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P4‐225: SYNTHETIC β‐AMYLOID DIMER IN ANTI‐PARALLEL CONFORMATION INDUCES IN VIVO SYNAPTIC PLASTICITY DEFICITS
Author(s) -
Kim Hye Yun,
Kim Hyunjin Vincent,
Lee Sejin,
Kim Dong Jin,
Kim Young Soo
Publication year - 2014
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2014.05.1743
Subject(s) - dimer , chemistry , monomer , synaptic plasticity , biophysics , covalent bond , in vivo , peptide , structural plasticity , biochemistry , neuroscience , biology , receptor , polymer , organic chemistry , microbiology and biotechnology
a secretory peptide which can inhibit the neurotoxicity of Ab. However, the neuroprotective effects and mechanism(s) of HN on Ab-induced AD-like pathological changes and memory deficits are yet incompletely defined. Methods: The animal models were established by injected of 2 ml Ab 42 into the hippocampus CA1. HN-treatment group was given 2 ml HN at the same site after the success of model making. Spatial memory was measured by Morris water maze test on the 7th day after injection. The dendritic morphology and dendritic spine density of the pyramidal neurons in the hippocampal CA1 of the rat was analyzed by the Golgi staining and the synaptic transmission was detected by electrophysiological recording. The expressions of several memory-associated proteins were detected by Western blotting, and the ultrastructure of neurons in hippocampal CA1 region of the rats was studied by transmission electron microscope. Results: In the present study, supplementation of HN has been approved to enhance long term potential and ameliorate memory deficits induced by Ab42, with increase dendritic branches and the density of the dendritic spines, and upregulation of preand post-synaptic protein levels. Supplementation of HN also attenuated the Ab42-induced tau hyperphosphorylation through activation protein phosphatase-2A (PP2A) with decreased inhibitory phosphorylated PP2A catalytic subunit (PP2AC) at Tyr307. At last, we also found that supplementation of HN ameliorated the Ab42-induced apoptosis and oxidative stress. Conclusions: The observations, in all, reveal the important roles of HN against Ab 42 -induced AD-like pathological changes and memory deficits.