Neurobiology of Disease Soluble -Amyloid1– 40 Induces NMDA-Dependent Degradation of Postsynaptic Density-95 at Glutamatergic Synapses
نویسندگان
چکیده
F. Roselli,1,2 M. Tirard,1 J. Lu,1 P. Hutzler,3 P. Lamberti,2 P. Livrea,2 M. Morabito,4 and O. F. X. Almeida1 1Max Planck Institute of Psychiatry, 80804 Munich, Germany, 2Department of Neurological and Psychiatric Sciences, University of Bari, 70124 Bari, Italy, 3Institute of Pathology, GSF National Research Center for Environment and Health, 85764 Neuherberg, Germany, and 4Department of Cell Biology, University of Massachusetts Medical School, E. K. Shriver Center, Waltham, Massachusetts 02452
منابع مشابه
Soluble beta-amyloid1-40 induces NMDA-dependent degradation of postsynaptic density-95 at glutamatergic synapses.
Amyloid-beta (Abeta) has been implicated in memory loss and disruption of synaptic plasticity observed in early-stage Alzheimer's disease. Recently, it has been shown that soluble Abeta oligomers target synapses in cultured rat hippocampal neurons, suggesting a direct role of Abeta in the regulation of synaptic structure and function. Postsynaptic density-95 (PSD-95) is a postsynaptic scaffoldi...
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تاریخ انتشار 2005