Complex interplay between brain function and structure during cerebral amyloidosis in APP transgenic mouse strains revealed by multi-parametric MRI comparison
Open accessAbstract
Alzheimer's disease is a fatal neurodegenerative disorder affecting the aging population. Neuroimaging methods, in particular magnetic resonance imaging (MRI), have helped reveal alterations in the brain structure, metabolism, and function of patients and in groups at risk of developing AD, yet the nature of these alterations is poorly understood. Neuroimaging in mice is attractive for investigating mechanisms underlying functional and structural changes associated with AD pathology. Several preclinical murine models of AD have been generated based on transgenic insertion of human mutated APP genes. Depending on the specific mutations, mouse strains express different aspects of amyloid pathology, e.g. intracellular amyloid-β (Aβ) aggregates, parenchymal plaques, or cerebral amyloid angiopathy. We have applied multi-parametric MRI in three transgenic mouse lines to compare changes in brain function with resting-state fMRI and structure with diffusion tensor imaging and high resolution anatomical imaging. E22ΔAβ developing intracellular Aβ aggregates did not present functional or structural alterations compared to their wild-type littermates. PSAPP mice displaying parenchymal amyloid plaques displayed mild functional changes within the supplementary and barrel field cortices, and increased isocortical volume relative to controls. Extensive reduction in functional connectivity in the sensory-motor cortices and within the default mode network, as well as local volume increase in…
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Our results of structural connectivity deficit might be the basis of decreased functional connectivity in the TG mice.
“Collectively, our results of structural connectivity deficit might be the basis of decreased functional connectivity in the TG mice (Grandjean et al., 2016).”
From Disrupted structural connectivity in ArcAβ mouse model of Aβ amyloidosis (2020) · cites this paper as Grandjean et al., 2016
The study was unable to include the MRI brain samples in the histology experiment because those brain samples were exhausted in a previous study.
“This study has some limitations, mainly that we were unable to include the MRI brain samples in our histology experiment, as those brain samples were exhausted in a previous study (Grandjean et al., 2016).”
From Disrupted structural connectivity in ArcAβ mouse model of Aβ amyloidosis (2020) · cites this paper as Grandjean et al., 2016
Extracellular Aβ can stimulate tau phosphorylation and aggregation in neurons with axons projecting into the injection site in p301L mice, but not wild type mice.
“extracellular accumulations of Aβ can stimulate tau phosphorylation and aggregation in neurons with axons projecting into the injection site in mice expressing the mutant FTDP-17 (p301L) form of human tau, but not wild type mice19,20,22.”
From Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model (2019) · cites this paper as [22]
Aβ-induced tau pathology may spread through axons in a retrograde manner.
“Aβ-induced tau pathology may spread through axons in a retrograde manner17,21,22.”
From Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model (2019) · cites this paper as [22]
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Self-citationMapping the mouse brain with rs-fMRI: an optimized pipeline for functional network identification
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Resting State fMRI Reveals Diminished Functional Connectivity in a Mouse Model of Amyloidosis
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“For instance, the ArcAβ model (Grandjean et al., 2014) is characterized by intracellular amyloid deposits, extracellular plaques, as well as marked vascular pathology (Klohs et al., 2011; Knobloch et al., 2007a; Merlini et al., 2011), thus rendering it difficult to attribute the fMRI changes to a…”
InfluentialSelf-citationVoxel-based diffusion tensor imaging of an APP/PS1 mouse model of Alzheimer’s disease.
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Colon-Perez, L. M., Ibanez, K. R., Suarez, M., Torroella, K., Acuna, K., Ofori, E., Levites, Y., Vaillancourt, D. E., Golde, T. E., Chakrabarty, P., et al. (2019) · NeuroImage · doi:10.1016/j.neuroimage.2019.116138 · Cited by 41 · see citing works
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Neuroimaging of mouse models of Alzheimer’s disease
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Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model
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Disrupted structural connectivity in ArcAβ mouse model of Aβ amyloidosis
Al-Amin, M. M., Grandjean, J., Klohs, J., & Kim, J. (2020) · doi:10.1101/2020.04.27.064634 · Cited by 2 · see citing works
“…(Anckaerts et al., 2019), 5XFAD mice (Kesler et al., 2018), APP/PS1 mice (Shah et al., 2013, Bero et al., 2012), ArcAβ mice (Grandjean et al., 2014, Grandjean et al., 2016), aging apoE4 and apoE-KO mice (Zerbi et al., 2014) and PSAPP mice (Grandjean et al., 2016), although not in E22AΔβ mice…”
BackgroundMethodResultInfluentialSelf-citation
- Authors
- Grandjean, J., Derungs, R., Kulic, L., Welt, T., Henkelman, M., Nitsch, R. M., & Rudin, M.
- Affiliations
- ETH Zurich (CH)
- University of Zurich (CH)
- Corresponding author
- Rudin, Markus
- Venue
- NeuroImage
- Publisher
- Elsevier BV
- Published
- 2016-07
- Volume
- 134
- Pages
- 1-11
- ISSN
- 1053-8119 (ISSN-L)
- OpenAlex
- W2308601713
- Cited by
- 48
- References
- 9
- Citations by year
- 2025: 8 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 5 · 2019: 10 · 2018: 6 · 2017: 4 · 2016: 1
- FWCI
- 5.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 291 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- NeuroImage (acceptedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Swiss National Science Foundation (310030-126029, 310030-160310)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Functional Brain Connectivity Studies
- Keywords
- Alzheimer's disease, cerebral amyloidosis, amyloid-beta aggregates, cerebral amyloid angiopathy, amyloid plaques, resting-state functional connectivity, default mode network, functional connectivity, diffusion tensor imaging, multiparametric MRI, strain differences, brain structure
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Brain, Disease Models, Animal, Magnetic Resonance Imaging, Male, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Transgenic, Sensitivity and Specificity, Reproducibility of Results, Amyloid beta-Protein Precursor, Mice, Multimodal Imaging
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