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http://eprints.org/relation/isVersionOf http://eprints.iliauni.edu.ge/id/document/13085 http://eprints.org/relation/isVolatileVersionOf http://eprints.iliauni.edu.ge/id/document/13085 http://eprints.org/relation/isIndexCodesVersionOf http://eprints.iliauni.edu.ge/id/document/13085 archive 8 disk0/00/00/28/35 2015-06-01 05:51:41 2015-06-01 05:51:41 2015-06-01 05:51:41 article 416 show Shrestha BR Vitolo OV Joshi P Lordkipanidze Tamar tamar_lordkipanidze@iliauni.edu.ge pub Q1 ins10 public Elevated levels of amyloid-beta peptide (Abeta) are found in Down's syndrome patients and alter synaptic function during the early stages of Alzheimer's disease. Dendritic spines, sites of most excitatory synaptic contacts, are considered to be an important locus for encoding synaptic plasticity. We used time-lapse two-photon imaging of hippocampal pyramidal neurons in organotypic slices to study the effects of Abeta on the development of dendritic spines. We report that exposure of hippocampal neurons to sub-lethal levels of Abeta decreased spine density, increased spine length and subdued spine motility. The effect of Abeta on spine density was reversible. Moreover, Abeta's effect on dendritic spine density was blocked by rolipram, a phosphodiesterase type IV inhibitor, suggesting the involvement of a cAMP dependent pathway. These findings raise the possibility that Abeta-induced spine alterations could underlie the cognitive defects in Alzheimer's disease and Down syndrome. 2006-11 Mol Cell Neurosci 33 3 Elsevier 274-282 TRUE http://www.ncbi.nlm.nih.gov/pubmed/16962789