| pubmed-article:16470685 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16470685 | lifeskim:mentions | umls-concept:C2333949 | lld:lifeskim |
| pubmed-article:16470685 | lifeskim:mentions | umls-concept:C0002716 | lld:lifeskim |
| pubmed-article:16470685 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
| pubmed-article:16470685 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:16470685 | lifeskim:mentions | umls-concept:C0013138 | lld:lifeskim |
| pubmed-article:16470685 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:16470685 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:16470685 | pubmed:dateCreated | 2006-3-23 | lld:pubmed |
| pubmed-article:16470685 | pubmed:abstractText | Accumulation of amyloid (Abeta) peptides has been suggested to be the primary event in Alzheimer's disease. In neurons, K+ channels regulate a number of processes, including setting the resting potential, keeping action potentials short, timing interspike intervals, synaptic plasticity, and cell death. In particular, A-type K+ channels have been implicated in the onset of LTP in mammalian neurons, which is thought to underlie learning and memory. A number of studies have shown that Abeta peptides alter the properties of K+ currents in mammalian neurons. We set out to determine the effects of Abeta peptides on the neuronal A-type K+ channels of Drosophila. Treatment of cells for 18 h with 1 microM Abeta1-42 altered the kinetics of the A-type K+ current, shifting steady-state inactivation to more depolarized potentials and increasing the rate of recovery from inactivation. It also caused a decrease in neuronal viability. Thus it seems that alteration in the properties of the A-type K+ current is a prelude to the amyloid-induced death of neurons. This alteration in the properties of the A-type K+ current may provide a basis for the early memory impairment that was observed prior to neurodegeneration in a recent study of a transgenic Drosophila melanogaster line over-expressing the human Abeta1-42 peptide. | lld:pubmed |
| pubmed-article:16470685 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16470685 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16470685 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16470685 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16470685 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16470685 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16470685 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16470685 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16470685 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16470685 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:16470685 | pubmed:issn | 0022-3034 | lld:pubmed |
| pubmed-article:16470685 | pubmed:author | pubmed-author:KiddJackie... | lld:pubmed |
| pubmed-article:16470685 | pubmed:author | pubmed-author:SattelleDavid... | lld:pubmed |
| pubmed-article:16470685 | pubmed:author | pubmed-author:BrownLaurence... | lld:pubmed |
| pubmed-article:16470685 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16470685 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:16470685 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16470685 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16470685 | pubmed:pagination | 476-87 | lld:pubmed |
| pubmed-article:16470685 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
| pubmed-article:16470685 | pubmed:meshHeading | pubmed-meshheading:16470685... | lld:pubmed |
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| pubmed-article:16470685 | pubmed:meshHeading | pubmed-meshheading:16470685... | lld:pubmed |
| pubmed-article:16470685 | pubmed:meshHeading | pubmed-meshheading:16470685... | lld:pubmed |
| pubmed-article:16470685 | pubmed:meshHeading | pubmed-meshheading:16470685... | lld:pubmed |
| pubmed-article:16470685 | pubmed:meshHeading | pubmed-meshheading:16470685... | lld:pubmed |
| pubmed-article:16470685 | pubmed:meshHeading | pubmed-meshheading:16470685... | lld:pubmed |
| pubmed-article:16470685 | pubmed:meshHeading | pubmed-meshheading:16470685... | lld:pubmed |
| pubmed-article:16470685 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16470685 | pubmed:articleTitle | Effects of amyloid peptides on A-type K+ currents of Drosophila larval cholinergic neurons. | lld:pubmed |
| pubmed-article:16470685 | pubmed:affiliation | Department of Human Anatomy and Genetics, MRC Functional Genetics Unit, University of Oxford, South Parks Road, Oxford OX1 3QX, United Kingdom. jackie.kidd@physiol.ox.ac.uk | lld:pubmed |
| pubmed-article:16470685 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16470685 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16470685 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16470685 | lld:pubmed |
