Alzheimer's disease is a synaptic failure.
In its earliest clinical phase, Alzheimer's disease characteristically produces a remarkably pure impairment of memory. Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfunction is caused by diffusible oligomeric assemblies of the amyloid beta protein.
Selkoe
Dennis J
DJ
Center for Neurologic Diseases, Brigham and Women's Hospital, and the Harvard Center for Neurodegeneration and Repair, Boston, MA 02115, USA. selkoe@cnd.bwh.harvard.edu
D000544:Alzheimer Disease / Q000473:pathology / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D003071:Cognition; D006801:Humans; D017774:Long-Term Potentiation; D008565:Membrane Proteins / Q000235:genetics; D008568:Memory; D051379:Mice; D008822:Mice, Transgenic; D053764:Presenilin-1; D013569:Synapses / Q000502:physiology* / Q000648:ultrastructure; D009435:Synaptic Transmission
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D008565:Membrane Proteins; C508853:PSEN1 protein, human; D053764:Presenilin-1