@article{18,
  keywords = {Peptide Fragments/metabolism, Neurons/*physiology, Nerve Net/physiopathology, Mice, Transgenic, Mice, Memory, Maze Learning, *Disease Models, Animal, Cerebral Cortex/pathology/*physiopathology, Calcium Signaling, Calcium/metabolism, Animals, Amyloid beta-Protein/metabolism, Alzheimer Disease/*pathology/*physiopathology, Synapses/*physiology, Senile Plaques/chemistry/*pathology},
  author = {M. Busche and G. Eichhoff and H. Adelsberger and D. Abramowski and K. Wiederhold and C. Haass and M. Staufenbiel and A Konnerth and O Garaschuk},
  title = {Clusters of hyperactive neurons near amyloid plaques in a mouse model of Alzheimer's disease},
  abstract = {The neurodegeneration observed in Alzheimer's disease has been associated with synaptic dismantling and progressive decrease in neuronal activity. We tested this hypothesis in vivo by using two-photon Ca2+ imaging in a mouse model of Alzheimer's disease. Although a decrease in neuronal activity was seen in 29% of layer 2/3 cortical neurons, 21% of neurons displayed an unexpected increase in the frequency of spontaneous Ca2+ transients. These "hyperactive" neurons were found exclusively near the plaques of amyloid beta-depositing mice. The hyperactivity appeared to be due to a relative decrease in synaptic inhibition. Thus, we suggest that a redistribution of synaptic drive between silent and hyperactive neurons, rather than an overall decrease in synaptic activity, provides a mechanism for the disturbed cortical function in Alzheimer's disease.},
  year = {2008},
  journal = {Science},
  volume = {321},
  number = {5896},
  pages = {1686-1689},
  month = {Sep 19},
  url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18802001},
  note = {1095-9203 (Electronic)Journal ArticleResearch Support, Non-U.S. Gov't},
  language = {eng},
}