Synaptic Targeting by Alzheimer's-Related Amyloid β Oligomers
Northwestern University · University of Southern California · +1 more institution
Abstract
The cognitive hallmark of early Alzheimer's disease (AD) is an extraordinary inability to form new memories. For many years, this dementia was attributed to nerve-cell death induced by deposits of fibrillar amyloid beta (Abeta). A newer hypothesis has emerged, however, in which early memory loss is considered a synapse failure caused by soluble Abeta oligomers. Such oligomers rapidly block long-term potentiation, a classic experimental paradigm for synaptic plasticity, and they are strikingly elevated in AD brain tissue and transgenic-mouse AD models. The current work characterizes the manner in which Abeta oligomers attack neurons. Antibodies raised against synthetic oligomers applied to AD brain sections…
Citation impact
- FWCI
- 19.82
- Percentile
- 100%
- References
- 64
Authors
12Topics & keywords
- Long-term potentiation
- Synaptic plasticity
- Neuroscience
- Synapse
- Hippocampal formation
- Postsynaptic potential
- Biology
- Amyloid (mycology)
- Good health and well-being