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P2‐326: Blocking the apoE/Aβ binding prevents apoE‐mediated intraneuronal accumulation of Aβ peptides and ameliorates synaptic degeneration
Author(s) -
Kuszczyk Magdalena A.,
Sadowski Martin J.
Publication year - 2010
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.2010.05.1377
Subject(s) - apolipoprotein e , hippocampal formation , astrocyte , chemistry , extracellular , neurotoxicity , receptor , nmda receptor , hippocampus , microbiology and biotechnology , neuroscience , biochemistry , pharmacology , biology , medicine , central nervous system , toxicity , disease , organic chemistry
Similarly, Ab40 and Ab42 strengthened or weakened F-type transmission, respectively. D-type connections faired equal increases in failure rates and further depression regardless of Ab species or concentration. Low dose Ab40 also stimulated two forms of short term plasticity, synaptic augmentation and post-tetanic potentiation, whereas Ab42 clearly inhibited both SA (30% decline vs. control) and PTP (10% decline). Conclusions: These results, together with our previous study of electrical synaptic networks in PFC (PLoS 4 (12) e8366 2009) have implications for the biological function of Ab. Our data suggests the ‘good’ peptide, Ab40, serves to improve excitatory synaptic transmission and plasticity while the ‘toxic’ peptide, Ab42, is detrimental to PFC synapses. Pharmacological efforts to eliminate Ab should probably seek to spare physiological levels of Ab40.