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Human Molecular Genetics|July 16, 2004
Identification of loci determining susceptibility to the lethal effects of amyloid precursor protein transgene overexpressionJoseph Krezowski, Danielle Knudson, Christine Ebeling, et al.
Journal of Virology|January 18, 2023
Therapeutic Trial of anle138b in Mouse Models of Genetic Prion DiseaseSonia M Vallabh, Dan Zou, Rose Pitstick, et al.
The American Journal of Pathology|May 14, 2017
Enhanced Tau Aggregation in the Presence of Amyloid βRachel E Bennett, Sarah L DeVos, Simon Dujardin, et al.
The American Journal of Pathology|August 23, 2011
Tau accumulation causes mitochondrial distribution deficits in neurons in a mouse model of tauopathy and in human Alzheimer's disease brainKatherine J Kopeikina, George A Carlson, Rose Pitstick, et al.
Proceedings of the National Academy of Sciences of the United States of America|March 9, 2011
Scavenger receptor CD36 is essential for the cerebrovascular oxidative stress and neurovascular dysfunction induced by amyloid-betaLaibaik Park, Gang Wang, Ping Zhou, et al.
Acta Neuropathologica|November 26, 2013
Soluble pathological tau in the entorhinal cortex leads to presynaptic deficits in an early Alzheimer's disease modelManuela Polydoro, Volodymyr I Dzhala, Amy M Pooler, et al.
Neuron|February 28, 2012
Propagation of tau pathology in a model of early Alzheimer's diseaseAlix de Calignon, Manuela Polydoro, Marc Suárez-Calvet, et al.
Neuron|December 22, 2010
Tau mislocalization to dendritic spines mediates synaptic dysfunction independently of neurodegenerationBrian R Hoover, Miranda N Reed, Jianjun Su, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|August 16, 2013
Reversal of neurofibrillary tangles and tau-associated phenotype in the rTgTauEC model of early Alzheimer's diseaseManuela Polydoro, Alix de Calignon, Marc Suárez-Calvet, et al.
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