Immunological mechanisms in poststroke dementia

Kristian P. Doyle, Marion S. Buckwalter

Research output: Contribution to journalReview articlepeer-review

7 Scopus citations


Purpose of reviewTo review new evidence on links between poststroke dementia and inflammation.Recent findingsAlthough 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.SummaryThis 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.

Original languageEnglish (US)
Pages (from-to)30-36
Number of pages7
JournalCurrent opinion in neurology
Issue number1
StatePublished - Feb 1 2020


  • inflammation
  • poststroke dementia
  • stroke recovery

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology


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