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Abeta(1-42) injection causes memory impairment, lowered cortical and serum BDNF levels, and decreased hippocampal 5-HT(2A) levels

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Authors:
  • Christensen, R ;
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    unknown
  • Marcussen, Anders Bue ;
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    Nutrient and Metabolite Sensing, NNF Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, Københavns Universitet
  • Wörtwein, Gitta ;
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    Orcid logo0000-0001-6981-7885
    Section of Environmental Health, Department of Public Health, Faculty of Health and Medical Sciences, Københavns Universitet
  • Knudsen, G M ;
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    unknown
  • Aznar, S
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    unknown
DOI:
10.1016/j.expneurol.2007.10.009
Abstract:
Aggregation of the beta-amyloid protein (Abeta) is a hallmark of Alzheimer's disease (AD) and is believed to be causally involved in a neurodegenerative cascade. In patients with AD, reduced levels of serum Brain Derived Neurotrophic Factor (BDNF) and cortical 5-HT(2A) receptor binding has recently been reported but it is unknown how these changes are related to beta-amyloid accumulation. In this study we examined in rats the effect of intrahippocampal injections of aggregated Abeta(1-42) (1 microg/microl) on serum and brain BDNF or 5-HT(2A) receptor levels. A social recognition test paradigm was used to monitor Abeta(1-42) induced memory impairment. Memory impairment was seen 22 days after injection of Abeta(1-42) in the experimental group and until termination of the experiments. In the Abeta(1-42) injected animals we saw an abolished increase in serum BDNF levels that was accompanied by significant lower BDNF levels in frontal cortex and by an 8.5% reduction in hippocampal 5-HT(2A) receptor levels. A tendency towards lowered cortical 5-HT(2A) was also observed. These results indicate that the Abeta(1-42) associated memory deficit is associated with an impaired BDNF regulation, which is reflected in lower cortical BDNF levels, and changes in hippocampal 5-HT(2A) receptor levels. This suggests that the BDNF and 5-HT2A changes observed in AD are related to the presence of Abeta(1-42) deposits.
Type:
Journal article
Language:
English
Published in:
Experimental Neurology, 2008, Vol 210, Issue 1, p. 164-71
Main Research Area:
Medical science
Publication Status:
Published
Review type:
Peer Review
Submission year:
2008
Scientific Level:
Scientific
ID:
1928991

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