To think or not to think: synaptic activity and Abeta release.
Accumulation of beta-amyloid protein (Abeta) in the extracellular space of the brain has been hypothesized to be a culprit in the pathogenesis of Alzheimer's disease. In this issue of Neuron, Cirrito et al. describe a series of experiments demonstrating that extracellular Abeta levels are directly modulated by neuronal and synaptic activity.
Schroeder
Brock E
BE
Department of Neurosciences, University of California, San Diego, La Jolla, California 92093, USA.
Koo
Edward H
EH
D000544:Alzheimer Disease / Q000378:metabolism* / Q000503:physiopathology; D053829:Amyloid Precursor Protein Secretases; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D016282:Aspartic Acid Endopeptidases; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D010450:Endopeptidases / Q000378:metabolism; D045604:Extracellular Fluid / Q000378:metabolism; D006801:Humans; D058225:Plaque, Amyloid / Q000378:metabolism; D017729:Presynaptic Terminals / Q000378:metabolism*; D009435:Synaptic Transmission / Q000502:physiology*; D013572:Synaptic Vesicles / Q000378:metabolism
D016229:Amyloid beta-Peptides; D053829:Amyloid Precursor Protein Secretases; D010450:Endopeptidases; D016282:Aspartic Acid Endopeptidases; C509280:BACE1 protein, human