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000012404 084__ $$2WoS$$aBiochemistry & Molecular Biology
000012404 084__ $$2WoS$$aChemistry, Medicinal
000012404 084__ $$2WoS$$aNeurosciences
000012404 1001_ $$0P:(DE-Juel1)VDB65869$$aFunke, S. A.$$b0$$uFZJ
000012404 245__ $$aOral Treatment with the D-Enantiomeric Peptide D3 Improves Pathology and Behavior of Alzheimers disease Transgenic Mice
000012404 260__ $$aWashington, DC$$bSoc.$$c2010
000012404 300__ $$a639 - 648
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000012404 440_0 $$023262$$aACS Chemical Neuroscience$$v1$$x1948-7193$$y9
000012404 500__ $$aThis work has been supported by a grant from Volkswagen-Stiftung to D.W., C.K., and H.S. (I/82 649). Support from the "Prasidentenfond der Helmholtzgemeinschaft" (HGF, "Virtual Institute of Structural Biology") to D.W. is acknowledged. C.M. was supported by a DGCIS grant (French state). The electron microscopy facility used for this work is part of the Partnership for Structural Biology (PSB). Part of this research was supported by P30 NS47466. I.K. and T.v.G have been supported by 5P50 AG16582-10.
000012404 520__ $$aSeveral lines of evidence suggest that the amyloid-β-peptide (Aβ) plays a central role in the pathogenesis of Alzheimer's disease (AD). Not only Aβ fibrils but also small soluble Aβ oligomers in particular are suspected to be the major toxic species responsible for disease development and progression. The present study reports on in vitro and in vivo properties of the Aβ targeting d-enantiomeric amino acid peptide D3. We show that next to plaque load and inflammation reduction, oral application of the peptide improved the cognitive performance of AD transgenic mice. In addition, we provide in vitro data elucidating the potential mechanism underlying the observed in vivo activity of D3. These data suggest that D3 precipitates toxic Aβ species and converts them into nonamyloidogenic, nonfibrillar, and nontoxic aggregates without increasing the concentration of monomeric Aβ. Thus, D3 exerts an interesting and novel mechanism of action that abolishes toxic Aβ oligomers and thereby supports their decisive role in AD development and progression.
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000012404 65320 $$2Author$$aMirror image phage display
000012404 65320 $$2Author$$aD-enantiomeric peptide
000012404 65320 $$2Author$$aAlzheimer's disease
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000012404 7001_ $$0P:(DE-HGF)0$$avan Groen, T.$$b1
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000012404 7001_ $$0P:(DE-Juel1)VDB65461$$aBartnik, D.$$b3$$uFZJ
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000012404 7001_ $$0P:(DE-HGF)0$$aMoriscot, C.$$b8
000012404 7001_ $$0P:(DE-HGF)0$$aSchoehn, G.$$b9
000012404 7001_ $$0P:(DE-HGF)0$$aHorn, A.H.C.$$b10
000012404 7001_ $$0P:(DE-HGF)0$$aMüller-Schiffmann, A.$$b11
000012404 7001_ $$0P:(DE-HGF)0$$aKorth, C.$$b12
000012404 7001_ $$0P:(DE-HGF)0$$aSticht, H.$$b13
000012404 7001_ $$0P:(DE-Juel1)132029$$aWillbold, D.$$b14$$uFZJ
000012404 773__ $$0PERI:(DE-600)2528493-9$$a10.1021/cn100057j$$gVol. 1, p. 639 - 648$$p639 - 648$$q1<639 - 648$$tACS chemical neuroscience$$v1$$x1948-7193$$y2010
000012404 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368690
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