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Beta-secretase-cleaved amyloid precursor protein in Alzheimer brain: a morphologic study
Kristina Sennvik1, N Bogdanovic, Inga Volkmann
1Karolinska Institutet, Neurotec, Section of Experimental Geriatrics, KFC Novum, Huddinge, S-141 86, Sweden.
Journal of Cellular and Molecular Medicine
|April 20, 2004
Summary
Alzheimer's disease brains show altered beta-secretase-cleaved amyloid precursor protein (beta-sAPP) in gray matter and impaired axonal transport. These findings suggest abnormal APP processing and transport in Alzheimer's disease.
Area of Science:
- Neuroscience
- Neuropathology
- Molecular Biology
Background:
- Beta-amyloid (Abeta) aggregates form senile plaques in Alzheimer's disease (AD).
- Abeta is produced from amyloid precursor protein (APP) cleavage by beta- and gamma-secretase enzymes.
Purpose of the Study:
- To investigate the content and location of beta-secretase-cleaved APP (beta-sAPP) in AD brain tissue.
- To compare beta-sAPP distribution in AD cases versus control subjects.
Main Methods:
- Immunohistochemical analysis of brain tissue sections from frontal, temporal, and occipital lobes.
- Examination of beta-sAPP localization in astrocytes and axons.
Main Results:
- Strong granular beta-sAPP staining was observed in gray matter, with weaker staining in white matter.
- beta-sAPP immunostaining was more intense and widespread in the gray matter of AD brains compared to controls.
- Axonal beta-sAPP staining in AD cases was patchy, suggesting impaired axonal transport.
- beta-sAPP was also found around senile plaques and cerebral blood vessels.
Conclusions:
- Altered beta-sAPP staining patterns in the AD brain indicate abnormal APP processing.
- Evidence suggests impaired axonal transport of APP in Alzheimer's disease.
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