12 RESULTS
COMMENT I think this method has potentially important applications. However, it is important to note that the analyses in this study were limited to presynaptic structures. Most synaptic studies in AD models that I’m aware of, but then I’m likely biased by my are
COMMENT This is potentially very interesting, and may be usable in a number of diseases in which synapse number is thought to be an important variable. It is not clear what is the sensitivity of this method; while differences were noted in temporal lobe epilepsy,
COMMENT This study is quite comprehensive and shows quite nicely that APP, and not Aβ, is responsible for the epileptiform activity in APP-overexpressing mice. This has always been a bit of a conundrum for me, since our work shows that Aβ reduces excitatory trans
COMMENT Interesting papers. It's quite amazing that a protein linked to enhanced memory performance can be linked to synaptic plasticity, and AMPAR trafficking. The study by Makuch et al. provides more evidence that AMPA-R trafficking is an important regulat
COMMENT This is a very nice study. It provides further support that synaptic activity controls neuronal release of Aβ, and argues that synaptic activity may be the dominant factor controlling Aβ levels and plaque formation (rather than the recently proposed chang
COMMENT This study nicely examines potential signaling activated by β amyloid that could perturb LTP. The signaling identified can play multiple roles, so their exact participation in the effects of β amyloid needs to be elucidated. As targets for Alzheimer'
COMMENT I am intrigued by the findings regarding changes in transmission in the dentate gyrus of APP Tg animals. The authors find an increase in miniature inhibitory post-synaptic (IPSC) current frequency, but a decrease in "spontaneous" IPSC frequency
COMMENT I’ve read the article and find it to be interesting and to provide important new information. It demonstrates that overproduction of β amyloid in the entorhinal cortex can lead to synaptic aberrations in the hippocampus. This supports the view that pre-sy
COMMENT Our findings reported in Neuron indicate that removal of synaptic AMPAR by Aβ leads to loss of spines and loss of NMDA responses. In other cases, removal of synaptic AMPAR does not lead to loss of NMDA responses (e.g., Shi et al., 2001; expression of GluR
COMMENT I've read this informative forum with interest. I believe our work may have some relevance to the question: Is secreted Aβ a pathogenic agent in Alzheimer disease? We have reported that transient viral overexpression of APP depresses excitatory synap
COMMENT I've read this informative forum with interest. I believe our work may have some relevance to the question: Is secreted Aβ a pathogenic agent in Alzheimer disease? We have reported that transient viral overexpression of APP depresses excitatory synap
COMMENT These are very interesting studies. There has been growing evidence that some of the primary targets of AD and APP are synapses. These studies support this view. Furthermore, there has been recent interest in the relation between APP processing and synapt
