20655461

Source:http://linkedlifedata.com/resource/pubmed/id/20655461

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0580836, umls-concept:C1998497
pubmed:issue	2
pubmed:dateCreated	2010-7-26
pubmed:abstractText	A dual goal for treating Alzheimer's disease (AD) is to decrease deposition of neurotoxic amyloid beta-peptide in the brain and to boost repair of damaged neurons. Donmez et al. (2010) now show that SIRT1 may mediate both processes by deacetylating the transcription factor retinoic acid receptor beta, a potential new therapeutic target for AD.
pubmed:commentsCorrections	http://linkedlifedata.com/resource/pubmed/commentcorrection/20655461-20655472
pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/0413066
pubmed:status	PubMed-not-MEDLINE
pubmed:month	Jul
pubmed:issn	1097-4172
pubmed:author	pubmed-author:SelkoeDennis JDJ, pubmed-author:WolfeMichael SMS
pubmed:copyrightInfo	Copyright 2010 Elsevier Inc. All rights reserved.
pubmed:issnType	Electronic
pubmed:day	23
pubmed:volume	142
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	194-6
pubmed:year	2010
pubmed:articleTitle	Giving Alzheimer's the old one-two.
pubmed:affiliation	Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. mwolfe@rics.bwh.harvard.edu
pubmed:publicationType	Journal Article, Comment