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Most Intriguing Documents 3Q08-Chemistry and Related Science

Following is one of the journal documents most requested by researchers using CAS online services.

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CAS indexed 1 chemical substance from this document. CAS subject entries for this document include: Alzheimer's disease; Anti-Alzheimer's agents; Cognition enhancers; and 9 additional concepts.

CAPLUS COPYRIGHT 2008 ACS on STN

TITLE:	CNI-1493 inhibits A.beta. production, plaque formation, and cognitive deterioration in an animal model of Alzheimer's disease
AUTHOR(S):	Bacher, Michael; Dodel, Richard; Aljabari, Bayan; Keyvani, Kathy; Marambaud, Philippe; Kayed, Rakez; Glabe, Charles; Goertz, Nicole; Hoppmann, Anne; Sachser, Norbert; Klotsche, Jens; Schnell, Susanne; Lewejohann, Lars; Al-Abed, Yousef
CORPORATE SOURCE:	Department of Neurology, Philipps-University Marburg, Marburg, 35039, Germany
SOURCE:	Journal of Experimental Medicine (2008), 205(7), 1593-1599 CODEN: JEMEAV; ISSN: 0022-1007
PUBLISHER:	Rockefeller University Press
LANGUAGE:	English

ABSTRACT:
Alzheimer's disease (AD) is characterized by neuronal atrophy caused by sol. amyloid .beta. protein (A.beta.) peptide "oligomers" and a microglial-mediated inflammatory response elicited by extensive amyloid deposition in the brain. We show that CNI-1493, a tetravalent guanylhydrazone with established antiinflammatory properties, interferes with A.beta. assembly and protects neuronal cells from the toxic effect of sol. A.beta. oligomers. Administration of CNI-1493 to TgCRND8 mice overexpressing human amyloid precursor protein (APP) for a treatment period of 8 wk significantly reduced A.beta. deposition. CNI-1493 treatment resulted in 70% redn. of amyloid plaque area in the cortex and 87% redn. in the hippocampus of these animals. Administration of CNI-1493 significantly improved memory performance in a cognition task compared with vehicle-treated mice. In vitro anal. of CNI-1493 on APP processing in an APP-overexpressing cell line revealed a significant dose-dependent decrease of total A.beta. accumulation. This study indicates that the antiinflammatory agent CNI-1493 can ameliorate the pathophysiol. and cognitive defects in a murine model of AD.