Single App knock-in mouse models of Alzheimer's disease.

Takashi Saito, Yukio Matsuba, Naomi Mihira, Jiro Takano, Per Nilsson, Shigeyoshi Itohara, Nobuhisa Iwata and Takaomi C Saido

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Dec 02, 2015
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One of the most pressing issues in modern AD research is the inability to tease out whether pathology observed in many mutant mouse lines is due to the mutation/protein dysfunction or due to the aberrant overexpression of APP and/or PS1. In this study, the authors generated one of the first mouse lines which express mutant APP at physiological levels.

Read the full article on Readcube for free here.

Nat Neurosci. 2014 May;17(5):661-3. doi: 10.1038/nn.3697

Also, click here to see the recent panel discussion by Dr. Saido and other AD experts on ALZforum regarding this new animal model and the problems faced by the field when trying to interpret animal model data.

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Tim Spencer

Senior Editor, Nature Neuroscience

Tim Spencer received his PhD from the City University of New York, where he studied the signaling mechanisms which underlie the promotion of axonal growth and regeneration following injury in the laboratory of Marie Filbin. He then moved to the laboratory of Chris Henderson at Columbia University, where he examined molecular markers of postnatal motor neuron maturation and elements of neurodegenerative diseases such as ALS and SMA. His research interests include neuronal development and maturation, axonal guidance and models of neuronal disease and dysfunction. Tim joined the editorial team of Nature Neuroscience in March of 2011, where he handles many of the manuscripts on neural development and neurogenesis, neurodegeneration, neuroinflammation and neuroimmune interactions, myelination/remyelination, molecular and cellular pathways, and "brain cancer" (glioblastoma, etc.).

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