A biochemical hypothesis - that Alzheimer's disease (AD) is a progressive cerebral amyloidosis caused by the aggregation of the amyloid b-protein (Ab) - preceded and enabled the discovery of etiologies. This volume serves as a record focused on bringing together investigators at the forefront of elucidating the structure and function of hippocampal synapses with investigators focused on understanding how early assemblies of Ab may compromise some of these synapses.
Indice testuale
Permanence of the synapse and molecular instability.- Cellular biology of AMPA receptor trafficking and synaptic plasticity.- Imaging of experience-dependent structural plasticity in the mouse neocortex in vivo.- Synapse loss, synaptic plasticity and the postsynaptic density.- Impact of Beta Amyloid on Excitatory Synaptic Transmission and Plasticity.- Quantitative neuropathology in Alzheimer's mouse models.- Multiple levels of synaptic regulation by NMDA-type glutamate receptor in normal and disease states.- Soluble Oligomers of the Amyloid ss-Protein Impair Synaptic Plasticity and Behavior.- Why Alzheimer's is a disease of memory: synaptic targeting by pathogenic Ass oligomers (ADDLs).- Synaptic transmission dynamically modulates interstitial fluid amyloid-b levels.- Ass-induced toxicity mediated by caspase cleavage of the amyloid precursor protein (APP).- Long-term potentiation and Ass: targeting Ass species, cellular mechanisms and putative receptors.- Genes, synapses and autism spectrum disorders.- Subject Index
