In vivo diffusion tensor imaging of amyloid‐β‐induced white matter damage in mice
Open accessAbstract
BACKGROUND: Diffusion tensor imaging (DTI) suggests the presence of white matter abnormality at the prodromal stage in human Alzheimer's disease (AD). OBJECTIVE: To use a mouse model of AD to determine whether the white matter abnormality detected by in vivo DTI is associated with functional deficits and axon damage. METHODS: Amyloid-β1-42 (Aβ1-42) was injected into the left lateral ventricle in mice. Two months after the injection, in vivo DTI and visual evoked potential (VEP) recordings were performed, followed by immunohistochemistry of phosphorylated neurofilament and myelin basic protein. RESULTS: DTI of Aβ1-42-treated mice showed a significant increase of radial diffusivity in white matter including the optic nerves and tracts. The abnormality was associated with decreased amplitude and increased latency of VEP. Immunohistochemistry confirmed a significant loss of axons and myelin integrity. CONCLUSION: White matter damage induced by Aβ1-42 in mice can be detected non-invasively by DTI.
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Significant directional alignment between MRI and transcriptional changes likely reflects co-occurring neuronal loss, dendritic degeneration, axonal disruption, and myelin damage, together with cellular responses to neuroinflammation and neuropathology.
“Significant directional alignment between MRI and transcriptional changes likely reflects co‐occurring neuronal loss, dendritic degeneration, axonal disruption, and myelin damage, 85 , 86 , 87 together with cellular responses to neuroinflammation and neuropathology. 69”
From Diffusion MRI reveals amyloid plaque–associated cellular signatures through spatial transcriptomic integration (2026) · cites this paper as [87]
The Results and Discussion report that DTI abnormalities in Aβ-treated mice were associated with axonal loss and myelin damage. They do not establish neuronal loss or dendritic degeneration, and the study did not compare MRI with transcriptional changes. The separate claim about cellular responses is attached to citation 69, not this source. (LLM, conf=0.84)
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- Authors
- Sun, S.-W., Liang, H.-F., Mei, J., Xu, D., & Shi, W.-X.
- Affiliations
- University of California, Riverside (US)
- Loma Linda University (US)
- ORCID
- Shi, Wei-Xing
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2013-10-29
- Volume
- 38
- Issue
- 1
- Pages
- 93-101
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC3962204
- OpenAlex
- W1495248241
- Cited by
- 27
- References
- 58
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 1 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 3 · 2015: 3 · 2014: 1
- FWCI
- 1.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Scholars Repository - LLU (Loma Linda University) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS062830)
- Topics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced Neuroimaging Techniques and Applications
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- amyloid-beta 42, white matter injury
- MeSH terms
- Animals, Body Weight, Disease Models, Animal, Myelin Basic Protein, Evoked Potentials, Visual, Female, Functional Laterality, Male, Mice, Inbred C57BL, Optic Nerve, Peptide Fragments, Amyloid beta-Peptides, Neurofilament Proteins, Diffusion Magnetic Resonance Imaging, Mice, Leukoencephalopathies
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