Abstract
How do soluble oligomers of amyloid β-protein impair hippocampal synaptic plasticity?
Highlights
Alzheimer’s disease (AD), the most common neurodegenerative disorder, is characterized by progressive memory and cognitive impairment and the cerebral accumulation of extracellular amyloid plaques and intraneuronal neurofibrillary tangles
We found that LTD induction was facilitated by pathophysiologically relevant low concentrations of soluble Aβ oligomers through activation of either NMDA receptors or metabotropic glutamate receptors, depending on the electrical stimulation protocol used to induce the LTD (Li et al, 2009)
We report that pharmacologically blocking glutamate uptake closely recapitulates the effects of Aβ on LTD induction, suggesting that Aβ oligomers bias towards synapse weakening in part through such a mechanism (Li et al, 2009)
Summary
Alzheimer’s disease (AD), the most common neurodegenerative disorder, is characterized by progressive memory and cognitive impairment and the cerebral accumulation of extracellular amyloid plaques and intraneuronal neurofibrillary tangles. Synthetic Aβ peptides were reported to potently enable the induction of LTD in CA1 in an NMDARdependent manner in vivo (Kim et al, 2001; Cheng et al, 2009), whereas other studies found no effect on LTD in slices (Wang et al, 2002, 2004; Raymond et al, 2003).
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