Early-onset behavioral and synaptic deficits in a mouse model of Alzheimer's disease.
By J. Jacobsen, Chi‐Cheng Wu, J. Redwine, T. Comery, Robert L. Arias, M. Bowlby, R. Martone, John H. Morrison, M. Pangalos, P. Reinhart and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2006
732 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/642a8b50f5d03c2913322c64d9d0b5db29b5dbc6
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Citations in the corpus
- Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease (2007, background): “In Tg mouse AD models, synapse abnormalities as well as memory impairments correlate poorly with plaque burden and can occur before plaque formation (Holcomb et al., 1999; Hsia et al., 1999; Larson et al., 1999; Mucke et al., 2000; Jacobsen et al., 2006).”
- ApoE promotes the proteolytic degradation of Abeta. (2008, background): “Finally, as preplaque Tg2576 mice have been shown to display an Ab-dependent deficit in contextual memory (Jacobsen et al., 2006), we examined the effects of GW3965 on memory processes in these animals.”
- Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway (2007, background): “Hsieh et al. found that neurons overexpressing human APP have decreased dendritic spine density compared with control neurons.”
- Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, unknown): “LPS administration), trauma, neurological diseases, severe or chronic stress and natural aging (Dong and Xiong, 2006; HaussWegrzyniak et al., 2002; Jacobsen et al., 2006; Kim et al., 1996; Li et al., 2004; Lynch, 1998a,b; O’Donnell et al., 2000).”