Abstract |
A marked and significant reduction of protease nexin-1 (PN-1) and PN-2/ amyloid beta protein precursor (A beta PP) was observed in selected regions of Alzheimer's disease (AD) brains as compared to those of aged-matched controls. Correlative analysis indicated a relationship between PN-1 reduction and the severity of pathologic alterations. A statistically significant inverse correlation was noted between the level of PN-1 activity and the density of tau-positive dystrophic neurites in the hippocampus. In view of the ability of thrombin and PN-1 activity to regulate neurite outgrowth, it is possible that abnormal thrombin and PN-1 interactions may play a role in dystrophic neurite formation. The presence of clusters of dystrophic neurites around the capillaries suggests that blood-brain barrier (BBB) dysfunction may enhance such abnormal interactions. The decrease in PN-2/A beta PP levels in AD brains could possibly contribute to neuronal degeneration in AD in view of the ability of PN-2/A beta PP to protect neurons against the toxic effects of the A beta.
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Authors | B H Choi, R C Kim, P J Vaughan, A Lau, W E Van Nostrand, C W Cotman, D D Cunningham |
Journal | Neurobiology of aging
(Neurobiol Aging)
1995 Jul-Aug
Vol. 16
Issue 4
Pg. 557-62
ISSN: 0197-4580 [Print] United States |
PMID | 8544905
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Amyloid beta-Protein Precursor
- Carrier Proteins
- Protease Nexins
- Receptors, Cell Surface
- SERPINE2 protein, human
- Serpin E2
- tau Proteins
- Thrombin
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Topics |
- Aged
- Alzheimer Disease
(enzymology, pathology)
- Amyloid beta-Protein Precursor
(metabolism)
- Blotting, Western
- Brain
(enzymology, pathology)
- Carrier Proteins
(metabolism)
- Hippocampus
(enzymology, pathology)
- Humans
- Neurites
(enzymology, pathology)
- Protease Nexins
- Receptors, Cell Surface
- Regression Analysis
- Serpin E2
- Thrombin
(metabolism)
- tau Proteins
(metabolism)
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