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Published on: March 16, 2016
Suppression of AIMP1 protects cognition in Alzheimer's disease model mice 3xTg-AD
Sooah Jang1, Jung Ho Lee, Bo Kyung Sohn
1Departments of aPsychiatry bPharmacology cInstitute of Behavioral Science in Medicine dBrain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine eDepartment of Psychiatry, SMG-SNU Boramae Medical Center fDepartment of Psychiatry and Behavioral Science, Seoul National University College of Medicine gDepartment of Neurosurgery, St Peter's Kangnam Hospital, Seoul hDepartment of Pharmacy, College of Pharmacy, Ajou University, Suwon, Gyunggido, Republic of Korea.
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.
