Journal
CURRENT MEDICINAL CHEMISTRY
Volume 15, Issue 23, Pages 2321-2328Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/092986708785909111
Keywords
Alzheimer disease; tau; neurodegeneration; GSK-3 beta; cdk5; protein phosphatases; O-GlcNAcylation; therapy
Funding
- New York State Office of Mental Retardation and Developmental Disabilities
- NIH [AG027429, AG019158]
- U. S. Alzheimer's Association [IIRG-05-13095]
- NATIONAL INSTITUTE ON AGING [R01AG027429, R01AG019158] Funding Source: NIH RePORTER
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Alzheimer disease (AD) is the most common cause of dementia in adults. The current therapy for AD has only moderate efficacy in controlling symptoms, and it does not cure the disease. Recent studies have suggested that abnormal hyperphosphorylation of tau in the brain plays a vital role in the molecular pathogenesis of AD and in neurodegeneration. This article reviews the current advances in understanding of tau protein, regulation of tau phosphorylation, and the role of its abnormal hyperphosphorylation in neurofibrillary degeneration. Furthermore, several therapeutic strategies for treating AD on the basis of the important role of tau hyperphosphorylation in the pathogenesis of the disease are described. These strategies include (1) inhibition of glycogen synthase kinase-3 (GSK-3 cyclin-dependent kinase 5 (cdk5), and other tau kinases; (2) restoration of PP2A activity; and (3) targeting tau O-GlcNAcylation. Development of drugs on the basis of these strategies is likely to lead to disease-modifying therapies for AD.
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