Synaptic dysfunction is involved in early stages of Alzheimers disease (AD). Amyloid-β peptides (Aβ), a neuropathologic hallmark of the disease, have been shown to alter synaptic function. Given that Aβ is present in different forms including monomeric, oligomeric and fibrillar species, we have investigated whether fibrillar Aβ impairs synaptic function. Here we report that a synthetic fibrillar form of Aβ impairs the late protein-synthesis dependent phase of LTP without affecting the early protein-synthesis independent phase. These findings add to previous reports that Aβ oligomers are highly toxic to cells and might cause synaptic dysfunction, and suggest that a therapeutic intervention in AD should include the use of drugs inhibiting and disassembling fibril formation in addition to drugs inhibiting oligomers formation.
Keywords: Synapse, amyloid, Alzheimer's disease, synaptic plasticity, fibrils
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