Journal
MOLECULAR NEURODEGENERATION
Volume 6, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1750-1326-6-63
Keywords
Alzheimer's disease; amyloid-beta; synapse loss; long-term depression; long-term potentiation; cognitive decline
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Funding
- Alzheimer's disease Drug Discovery Foundation/Association for Frontotemporal Dementias [K99 AG033670-01A1, P50 AG005134, AG12406, AG08487]
- NIH [T32 GM07753]
- Paul and Daisy Soros Foundation
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Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by insidious cognitive decline and memory dysfunction. Synapse loss is the best pathological correlate of cognitive decline in AD and mounting evidence suggests that AD is primarily a disease of synaptic dysfunction. Soluble oligomeric forms of amyloid beta (A beta), the peptide that aggregates to form senile plaques in the brain of AD patients, have been shown to be toxic to neuronal synapses both in vitro and in vivo. A beta oligomers inhibit long-term potentiation (LTP) and facilitate long-term depression (LTD), electrophysiological correlates of memory formation. Furthermore, oligomeric A beta has also been shown to induce synapse loss and cognitive impairment in animals. The molecular underpinnings of these observations are now being elucidated, and may provide clear therapeutic targets for effectively treating the disease. Here, we review recent findings concerning AD pathogenesis with a particular focus on how A beta impacts synapses.
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