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Brain RAS is\nreported to interact with pathophysiological mechanisms of many neurological and psychiatric\ndiseases, including Alzheimer\u2019s Disease (AD). Even though AD is the most common cause of\ndementia worldwide, its pathophysiology is far from elucidated. Currently, no treatment can\nhalt the disease course. Successive failures of amyloid-targeting drugs have challenged the\namyloid hypothesis and increased the interest in the inflammatory and vascular aspects of AD.\nRAS compounds, both centrally and peripherally, potentially interact with neuroinflammation\nand cerebrovascular regulation. This narrative review discusses the AD pathophysiology and\nits possible interaction with RAS, looking forward to potential therapeutic approaches. RAS\nmolecules affect BP, cerebral blood flow, neuroinflammation, and oxidative stress.\nAngiotensin (Ang) II, via angiotensin type 1 receptors may promote brain tissue damage, while\nAng-(1-7) seems to elicit neuroprotection. Several studies dosed RAS molecules in AD\npatients&amp;#039; biological material, with heterogeneous results. The link between AD and clinical\nconditions related to classical RAS axis overactivation (hypertension, heart failure, and chronic\nkidney disease) supports the hypothesized role of this system in AD. Additionally, RAStargeting\ndrugs as Angiotensin Converting Enzyme inhibitors (ACEis) and Angiotensin\nReceptor Blockers (ARBs) seem to exert beneficial effects on AD. Results of randomized\ncontrolled trials testing ACEi or ARBs in AD are awaited to elucidate whether AD-RAS\ninteraction has implications on AD therapeutics.<\/jats:p>\n<\/jats:sec>","DOI":"10.2174\/0929866527666191230103739","type":"journal-article","created":{"date-parts":[[2019,12,30]],"date-time":"2019-12-30T14:11:02Z","timestamp":1577715062000},"page":"484-511","update-policy":"https:\/\/doi.org\/10.2174\/bsp_crossmark_policy","source":"Crossref","is-referenced-by-count":46,"title":["Renin-Angiotensin System and Alzheimer\u2019s Disease Pathophysiology: From the Potential Interactions to Therapeutic Perspectives"],"prefix":"10.2174","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3319-2833","authenticated-orcid":true,"given":"Victor Teatini","family":"Ribeiro","sequence":"first","affiliation":[{"name":"Interdisciplinary Laboratory of Medical Investigation, Faculty of Medicine, Federal University of Minas Gerais (UFMG), Belo Horizonte, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5027-9722","authenticated-orcid":true,"given":"Leonardo Cruz","family":"de Souza","sequence":"additional","affiliation":[{"name":"Interdisciplinary Laboratory of Medical Investigation, Faculty of Medicine, Federal University of Minas Gerais (UFMG), Belo Horizonte, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9222-3882","authenticated-orcid":true,"given":"Ana Cristina","family":"Sim\u00f5es e Silva","sequence":"additional","affiliation":[{"name":"Interdisciplinary Laboratory of Medical Investigation, Faculty of Medicine, Federal University of Minas Gerais (UFMG), Belo Horizonte, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"965","reference":[{"key":"ref=1","doi-asserted-by":"publisher","first-page":"317","DOI":"10.1016\/j.biopha.2017.07.091","volume":"94","author":"Patel S.","year":"2017","unstructured":"Patel S.; Rauf A.; Khan H.; Abu-Izneid T.; Renin-angiotensin-aldosterone (RAAS): The ubiquitous system for homeostasis and pathologies. 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