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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
24
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pubmed:dateCreated |
2007-6-14
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pubmed:abstractText |
Hyperphosphorylation of the microtubule-associated protein tau is a key event in the development of Alzheimer's disease (AD) neuropathology. Acute stress can induce hippocampal tau phosphorylation (tau-P) in rodents, but the mechanisms and pathogenic relevance of this response are unclear. Here, we find that hippocampal tau-P elicited by an acute emotional stressor, restraint, was not affected by preventing the stress-induced rise in glucocorticoids but was blocked by genetic or pharmacologic disruption of signaling through the type 1 corticotropin-releasing factor receptor (CRFR1). Conversely, these responses were exaggerated in CRFR2-deficient mice. Parallel CRFR dependence was seen in the stress-induced activation of specific tau kinases. Repeated stress exposure elicited cumulative effects on tau-P and its sequestration in an insoluble, and potentially pathogenic, form. These findings support differential regulatory roles for CRFRs in an AD-relevant form of neuronal plasticity and may link datasets documenting alterations in the CRF signaling system in AD and implicating chronic stress as a risk factor in age-related neurological disorders.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Corticosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Corticotropin-Releasing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/PHF-1 monoclonal antibody,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrimidines,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrroles,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Corticotropin-Releasing...,
http://linkedlifedata.com/resource/pubmed/chemical/antalarmin,
http://linkedlifedata.com/resource/pubmed/chemical/tau Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1529-2401
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
13
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6552-62
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pubmed:dateRevised |
2011-8-2
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pubmed:meshHeading |
pubmed-meshheading:17567816-Adrenalectomy,
pubmed-meshheading:17567816-Analysis of Variance,
pubmed-meshheading:17567816-Animals,
pubmed-meshheading:17567816-Antibodies, Monoclonal,
pubmed-meshheading:17567816-Corticosterone,
pubmed-meshheading:17567816-Corticotropin-Releasing Hormone,
pubmed-meshheading:17567816-Gene Expression Regulation,
pubmed-meshheading:17567816-Immunoprecipitation,
pubmed-meshheading:17567816-Injections, Intraventricular,
pubmed-meshheading:17567816-Male,
pubmed-meshheading:17567816-Mice,
pubmed-meshheading:17567816-Mice, Inbred C57BL,
pubmed-meshheading:17567816-Mice, Knockout,
pubmed-meshheading:17567816-Phosphorylation,
pubmed-meshheading:17567816-Protein Kinases,
pubmed-meshheading:17567816-Pyrimidines,
pubmed-meshheading:17567816-Pyrroles,
pubmed-meshheading:17567816-Receptors, Corticotropin-Releasing Hormone,
pubmed-meshheading:17567816-Stress, Physiological,
pubmed-meshheading:17567816-Time Factors,
pubmed-meshheading:17567816-tau Proteins
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pubmed:year |
2007
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pubmed:articleTitle |
Corticotropin-releasing factor receptors differentially regulate stress-induced tau phosphorylation.
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pubmed:affiliation |
Laboratory of Neuronal Structure and Function, The Salk Institute for Biological Studies and Foundation for Medical Research, La Jolla, California 92037, USA. rrissman@salk.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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