Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 107, Issue 44, Pages 19014-19019Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1013543107
Keywords
beta amyloid; glutamate receptor trafficking; protein tyrosine phosphatase; long-term potentiation
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Funding
- American Health Assistance Foundation
- National Institutes of Health [MH081190, AG09464, NS42304, NS39962, MH01527, MH52711]
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Alzheimer's disease (AD) is a progressive and incurable neurodegenerative disorder. Early in the pathophysiology of AD, synaptic function is disrupted by soluble A beta oligomers, possibly through A beta-mediated internalization of NMDA receptors. Striatal-enriched phosphatase (STEP) is a tyrosine phosphatase that regulates the internalization of NMDA receptors. Recent work shows that STEP is elevated in the prefrontal cortex of human AD patients and in animal models of AD. Here, we use genetic manipulations to reduce STEP activity in a triple transgenic AD mouse model and show that a decrease in STEP levels reverses cognitive and cellular deficits observed in these mice. Our results suggest that STEP inhibitors may prove therapeutic for this devastating disorder.
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