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Abstract #0018

Neuroprotective Mechanism of Minocycline in an Accelerated Macaque Model of NeuroAIDS

Eva-Maria Ratai1,2, Chan-Gyu Joo1,2, Jeffrey Bombardier1, Robert Fell1, Julian He1,2, Reza Hakimelahi1,2, Tricia Burdo3, Jennifer Campbell3, Patrick Autissier3, Lakshmanan Annamalai4, Eliezer Masliah5, Susan Westmoreland, 2,4, Kenneth Williams3, Ramon Gilberto Gonzalez1,2

1Department of Radiology, A. A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, United States; 2Harvard Medical School, Boston, MA, United States; 3Biology Department, Boston College, Boston, MA, United States; 4Division of Comparative Pathology, New England Primate Research Center, Southborough, MA, United States; 5Department of Neurosciences, University of California at San Diego, La Jolla, CA, United States

HIV-associated neurocognitive disorders continue to be a significant problem. Using the accelerated macaque model of neuroAIDS in combination with in vivo MR spectroscopy minocycline was found to be neuroprotective and able to reverse increased high energy metabolism, most likely localized to glia. Evaluating our observations, clues into the mechanisms underlying neuroprotection included reduction of microglial activation, reductions of CSF and plasma viral loads during treatment, and a reduction in a subset of circulating monocytes considered to be responsible for viral infection of the CNS by cell trafficking mechanisms.