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Impaired brain glucose metabolism leads to Alzheimer neurofibrillary degeneration through a decrease in tau
Cheng-Xin Gong1, Fei Liu, Inge Grundke-Iqbal
1Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314-6399, USA. cxgong@ultinet.net
Journal of Alzheimer'S Disease : JAD
|April 22, 2006
Summary
Impaired brain glucose metabolism in Alzheimer disease (AD) may worsen tau pathology. This study proposes that reduced glucose uptake facilitates tau hyperphosphorylation, offering a new therapeutic target for AD.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Neurofibrillary degeneration, driven by tau hyperphosphorylation and aggregation, is central to Alzheimer disease (AD) pathogenesis.
- Impaired brain glucose metabolism is a known feature of AD, but its direct contribution to tau pathology remains unclear.
Purpose of the Study:
- To investigate the link between impaired glucose metabolism and tau hyperphosphorylation in Alzheimer disease.
- To propose a novel hypothesis on the role of glucose metabolism in AD pathogenesis.
Main Methods:
- The study integrates existing knowledge on tau phosphorylation and O-GlcNAcylation.
- It proposes a hypothesis based on recent findings of tau O-GlcNAcylation in the human brain.
Main Results:
- Tau protein in the human brain is modified by O-GlcNAcylation, a process that negatively regulates tau phosphorylation.
- A novel hypothesis is proposed linking impaired glucose metabolism to tau hyperphosphorylation in AD.
Conclusions:
- Impaired brain glucose uptake/metabolism may contribute to AD by promoting abnormal tau hyperphosphorylation.
- Understanding this mechanism could reveal new therapeutic targets for AD prevention and treatment.