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From the Departments of Neurosciences (L.C., A.A., R.E., E.M.), Pathology (D.L., E.M.), and Psychiatry (G.C., I.P.E., I.G., M.C., D.L., R.H.) and the HIV Neurobehavioral Research Center, University of California, San Diego/La Jolla, CA; and Veterans Affairs Healthcare System (I.G.), La Jolla, CA.
Address correspondence and reprint requests to Dr. Eliezer Masliah, Department of Neurosciences, University of California San Diego, La Jolla, CA 92093-0624; e-mail: emasliah{at}ucsd.edu
The cellular basis for cognitive deficits in HIV+ patients with and without a history of methamphetamine (METH) use is unclear. We found that HIV+ METH users had more severe loss of interneurons that was associated with cognitive impairment. Compared with other markers, loss of calbindin and parvalbumin interneurons in the frontal cortex was the most significant correlate to memory deficits, suggesting a role in neurobehavioral alterations of HIV+ METH users.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the October 24 issue to find the title link for this article.
*See appendix for a list of Group members.
This work was supported by NIH Grants MH59745, MH45294, MH58164, and DA12065, and an HNRC pilot project award. The HIV Neurobehavioral Research Center is supported by Center award MH 62512 from the National Institute of Mental Health.
Disclosure: The authors report no conflicts of interest.
The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Navy, Department of Defense, nor the United States Government.
Received November 28, 2005. Accepted in final form June 22, 2006.
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