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Fiber Tracts Anomalies in APPxPS1 Transgenic Mice Modeling Alzheimer's Disease
H Chen1, S Epelbaum, B Delatour
1CNRS, Laboratoire NAMC, UMR 8620, Université Paris-Sud 11, 91405 Orsay, France.
Journal of Aging Research
|September 14, 2011
Summary
Alzheimer's disease (AD) involves amyloid beta (Aβ) buildup. This study shows Aβ overproduction in mice damages brain fiber tracts, suggesting early intracellular Aβ may trigger these anomalies.
Area of Science:
- Neuroscience
- Neuropathology
- Alzheimer's Disease Research
Background:
- Amyloid beta (Aβ) peptides accumulate in Alzheimer's disease (AD) brains.
- The connection between brain amyloidosis and AD symptoms is unclear, potentially involving neuropathological changes like fiber tract anomalies.
Purpose of the Study:
- Investigate the impact of Aβ overproduction on forebrain axonal bundle integrity in APPxPS1 transgenic mice.
- Examine the relationship between Aβ accumulation and fiber tract alterations.
Main Methods:
- Utilized APPxPS1 transgenic mice overproducing Aβ.
- Assessed the integrity of corpus callosum and anterior commissure axonal bundles.
- Analyzed neurofilament loss and myelin breakdown.
Main Results:
- APPxPS1 mice exhibited reduced fiber tract volumes.
- Observed accelerated age-related axonal neurofilament loss and myelin breakdown.
- Found no correlation between defect severity, amyloid plaque density, or neurodegeneration.
Conclusions:
- Commissural fiber tract alterations occur in Aβ-overproducing mice.
- Intracellular Aβ accumulation may precede and trigger these morphological anomalies, independent of plaque density or cell death.
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