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Items: 1 to 20 of 79

1.

RAGE potentiates Abeta-induced perturbation of neuronal function in transgenic mice.

Arancio O, Zhang HP, Chen X, Lin C, Trinchese F, Puzzo D, Liu S, Hegde A, Yan SF, Stern A, Luddy JS, Lue LF, Walker DG, Roher A, Buttini M, Mucke L, Li W, Schmidt AM, Kindy M, Hyslop PA, Stern DM, Du Yan SS.

EMBO J. 2004 Oct 13;23(20):4096-105. Epub 2004 Sep 30.

2.

RAGE-dependent signaling in microglia contributes to neuroinflammation, Abeta accumulation, and impaired learning/memory in a mouse model of Alzheimer's disease.

Fang F, Lue LF, Yan S, Xu H, Luddy JS, Chen D, Walker DG, Stern DM, Yan S, Schmidt AM, Chen JX, Yan SS.

FASEB J. 2010 Apr;24(4):1043-55. doi: 10.1096/fj.09-139634. Epub 2009 Nov 11.

3.

RAGE and Alzheimer's disease: a progression factor for amyloid-beta-induced cellular perturbation?

Yan SD, Bierhaus A, Nawroth PP, Stern DM.

J Alzheimers Dis. 2009;16(4):833-43. doi: 10.3233/JAD-2009-1030. Review.

4.

RAGE does not affect amyloid pathology in transgenic ArcAbeta mice.

Vodopivec I, Galichet A, Knobloch M, Bierhaus A, Heizmann CW, Nitsch RM.

Neurodegener Dis. 2009;6(5-6):270-80. doi: 10.1159/000261723. Epub 2010 Feb 10.

PMID:
20145420
5.

RAGE is a key cellular target for Abeta-induced perturbation in Alzheimer's disease.

Yan SS, Chen D, Yan S, Guo L, Du H, Chen JX.

Front Biosci (Schol Ed). 2012 Jan 1;4:240-50. Review.

6.

Receptor for advanced glycation end product-dependent activation of p38 mitogen-activated protein kinase contributes to amyloid-beta-mediated cortical synaptic dysfunction.

Origlia N, Righi M, Capsoni S, Cattaneo A, Fang F, Stern DM, Chen JX, Schmidt AM, Arancio O, Yan SD, Domenici L.

J Neurosci. 2008 Mar 26;28(13):3521-30. doi: 10.1523/JNEUROSCI.0204-08.2008.

7.

Preventing activation of receptor for advanced glycation endproducts in Alzheimer's disease.

Lue LF, Yan SD, Stern DM, Walker DG.

Curr Drug Targets CNS Neurol Disord. 2005 Jun;4(3):249-66. Review.

PMID:
15975028
8.

Involvement of microglial receptor for advanced glycation endproducts (RAGE) in Alzheimer's disease: identification of a cellular activation mechanism.

Lue LF, Walker DG, Brachova L, Beach TG, Rogers J, Schmidt AM, Stern DM, Yan SD.

Exp Neurol. 2001 Sep;171(1):29-45.

PMID:
11520119
9.

RAGE: a potential target for Abeta-mediated cellular perturbation in Alzheimer's disease.

Chen X, Walker DG, Schmidt AM, Arancio O, Lue LF, Yan SD.

Curr Mol Med. 2007 Dec;7(8):735-42. Review.

PMID:
18331231
10.

RAGE regulates BACE1 and Abeta generation via NFAT1 activation in Alzheimer's disease animal model.

Cho HJ, Son SM, Jin SM, Hong HS, Shin DH, Kim SJ, Huh K, Mook-Jung I.

FASEB J. 2009 Aug;23(8):2639-49. doi: 10.1096/fj.08-126383. Epub 2009 Mar 30.

11.

Conditional inactivation of presenilin 1 prevents amyloid accumulation and temporarily rescues contextual and spatial working memory impairments in amyloid precursor protein transgenic mice.

Saura CA, Chen G, Malkani S, Choi SY, Takahashi RH, Zhang D, Gouras GK, Kirkwood A, Morris RG, Shen J.

J Neurosci. 2005 Jul 20;25(29):6755-64.

12.

Amyloid-beta deposition is associated with decreased hippocampal glucose metabolism and spatial memory impairment in APP/PS1 mice.

Sadowski M, Pankiewicz J, Scholtzova H, Ji Y, Quartermain D, Jensen CH, Duff K, Nixon RA, Gruen RJ, Wisniewski T.

J Neuropathol Exp Neurol. 2004 May;63(5):418-28.

13.

The role of RAGE in amyloid-beta peptide-mediated pathology in Alzheimer's disease.

Schmidt AM, Sahagan B, Nelson RB, Selmer J, Rothlein R, Bell JM.

Curr Opin Investig Drugs. 2009 Jul;10(7):672-80. Review.

PMID:
19579173
14.

Hypercholesterolemia accelerates intraneuronal accumulation of Aβ oligomers resulting in memory impairment in Alzheimer's disease model mice.

Umeda T, Tomiyama T, Kitajima E, Idomoto T, Nomura S, Lambert MP, Klein WL, Mori H.

Life Sci. 2012 Dec 10;91(23-24):1169-76. doi: 10.1016/j.lfs.2011.12.022. Epub 2012 Jan 17.

PMID:
22273754
15.

Specific spatial learning deficits become severe with age in beta -amyloid precursor protein transgenic mice that harbor diffuse beta -amyloid deposits but do not form plaques.

Koistinaho M, Ort M, Cimadevilla JM, Vondrous R, Cordell B, Koistinaho J, Bures J, Higgins LS.

Proc Natl Acad Sci U S A. 2001 Dec 4;98(25):14675-80. Epub 2001 Nov 27.

17.

Cerebrolysin decreases amyloid-beta production by regulating amyloid protein precursor maturation in a transgenic model of Alzheimer's disease.

Rockenstein E, Torrance M, Mante M, Adame A, Paulino A, Rose JB, Crews L, Moessler H, Masliah E.

J Neurosci Res. 2006 May 15;83(7):1252-61.

PMID:
16511867
18.

Myeloid differentiation factor 88-deficient bone marrow cells improve Alzheimer's disease-related symptoms and pathology.

Hao W, Liu Y, Liu S, Walter S, Grimm MO, Kiliaan AJ, Penke B, Hartmann T, Rübe CE, Menger MD, Fassbender K.

Brain. 2011 Jan;134(Pt 1):278-92. doi: 10.1093/brain/awq325. Epub 2010 Nov 28.

19.

Deletion of tumor necrosis factor death receptor inhibits amyloid beta generation and prevents learning and memory deficits in Alzheimer's mice.

He P, Zhong Z, Lindholm K, Berning L, Lee W, Lemere C, Staufenbiel M, Li R, Shen Y.

J Cell Biol. 2007 Aug 27;178(5):829-41.

20.

Aβ-AGE aggravates cognitive deficit in rats via RAGE pathway.

Chen C, Li XH, Tu Y, Sun HT, Liang HQ, Cheng SX, Zhang S.

Neuroscience. 2014 Jan 17;257:1-10. doi: 10.1016/j.neuroscience.2013.10.056. Epub 2013 Nov 1.

PMID:
24188791
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