CEREBROVASCULAR DISEASE: Edited by Mitchell S.V. ElkindImmunological mechanisms in poststroke dementiaDoyle, Kristian P.a; Buckwalter, Marion S.bAuthor Information aDepartments of Immunobiology and Neurology and the Arizona Center on Aging, University of Arizona, Tucson, Arizona bDepartments of Neurology and Neurological Sciences, and Neurosurgery, Wu Tsai Neurosciences Institute, Stanford School of Medicine, Stanford, California, USA Correspondence to Marion S. Buckwalter, Associate Professor, Departments of Neurology and Neurological Sciences, and Neurosurgery, Wu Tsai Neurosciences Institute, Stanford School of Medicine, 1201 Welch Road, P209, Stanford, CA 94305-5489, USA. Tel: +1 650 724 9098; e-mail: [email protected] Current Opinion in Neurology: February 2020 - Volume 33 - Issue 1 - p 30-36 doi: 10.1097/WCO.0000000000000783 Buy Metrics Abstract Purpose of review To review new evidence on links between poststroke dementia and inflammation. Recent findings Although there are still no treatments for poststroke dementia, recent evidence has improved our understanding that stroke increases the risk of incident dementia and worsens cognitive trajectory for at least a decade afterwards. Within approximately the first year dementia onset is associated with stroke severity and location, whereas later absolute risk is associated with more traditional dementia risk factors, such as age and imaging findings. The molecular mechanisms that underlie increased risk of incident dementia in stroke survivors remain unproven; however new data in both human and animal studies suggests links between cognitive decline and inflammation. These point to a model where chronic brain inflammation, provoked by inefficient clearance of myelin debris and a prolonged innate and adaptive immune response, causes poststroke dementia. These localized immune events in the brain may themselves be influenced by the peripheral immune state at key times after stroke. Summary This review recaps clinical evidence on poststroke dementia, new mechanistic links between the chronic inflammatory response to stroke and poststroke dementia, and proposes a model of immune-mediated neurodegeneration after stroke. Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.