Cited 4 times in
Suppression of AIMP1 protects cognition in Alzheimer's disease model mice 3xTg-AD
DC Field | Value | Language |
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dc.contributor.author | 김어수 | - |
dc.contributor.author | 김철훈 | - |
dc.contributor.author | 남궁기 | - |
dc.contributor.author | 이정호 | - |
dc.contributor.author | 장수아 | - |
dc.date.accessioned | 2017-11-02T08:19:43Z | - |
dc.date.available | 2017-11-02T08:19:43Z | - |
dc.date.issued | 2017 | - |
dc.identifier.issn | 0959-4965 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/154338 | - |
dc.description.abstract | Neuroinflammation has been raised as a candidate of unifying pathogenesis and a target of a disease-modifying strategy for Alzheimer's disease (AD). Aminoacyl-tRNA synthetase complex (ARS)-interacting multifunctional protein 1 (AIMP1) is a cytokine that is known to amplify the actions of tumor necrosis factor-α and to be involved in microglial activation and neuronal death. In this respect, AIMP1 could be a plausible target for the treatment of AD. Therefore, we aimed to examine whether anti-AIMP1 antibody could exert therapeutic effects against cognitive impairment using 3xTg-AD mice. Through the passive avoidance test, we found that an intraperitoneal injection of anti-AIMP1 antibody over 4 weeks was effective in protecting memory function in 3xTg-AD mice (16 weeks old). In addition, to address the translational implications of AIMP1, we measured blood AIMP1 levels in patients with AD (n=22), mild cognitive impairment (n=25), and normal cognition (n=23). Blood AIMP1 levels were associated negatively with global cognitive function and were significantly higher in individuals with a higher degree of medial temporal lobe atrophy, which is one of the representative clinical markers of AD. Our results suggested a possible association of AIMP1 with AD pathogenesis, as well as the potential of the anti-AIMP1 antibody as a novel therapeutic option for AD. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Lippincott Williams & Wilkins | - |
dc.relation.isPartOf | NEUROREPORT | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Aged | - |
dc.subject.MESH | Aged, 80 and over | - |
dc.subject.MESH | Alzheimer Disease/blood | - |
dc.subject.MESH | Alzheimer Disease/complications* | - |
dc.subject.MESH | Alzheimer Disease/genetics | - |
dc.subject.MESH | Alzheimer Disease/pathology | - |
dc.subject.MESH | Amyloid beta-Protein Precursor/genetics | - |
dc.subject.MESH | Animals Antibodies/therapeutic use | - |
dc.subject.MESH | Avoidance Learning/drug effects | - |
dc.subject.MESH | Brain/diagnostic imaging | - |
dc.subject.MESH | Cognition Disorders/metabolism* | - |
dc.subject.MESH | Cognition Disorders/prevention & control* | - |
dc.subject.MESH | Cytokines/immunology | - |
dc.subject.MESH | Cytokines/metabolism* | - |
dc.subject.MESH | Disease Models, Animal | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Magnetic Resonance Imaging | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Memory Disorders/etiology | - |
dc.subject.MESH | Mental Status Schedule | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Inbred C57BL | - |
dc.subject.MESH | Mice, Transgenic | - |
dc.subject.MESH | Middle Aged | - |
dc.subject.MESH | Mutation/genetics | - |
dc.subject.MESH | Presenilin-1/genetics | - |
dc.subject.MESH | Rotarod Performance Test | - |
dc.subject.MESH | tau Proteins/genetics | - |
dc.title | Suppression of AIMP1 protects cognition in Alzheimer's disease model mice 3xTg-AD | - |
dc.type | Article | - |
dc.publisher.location | England | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Psychiatry | - |
dc.contributor.googleauthor | Sooah Jang | - |
dc.contributor.googleauthor | Jung Ho Lee | - |
dc.contributor.googleauthor | Bo Kyung Sohn | - |
dc.contributor.googleauthor | Eosu Kim | - |
dc.contributor.googleauthor | Sang Gyu Park | - |
dc.contributor.googleauthor | Kang Jun Yoon | - |
dc.contributor.googleauthor | Minsun Park | - |
dc.contributor.googleauthor | Eun Woo Kim | - |
dc.contributor.googleauthor | Jihyeon Jeong | - |
dc.contributor.googleauthor | Jun-Young Lee | - |
dc.contributor.googleauthor | Chul Hoon Kim | - |
dc.contributor.googleauthor | Kee Namkoong | - |
dc.identifier.doi | 10.1097/WNR.0000000000000710 | - |
dc.contributor.localId | A01057 | - |
dc.contributor.localId | A01240 | - |
dc.contributor.localId | A03130 | - |
dc.contributor.localId | A04657 | - |
dc.contributor.localId | A00686 | - |
dc.relation.journalcode | J02361 | - |
dc.identifier.eissn | 1473-558X | - |
dc.identifier.pmid | 27906773 | - |
dc.identifier.url | http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00001756-201702010-00004&LSLINK=80&D=ovft | - |
dc.subject.keyword | Alzheimer’s disease | - |
dc.subject.keyword | aminoacyl-tRNA synthetase complex interacting multifunctional protein 1 | - |
dc.subject.keyword | antiaminoacyl-tRNA synthetase complex interacting multifunctional protein 1 antibody | - |
dc.subject.keyword | neuroinflammation | - |
dc.contributor.alternativeName | Kim, Eo Su | - |
dc.contributor.alternativeName | Kim, Chul Hoon | - |
dc.contributor.alternativeName | Namkoong, Kee | - |
dc.contributor.alternativeName | Lee, Jeong Ho | - |
dc.contributor.alternativeName | Jang, Soo Ah | - |
dc.contributor.affiliatedAuthor | Kim, Chul Hoon | - |
dc.contributor.affiliatedAuthor | Namkoong, Kee | - |
dc.contributor.affiliatedAuthor | Lee, Jeong Ho | - |
dc.contributor.affiliatedAuthor | Jang, Soo Ah | - |
dc.contributor.affiliatedAuthor | Kim, Eo Su | - |
dc.citation.title | Neuroreport | - |
dc.citation.volume | 28 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 82 | - |
dc.citation.endPage | 86 | - |
dc.identifier.bibliographicCitation | NEUROREPORT, Vol.28(2) : 82-86, 2017 | - |
dc.date.modified | 2017-11-01 | - |
dc.identifier.rimsid | 42907 | - |
dc.type.rims | ART | - |
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