Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 299, Issue -, Pages 164-171Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2016.09.008
Keywords
Chronic cerebral hypoperfusion; Cognitive deficits; mTOR pathway; M1/M2 balance; RAD001
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Funding
- National Basic Research Program of China [2013CB966900]
- National Natural Science Foundation of China [81571600, 81322018, 81273287, 81100887]
- Youth Top-notch Talent Support Program
- Natural Science Foundation of Tianjin Municipal Science and Technology Commission [13JCYBJC22700]
- National Key Clinical Specialty Construction Project of China
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Vascular dementia (VaD) is a widely prevalent and devastating disease. Despite the tremendous complexity that limits understanding of the pathophysiology of VaD, microglial dysfunction has been attributed, in part, to immune microenviroment disorder and finally leads to cognitive deficits. Considered the mammalian target of rapamycin complex 1 (mTORC1) is a key player in regulation of glial function, our work focused on whether the mTOR inhibitor everolimus (RAD001) could overcome the destructive microglial function, change the phenotype and ameliorate cognitive decline induced by chronic cerebral hypoperfusion. Strikingly, the results suggest that inhibition of the mTORC1 activity by RAD001 ameliorates VaD by restoring microglia's M1/M2 balance. Therefore, RAD001 may have promise as a therapy for VaD disease. (C) 2016 Elsevier B.V. All rights reserved.
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