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Picomolar Amyloid-beta Positively Modulates Synaptic Plasticity and Memory in Hippocampus

Overview
Journal J Neurosci
Specialty Neurology
Date 2009 Jan 2
PMID 19118188
Citations 385
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Abstract

Amyloid-beta (Abeta) peptides are produced in high amounts during Alzheimer's disease, causing synaptic and memory dysfunction. However, they are also released in lower amounts in normal brains throughout life during synaptic activity. Here we show that low picomolar concentrations of a preparation containing both Abeta(42) monomers and oligomers cause a marked increase of hippocampal long-term potentiation, whereas high nanomolar concentrations lead to the well established reduction of potentiation. Picomolar levels of Abeta(42) also produce a pronounced enhancement of both reference and contextual fear memory. The mechanism of action of picomolar Abeta(42) on both synaptic plasticity and memory involves alpha7-containing nicotinic acetylcholine receptors. These findings strongly support a model for Abeta effects in which low concentrations play a novel positive, modulatory role on neurotransmission and memory, whereas high concentrations play the well known detrimental effect culminating in dementia.

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References
1.
Phinney A, Calhoun M, Wolfer D, Lipp H, Zheng H, Jucker M . No hippocampal neuron or synaptic bouton loss in learning-impaired aged beta-amyloid precursor protein-null mice. Neuroscience. 1999; 90(4):1207-16. DOI: 10.1016/s0306-4522(98)00645-9. View

2.
Wang H, Lee D, Dandrea M, Peterson P, Shank R, Reitz A . beta-Amyloid(1-42) binds to alpha7 nicotinic acetylcholine receptor with high affinity. Implications for Alzheimer's disease pathology. J Biol Chem. 2000; 275(8):5626-32. DOI: 10.1074/jbc.275.8.5626. View

3.
Ishida A, Furukawa K, Keller J, Mattson M . Secreted form of beta-amyloid precursor protein shifts the frequency dependency for induction of LTD, and enhances LTP in hippocampal slices. Neuroreport. 1997; 8(9-10):2133-7. DOI: 10.1097/00001756-199707070-00009. View

4.
Araki W, Kitaguchi N, Tokushima Y, Ishii K, Aratake H, Shimohama S . Trophic effect of beta-amyloid precursor protein on cerebral cortical neurons in culture. Biochem Biophys Res Commun. 1991; 181(1):265-71. DOI: 10.1016/s0006-291x(05)81412-3. View

5.
Schenk F, Morris R . Dissociation between components of spatial memory in rats after recovery from the effects of retrohippocampal lesions. Exp Brain Res. 1985; 58(1):11-28. DOI: 10.1007/BF00238949. View