| pubmed-article:18385378 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18385378 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:18385378 | lifeskim:mentions | umls-concept:C1367656 | lld:lifeskim |
| pubmed-article:18385378 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:18385378 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:18385378 | lifeskim:mentions | umls-concept:C0812267 | lld:lifeskim |
| pubmed-article:18385378 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:18385378 | lifeskim:mentions | umls-concept:C1515926 | lld:lifeskim |
| pubmed-article:18385378 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:18385378 | pubmed:dateCreated | 2008-4-9 | lld:pubmed |
| pubmed-article:18385378 | pubmed:abstractText | beta-Site APP-cleaving enzyme 1 (BACE1) is required for the penultimate cleavage of the amyloid-beta precursor protein (APP) leading to the generation of amyloid-beta peptides that is central to the pathogenesis of Alzheimer's disease. In addition to its role in endoproteolysis of APP, BACE1 participates in the proteolytic processing of neuregulin 1 (NRG1) and influences the myelination of central and peripheral axons. Although NRG1 has been genetically linked to schizophrenia and NRG1(+/-) mice exhibit a number of schizophrenia-like behavioral traits, it is not known whether altered BACE1-dependent NRG1 signaling can cause similar behavioral abnormalities. To test this hypothesis, we analyze the behaviors considered to be rodent analogs of clinical features of schizophrenia in BACE1(-/-) mice with impaired processing of NRG1. We demonstrate that BACE1(-/-) mice exhibit deficits in prepulse inhibition, novelty-induced hyperactivity, hypersensitivity to a glutamatergic psychostimulant (MK-801), cognitive impairments, and deficits in social recognition. Importantly, some of these manifestations were responsive to treatment with clozapine, an atypical antipsychotic drug. Moreover, although the total amount of ErbB4, a receptor for NRG1 was not changed, binding of ErbB4 with postsynaptic density protein 95 (PSD95) was significantly reduced in the brains of BACE1(-/-) mice. Consistent with the role of ErbB4 in spine morphology and synaptic function, BACE1(-/-) mice displayed reduced spine density in hippocampal pyramidal neurons. Collectively, our findings suggest that alterations in BACE1-dependent NRG1/ErbB4 signaling may participate in the pathogenesis of schizophrenia and related psychiatric disorders. | lld:pubmed |
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| pubmed-article:18385378 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18385378 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18385378 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18385378 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18385378 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:18385378 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:18385378 | pubmed:author | pubmed-author:WongP CPC | lld:pubmed |
| pubmed-article:18385378 | pubmed:author | pubmed-author:PriceD LDL | lld:pubmed |
| pubmed-article:18385378 | pubmed:author | pubmed-author:SavonenkoA... | lld:pubmed |
| pubmed-article:18385378 | pubmed:author | pubmed-author:LairdF MFM | lld:pubmed |
| pubmed-article:18385378 | pubmed:author | pubmed-author:MelnikovaTT | lld:pubmed |
| pubmed-article:18385378 | pubmed:author | pubmed-author:StewartK-AKA | lld:pubmed |
| pubmed-article:18385378 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18385378 | pubmed:day | 8 | lld:pubmed |
| pubmed-article:18385378 | pubmed:volume | 105 | lld:pubmed |
| pubmed-article:18385378 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18385378 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18385378 | pubmed:pagination | 5585-90 | lld:pubmed |
| pubmed-article:18385378 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:18385378 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18385378 | pubmed:articleTitle | Alteration of BACE1-dependent NRG1/ErbB4 signaling and schizophrenia-like phenotypes in BACE1-null mice. | lld:pubmed |
| pubmed-article:18385378 | pubmed:affiliation | Departments of Pathology, Neurology, and Neuroscience, Johns Hopkins University School of Medicine, 558 Ross Research Building, 720 Rutland Avenue, Baltimore, MD 21205, USA. | lld:pubmed |
| pubmed-article:18385378 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18385378 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18385378 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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