Stereological analysis of microvascular parameters in a double transgenic model of Alzheimer's disease

Morphological alterations in microvasculature occur as a common finding in the brains of non-demented aged persons and patients with Alzheimer's disease. Quantifying the extent of this vascular pathology, however, has been complicated by systematic error (bias) associated with the applications...

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Bibliographic Details
Published in:Brain research bulletin 2005-04, Vol.65 (4), p.317-322
Main Authors: Lee, Garrick D., Aruna, Juliana H., Barrett, Patrick M., Lei, De-Liang, Ingram, Donald K., Mouton, Peter R.
Format: Article
Language:English
Subjects:
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer Disease - physiopathology
Amyloid beta-Protein Precursor - genetics
Amyloid beta-Protein Precursor - metabolism
Animals
Blood Vessels - pathology
Body Weight - genetics
Capillaries - metabolism
Capillaries - pathology
Capillary segments
Cerebrovascular Circulation
Corpus callosum
Design-based
Disease Models, Animal
Humans
Male
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
Mice, Transgenic
Microvasculature
Presenilin-1
Reference Values
Space balls
Stereotaxic Techniques
Total capillary length
Unbiased stereology
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Summary:Morphological alterations in microvasculature occur as a common finding in the brains of non-demented aged persons and patients with Alzheimer's disease. Quantifying the extent of this vascular pathology, however, has been complicated by systematic error (bias) associated with the applications of assumption- and model-based morphometric techniques to human and animal tissues. The current study used novel assumption- and model-free stereological approaches to quantify capillary parameters in the corpus callosum of a double amyloid precursor protein/presenilin-1 transgenic murine model of Alzheimer's disease. The results revealed significant reductions in the total number of capillary segments in white matter of transgenic mice compared to non-transgenic littermates, with no differences in total capillary length. These findings support the view that the expression of mutant human genes for β-amyloid peptides alters the normal architecture of cerebral capillary vessels in the white matter of mouse brain, which may model microvasculature changes reported in Alzheimer's disease.
ISSN:0361-9230
1873-2747
DOI:10.1016/j.brainresbull.2004.11.024