Synaptic Plasticity and the Mechanism of Alzheimer''s Disease

In disorders like Huntington’s disease, amyotrophic lateral sclerosis and even Parkinson’s disease, unbiased genetic screens, linkage analysis and positional cloning have identified causative genes that subsequently allowed the formulation of specific biochemical hypotheses.

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