| pubmed-article:15120860 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15120860 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:15120860 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
| pubmed-article:15120860 | lifeskim:mentions | umls-concept:C0085151 | lld:lifeskim |
| pubmed-article:15120860 | lifeskim:mentions | umls-concept:C0299212 | lld:lifeskim |
| pubmed-article:15120860 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:15120860 | lifeskim:mentions | umls-concept:C1517676 | lld:lifeskim |
| pubmed-article:15120860 | lifeskim:mentions | umls-concept:C0205099 | lld:lifeskim |
| pubmed-article:15120860 | lifeskim:mentions | umls-concept:C0599668 | lld:lifeskim |
| pubmed-article:15120860 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:15120860 | pubmed:dateCreated | 2004-5-3 | lld:pubmed |
| pubmed-article:15120860 | pubmed:abstractText | Alzheimer's disease is characterized by amyloid peptide formation and deposition, neurofibrillary tangles, central cholinergic dysfunction, and dementia; however, the relationship between these parameters is not well understood. We studied the effect of amyloid peptide formation and deposition on central cholinergic function in knock-in mice carrying the human amyloid precursor protein (APP) gene with the Swedish/London double mutation (APP-SL mice) which were crossbred with transgenic mice overexpressing normal (PS1wt) or mutated (M146L; PS1mut) human presenilin-1. APP-SLxPS1mut mice had increased levels of Abeta peptides at 10 months of age and amyloid plaques at 14 months of age while APP-SLxPS1wt mice did not have increased peptide levels and did not develop amyloid plaques. We used microdialysis in 15-27 months old mice to compare hippocampal acetylcholine (ACh) levels in the two mouse lines and found that extracellular ACh levels were slightly but significantly reduced in the APP-SLxPS1mut mice (-26%; P=0.044). Exploratory activity in the open field increased hippocampal ACh release by two-fold in both mouse lines; total and relative increases were not significantly different for the two strains under study. Similarly, infusion of scopolamine (1 microM) increased hippocampal ACh release to a similar extent (3-5-fold) in both groups. High-affinity choline uptake, a measure of the ACh turnover rate, was identical in both mouse lines. Neurons expressing choline acetyltransferase were increased in the septum of APP-SLxPS1mut mice (+26%; P=0.046). We conclude that amyloid peptide production causes a small decrease of extracellular ACh levels. The deposition of amyloid plaques, however, does not impair stimulated ACh release and proceeds without major changes of central cholinergic function. | lld:pubmed |
| pubmed-article:15120860 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15120860 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15120860 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15120860 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15120860 | pubmed:issn | 0306-4522 | lld:pubmed |
| pubmed-article:15120860 | pubmed:author | pubmed-author:KleinJJ | lld:pubmed |
| pubmed-article:15120860 | pubmed:author | pubmed-author:PopeJJ | lld:pubmed |
| pubmed-article:15120860 | pubmed:author | pubmed-author:HartmannJJ | lld:pubmed |
| pubmed-article:15120860 | pubmed:author | pubmed-author:KönigGG | lld:pubmed |
| pubmed-article:15120860 | pubmed:author | pubmed-author:EbertUU | lld:pubmed |
| pubmed-article:15120860 | pubmed:author | pubmed-author:ErbCC | lld:pubmed |
| pubmed-article:15120860 | pubmed:author | pubmed-author:BaumannK HKH | lld:pubmed |
| pubmed-article:15120860 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15120860 | pubmed:volume | 125 | lld:pubmed |
| pubmed-article:15120860 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15120860 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15120860 | pubmed:pagination | 1009-17 | lld:pubmed |
| pubmed-article:15120860 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:15120860 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15120860 | pubmed:articleTitle | Central cholinergic functions in human amyloid precursor protein knock-in/presenilin-1 transgenic mice. | lld:pubmed |
| pubmed-article:15120860 | pubmed:affiliation | Alzheimer Research Group, Bayer Health Care AG, D-42096 Wuppertal, Germany. | lld:pubmed |
| pubmed-article:15120860 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15120860 | pubmed:publicationType | Comparative Study | lld:pubmed |
| entrez-gene:11820 | entrezgene:pubmed | pubmed-article:15120860 | lld:entrezgene |
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