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These are risk factors leading to neuronal injury, the incidence and progression of neurodegerative, mood and traumatic brain disorders, and cognitive decline. In rodents, ARBs (AT1 receptor blockers) ameliorate stress-induced disorders, anxiety and depression, protect cerebral blood flow during stroke, decrease brain inflammation and amyloid-\u03b2 neurotoxicity and reduce traumatic brain injury. Direct anti-inflammatory protective effects, demonstrated in cultured microglia, cerebrovascular endothelial cells, neurons and human circulating monocytes, may result not only in AT1 receptor blockade, but also from PPAR\u03b3 (peroxisome-proliferator-activated receptor \u03b3) stimulation. Controlled clinical studies indicate that ARBs protect cognition after stroke and during aging, and cohort analyses reveal that these compounds significantly reduce the incidence and progression of Alzheimer's disease. ARBs are commonly used for the therapy of hypertension, diabetes and stroke, but have not been studied in the context of neurodegenerative, mood or traumatic brain disorders, conditions lacking effective therapy. These compounds are well-tolerated pleiotropic neuroprotective agents with additional beneficial cardiovascular and metabolic profiles, and their use in central nervous system disorders offers a novel therapeutic approach of immediate translational value. ARBs should be tested for the prevention and therapy of neurodegenerative disorders, in particular Alzheimer's disease, affective disorders, such as co-morbid cardiovascular disease and depression, and traumatic brain injury.<\/jats:p>","DOI":"10.1042\/cs20120078","type":"journal-article","created":{"date-parts":[[2012,7,24]],"date-time":"2012-07-24T10:21:32Z","timestamp":1343125292000},"page":"567-590","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":195,"title":["Angiotensin II AT1 receptor blockers as treatments for inflammatory brain disorders"],"prefix":"10.1042","volume":"123","author":[{"given":"Juan\u00a0M.","family":"Saavedra","sequence":"first","affiliation":[{"name":"Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2012,7,23]]},"reference":[{"key":"2021113010211763100_B1","doi-asserted-by":"crossref","first-page":"2381","DOI":"10.1111\/j.1582-4934.2010.01164.x","article-title":"Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury","volume":"14","author":"Andriessen","year":"2010","journal-title":"J. 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