Principal Investigator: Juan Saavedra, MD
Juan Saavedra, MD
Section on Pharmacology
Dr. Saavedra is chief of the Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health. He graduated from Medical School in 1965 and was board certified in Psychiatry in 1970 at the University of Buenos Aires, Argentina. He joined the laboratory of Julius Axelrod (Section on Pharmacology, Laboratory of Clinical Science, NIMH) as a Guest Researcher in 1971, was a Fogarty International Fellow from 1972-1973, Visiting Scientist from 1973 to 1979 and Medical Officer (Psychiatry, Civil Service Excepted Appointment) from 1979 to 1983. From 1983-1988 he joined the Section on Clinical Pharmacology, Laboratory of Clinical Science, NIMH, and in 1989 he became chief of the newly created Section on Pharmacology, DIRP, NIMH. Dr. Saavedra is also a Research Professor of Psychiatry, Department of Psychiatry, Uniformed Services School of the Health Sciences, Bethesda, Maryland.
Dr. Saavedra’s laboratory is focused on the analysis of basic molecular mechanisms controlling the reaction to stress, and of those involved in brain inflammation. The goal of these studies is to develop novel therapies for the treatment of major diseases of the brain. The main interest is the treatment of anxiety, depression and post-traumatic stress disorder. Brain inflammation and failure to control and adapt to stress are recognized as important factors in the development and progression of these diseases. The Section on Pharmacology studies novel centrally–acting compounds that decrease anxiety and prevent stress-induced disorders, brain inflammation and brain ischemia, such as antagonists of Angiotensin II AT1 receptors. The investigators attempt to elucidate their mechanisms of action and determine their therapeutic spectrum. In complementary studies on human circulating cells, they search for biological markers of inflammation and their relationship to brain disorders. The approach is multidisciplinary, and includes neuroanatomy, biochemistry, pharmacology and molecular biology components.
Candesartan, an angiotensin II AT₁-receptor blocker and PPAR-γ agonist, reduces lesion volume and improves motor and memory function after traumatic brain injury in mice . Villapol S, Yaszemski AK, Logan TT, Sánchez-Lemus E, Saavedra JM, Symes AJ. Neuropsychopharmacology. 2012 Dec;37(13):2817-29. doi: 10.1038/npp.2012.152. Epub 2012 Aug 15. PMID: 22892395.
Regulation of angiotensin II type 2 receptor gene expression in the adrenal medulla by acute and repeated immobilization stress . Nostramo R, Tillinger A, Saavedra JM, Kumar A, Pandey V, Serova L, Kvetnansky R, Sabban EL. J Endocrinol. 2012 Nov;215(2):291-301. doi: 10.1530/JOE-12-0181. Epub 2012 Aug 21. PMID: 22911895.
Angiotensin II AT(1) receptor blockers as treatments for inflammatory brain disorders . Saavedra JM. Clin Sci (Lond). 2012 Nov;123(10):567-90. doi: 10.1042/CS20120078. PMID: 22827472.
Angiotensin II AT1 receptor blocker candesartan prevents the fast up-regulation of cerebrocortical benzodiazepine-1 receptors induced by acute inflammatory and restraint stress . Sánchez-Lemus E, Honda M, Saavedra JM. Behav Brain Res. 2012 Jun 15;232(1):84-92. doi: 10.1016/j.bbr.2012.03.041. Epub 2012 Apr 4. PMID: 22503782.
Telmisartan directly ameliorates the neuronal inflammatory response to IL-1β partly through the JNK/c-Jun and NADPH oxidase pathways . Pang T, Wang J, Benicky J, Sánchez-Lemus E, Saavedra JM. J Neuroinflammation. 2012 May 29;9:102. doi: 10.1186/1742-2094-9-102. PMID: 22642771.
Magnuson Clinical Center, Room 2D57, MSC 1514
Bethesda, MD 20814
Phone: +1 301 496 0160
Fax: +1 301 402 0337