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Updated: May 11, 2026

Assessment of Spontaneous Alternation, Novel Object Recognition and Limb Clasping in Transgenic Mouse Models of Amyloid-β and Tau Neuropathology
Published on: May 28, 2017
A core proteome profile unites mouse models and patients in Alzheimer disease
Grigoria Tsaka1, Frederic Rousseau2, Joost Schymkowitz2
1Switch Laboratory, VIB Center for Brain and Disease Research, Leuven, Belgium; Switch Laboratory, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium; Laboratory for Neuropathology, Department of Imaging and Pathology, KU Leuven, Leuven, Belgium; Leuven Brain Institute, KU Leuven, Leuven, Belgium.
Abstract:
Levites et al. demonstrate that mouse models of Alzheimer disease (AD), exhibiting amyloid-beta (Αβ) plaque formation, share Αβ responsome proteins with humans. Their work underscores the value of these models in studying Αβ aggregation, cellular vulnerability, and early-stage AD pathology.
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