016229:Amyloid beta-Peptides; D017630:Connexins