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12740129
Synaptic plasticity in animal models of early Alzheimer's disease.
Rowan MJ, Klyubin I, Cullen WK, Anwyl R
Amyloid beta-protein (Abeta) is believed to be a primary cause of Alzheimer's disease (AD). Recent research has examined the potential importance of soluble species of Abeta in synaptic dysfunction, long before fibrillary Abeta is deposited and neurodegenerative changes occur. Hippocampal excitatory synaptic transmission and plasticity are disrupted in transgenic mice overexpressing human amyloid precursor protein with early onset familial AD mutations, and in rats after exogenous application of synthetic Abeta both in vitro and in vivo. Recently, naturally produced soluble Abeta was shown to block the persistence of long-term potentiation (LTP) in the intact hippocampus. Sub-nanomolar concentrations of oligomeric Abeta were sufficient to inhibit late LTP, pointing to a possible reason for the sensitivity of hippocampus-dependent memory to impairment in the early preclinical stages of AD. Having identified the active species of Abeta that can play havoc with synaptic plasticity, it is hoped that new ways of targeting early AD can be developed.
358
821-8
2003
Other categories referring to 12740129
Pathological mechanism.Citation   (1)
Revisions: 2
Last Time: 8/29/2006 1:30:48 PM
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Owner: Tom Morse