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Glycobiology Advance Access published online on January 12, 2004
Glycobiology, doi:10.1093/glycob/cwh042
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Submitted on July 29, 2003
Revised on October 27, 2003
Accepted on November 28, 2003

© 2004 Oxford University Press

ORIGINAL MANUSCRIPT

Accumulation of high molecular weight amylose in Alzheimer's disease brains

Linjuan Huang 1, Rawle I. Hollingsworth 2, Rudy Castellani 3, and Birgit Zipser 1*

1 Department of Physiology, Michigan State University, East Lansing, MI 48824
2 Department of Biochemistry, Michigan State University, East Lansing, MI 48824
3 Department of Physiology, Division of Pathology, Michigan State University, East Lansing, MI 48824

* To whom correspondence should be addressed. E-mail: zipserb{at}msu.edu.

Abstract

While most of the glucose metabolized in the brain is taken up from the blood, glucose derived from glycogen stores is increasingly implicated in both normal brain function and injury repair. An impaired glucose metabolism is one of the features of Alzheimer's disease (AD) entailing a reduction in glucose transporters and the uptake of glucose as well as alterations in the specific activity of glycolytic enzymes. Here we report that AD brains accumulate amylose, the unbranched {alpha} (1,4) linked glucose polymer that is resistant to degradation by glycolytic enzymes. Neutral polysaccharides harvested from postmortem brains were purified with hydrazinolysis, ion exchange and sizing chromatography and subjected to NMR spectroscopy, GC, GC-MS, and methylation analysis. Five percent of the polysaccharides (50 µg [0.3µmol]/g of wet weight brain tissue) consisted of amylose with molecular weights exceeding 600,000Da. There is no evidence for 1,6 branching indicating that the polymer is not a form of high molecular weight glycogen. By GC analysis, the glucose content of the AD brains was almost 3 times greater than that of the age-matched control brains. A synthesis of amylose in AD brains at the expense of glycogen would compromise glucose metabolism and enhance neural degeneration.


glucose metabolism, glycopathobiochemistry, glycogen stores, glycogen storage disease, corpora amylacea
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