Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 58, Issue 3, Pages 841-853Publisher
IOS PRESS
DOI: 10.3233/JAD-170136
Keywords
3xTg; Alzheimer's disease; diffusion tensor imaging; gray matter; hippocampus; neurofibrillary tangles
Categories
Funding
- Research Manitoba
- St. Boniface Hospital Research Foundation [1406-3216, 1410-3216]
- Alzheimer's Society of Manitoba
- Honourable Douglas and Patricia Everett and Royal Canadian Properties Limited Endowment Fund [1403-3131]
- Honourable Douglas and Patricia Everett and Royal Canadian Properties Limited Endowment Fund Chair
- Manitoba Dementia Chair (Alzheimer's Society of Manitoba)
- Manitoba Dementia Chair (Research Manitoba)
- Centre on Aging at the University of Manitoba
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A diagnosis of Alzheimer's disease (AD), a neurodegenerative disorder accompanied by severe functional and cognitive decline, is based on clinical findings, with final confirmation of the disease at autopsy by the presence of amyloid-beta (A beta) plaques and neurofibrillary tangles. Given that microstructural brain alterations occur years prior to clinical symptoms, efforts to detect brain changes early could significantly enhance our ability to diagnose AD sooner. Diffusion tensor imaging (DTI), a type of MRI that characterizes the magnitude, orientation, and anisotropy of the diffusion ofwater in tissues, has been used to infer neuropathological changes in vivo. Its utility in AD, however, is still under investigation. The current study used DTI to examine brain regions susceptible to AD-related pathology; the cerebral cortex, entorhinal cortex, and hippocampus, in 12-14-month-old 3xTg AD mice that possess both A beta plaques and neurofibrillary tangles. Mean diffusivity did not differ between 3xTg and control mice in any region. Decreased fractional anisotropy (p < 0.01) and axial diffusivity (p < 0.05) were detected only in the hippocampus, in which both congophilic A beta plaques and hyperphosphorylated tau accumulation, consistent with neurofibrillary tangle formation, were detected. Pathological tau accumulation was seen in the cortex. The entorhinal cortexwas largely spared from AD-related neuropathology. This is the first study to demonstrate DTI abnormalities in gray matter in a mouse model of AD in which both pathological hallmarks are present, suggesting the feasibility of DTI as a non-invasive means of detecting brain pathology in vivo in early-stage AD.
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