Literature DB >> 25697885

Unfolding the promise of translational targeting in neurodegenerative disease.

Thomas M Drake1.   

Abstract

With the rise of aging populations, new challenges for health care systems are emerging. Degenerative conditions of the central nervous system share a strikingly great deal of similarities, particularly the production and buildup of malfolded proteins. As a result, stress pathways within the endoplasmic reticulum become activated, triggering widespread neuronal apoptosis. New pharmacological compounds targeting this response are emerging as promising treatment strategies. This review examines the current evidence for protein aggregation in neurodegenerative disease states and discusses future mechanisms of therapeutically targeting the endoplasmic reticulum.

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Year:  2015        PMID: 25697885     DOI: 10.1007/s12017-015-8346-x

Source DB:  PubMed          Journal:  Neuromolecular Med        ISSN: 1535-1084            Impact factor:   3.843


  66 in total

1.  Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta.

Authors:  T Nakagawa; H Zhu; N Morishima; E Li; J Xu; B A Yankner; J Yuan
Journal:  Nature       Date:  2000-01-06       Impact factor: 49.962

Review 2.  Mediators of endoplasmic reticulum stress-induced apoptosis.

Authors:  Eva Szegezdi; Susan E Logue; Adrienne M Gorman; Afshin Samali
Journal:  EMBO Rep       Date:  2006-09       Impact factor: 8.807

3.  The unfolded protein response and proteostasis in Alzheimer disease: preferential activation of autophagy by endoplasmic reticulum stress.

Authors:  Wiep Scheper; Diana A T Nijholt; Jeroen J M Hoozemans
Journal:  Autophagy       Date:  2011-08-01       Impact factor: 16.016

Review 4.  Endoplasmic reticulum stress, the unfolded protein response, autophagy, and the integrated regulation of breast cancer cell fate.

Authors:  Robert Clarke; Katherine L Cook; Rong Hu; Caroline O B Facey; Iman Tavassoly; Jessica L Schwartz; William T Baumann; John J Tyson; Jianhua Xuan; Yue Wang; Anni Wärri; Ayesha N Shajahan
Journal:  Cancer Res       Date:  2012-03-15       Impact factor: 12.701

5.  Lipid-mediated cell signaling protects against injury and neurodegeneration.

Authors:  Changde Zhang; Nicolas G Bazan
Journal:  J Nutr       Date:  2010-02-24       Impact factor: 4.798

6.  Alpha-synuclein activates microglia by inducing the expressions of matrix metalloproteinases and the subsequent activation of protease-activated receptor-1.

Authors:  Eun-Jung Lee; Moon-Sook Woo; Pyong-Gon Moon; Moon-Chang Baek; In-Young Choi; Won-Ki Kim; Eunsung Junn; Hee-Sun Kim
Journal:  J Immunol       Date:  2010-05-28       Impact factor: 5.422

7.  Unfolded proteins are Ire1-activating ligands that directly induce the unfolded protein response.

Authors:  Brooke M Gardner; Peter Walter
Journal:  Science       Date:  2011-08-18       Impact factor: 47.728

Review 8.  GRP78 induction in cancer: therapeutic and prognostic implications.

Authors:  Amy S Lee
Journal:  Cancer Res       Date:  2007-04-15       Impact factor: 12.701

Review 9.  The mammalian unfolded protein response.

Authors:  Martin Schröder; Randal J Kaufman
Journal:  Annu Rev Biochem       Date:  2005       Impact factor: 23.643

10.  The unfolded protein response is activated in disease-affected brain regions in progressive supranuclear palsy and Alzheimer's disease.

Authors:  Lauren D Stutzbach; Sharon X Xie; Adam C Naj; Roger Albin; Sid Gilman; Virginia M Y Lee; John Q Trojanowski; Bernie Devlin; Gerard D Schellenberg
Journal:  Acta Neuropathol Commun       Date:  2013-07-06       Impact factor: 7.801

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  2 in total

Review 1.  Endoplasmic reticulum stress and inflammation in the central nervous system.

Authors:  Neil T Sprenkle; Savannah G Sims; Cristina L Sánchez; Gordon P Meares
Journal:  Mol Neurodegener       Date:  2017-05-25       Impact factor: 14.195

Review 2.  GRP78 at the Centre of the Stage in Cancer and Neuroprotection.

Authors:  Caty Casas
Journal:  Front Neurosci       Date:  2017-04-05       Impact factor: 4.677

  2 in total

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