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Proteome analysis of three mouse models for Alzheimer's disease suggests impairment of adolescent hippocampal plasticity
Author(s) -
Hartl Daniela,
Zabel Claus,
Rohe Michael,
Mao Lei,
Klose Joachim
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.507.4
Subject(s) - hippocampal formation , genetically modified mouse , proteome , transgene , biology , plasticity , neuroplasticity , neuroscience , synaptic plasticity , disease , microbiology and biotechnology , pathology , medicine , bioinformatics , biochemistry , receptor , gene , physics , thermodynamics
We have analyzed three mouse models for Alzheimer's disease (AD) using our high‐resolution 2‐dimensional gel electrophoresis technology in combination with fluorescent dyes and mass spectrometry. We found numerous protein expression changes in brain regions of transgenic mice which largely preceeded the occurrence of amyloid plaques. Interestingly, we also found a considerable peak in the number of hippocampal protein changes of adolescent transgenic mice. Furthermore, the absence of normal developmental proteome alterations as well as a down‐regulation of proteins related to synaptic plasticity were observed in this early phase. Together, our results suggest the disturption of hippocampal plasticity during adolescence in APP transgenic mice. Our findings are in line with the observation that AD is preceded by a clinically silent period lasting several years to decades.

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