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Updated: Oct 7, 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 murine model of amyloid enhanced tauopathy: progressive changes in tau pathology and behavior
Dylan J Finneran1, Taylor Desjarlais1, Brianna M Jackman1
1Dept of Translational Neuroscience, College of Human Medicine, Michigan State University, Grand Rapids, Michigan, USA.
Background:
Our prior work demonstrated systemic P301L-tau injections in mice with mature amyloid resulted in several-fold enhancement of tauopathy compared to non-transgenic (NTg) littermates.
Methods:
APP+PS1 mice were injected intravenously with AAV.CAP-B10 expressing P301L tau (A/P+P301L). Mice were tested behaviorally and tissues collected for measurement of amyloid and tau pathology.
Results:
A/P+P301L mice have greater spatial navigation memory impairments than control APP+PS1 mice, or AAV-tau injected NTg mice. Tau phosphorylation and deposition increased from 5 to 9 months after injection, culminating in numerous Gallyas-positive presumptive neurofibrillary tangles.
Discussion:
In this model of amyloid-enhanced tauopathy, tau pathology acts synergistically with amyloidosis to exacerbate cognitive impairments compared to amyloid-only mice. The tauopathy is progressive, with more severe behavioral impairments and neurofibrillary deposits at longer survival times. The temporal staging of pathology in this model resembles that of Alzheimer's disease and may be useful for interrogating the linkage between amyloid and tau pathology.
