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A transgenic Alzheimer rat with plaques, tau pathology, behavioral impairment, oligomeric aβ, and frank neuronal loss.
Cohen RM, Rezai-Zadeh K, Weitz TM, Rentsendorj A, Gate D, Spivak I, Bholat Y, Vasilevko V, Glabe CG, Breunig JJ, Rakic P, Davtyan H, Agadjanyan MG, Kepe V, Barrio JR, Bannykh S, Szekely CA, Pechnick RN, Town T. Cohen RM, et al. Among authors: glabe cg. J Neurosci. 2013 Apr 10;33(15):6245-56. doi: 10.1523/JNEUROSCI.3672-12.2013. J Neurosci. 2013. PMID: 23575824 Free PMC article.
Intracellular amyloid and the neuronal origin of Alzheimer neuritic plaques.
Pensalfini A, Albay R 3rd, Rasool S, Wu JW, Hatami A, Arai H, Margol L, Milton S, Poon WW, Corrada MM, Kawas CH, Glabe CG. Pensalfini A, et al. Among authors: glabe cg. Neurobiol Dis. 2014 Nov;71:53-61. doi: 10.1016/j.nbd.2014.07.011. Epub 2014 Aug 1. Neurobiol Dis. 2014. PMID: 25092575 Free PMC article.
Progressive accumulation of amyloid-beta oligomers in Alzheimer's disease and in amyloid precursor protein transgenic mice is accompanied by selective alterations in synaptic scaffold proteins.
Pham E, Crews L, Ubhi K, Hansen L, Adame A, Cartier A, Salmon D, Galasko D, Michael S, Savas JN, Yates JR, Glabe C, Masliah E. Pham E, et al. FEBS J. 2010 Jul;277(14):3051-67. doi: 10.1111/j.1742-4658.2010.07719.x. Epub 2010 Jun 22. FEBS J. 2010. PMID: 20573181 Free PMC article.
158 results