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Gene Expression Changes Related to Synaptic Deficits in the Tg2576 Mouse Model of Alzheimer's Disease

Jeffrey F. Waring, David J. Anderson, Paul E. Kroeger, Jinhe Li, Sarah P. Chen, Bradley A. Hooker, Murali Gopalakrishnan and Clark A. Briggs

Aβ in the form of soluble oligomers or amyloid deposits has been identified as an endogenous substance responsible for the induction of neurodegeneration in Alzheimer’s disease. To study Aβ-related processes, we evaluated both input-output electrophysiology and gene expression in hippocampi from Tg2576 and wild-type control mice 7 months of age. In hippocampal CA1 f-EPSP recordings, the postsynaptic response was reduced in Tg2576, while there was no significant difference in fiber volley amplitude or paired-pulse facilitation. Gene expression was evaluated on RNA extracted from hippocampi contralateral to those used for electrophysiology. Robust gene expression differences were observed between Tg2576 and WT hippocampi, many of which reflected deficits in glutamatergic synaptic transmission. These results support the identification of synaptic deficits in young adult Tg2576 mice, and identify gene products that potentially could be used as biomarkers for Aβ toxicity or as mechanistic targets in further studies