Models and mechanisms of post-stroke dementia and cognitive impairment
Stroke is a leading cause of death and disability globally, with significant long-term impacts such as post-stroke cognitive impairment (PSCI). PSCI affects up to one-third of stroke survivors, substantially increasing their risk of dementia, especially after recurrent strokes. Despite advances in a...
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| Format: | Article |
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Frontiers Media S.A.
2025-05-01
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| Series: | Frontiers in Stroke |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fstro.2025.1563924/full |
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| author | Romeesa Khan Romeesa Khan Patrick Devlin Akihiko Urayama Rodney M. Ritzel Rodney M. Ritzel |
| author_facet | Romeesa Khan Romeesa Khan Patrick Devlin Akihiko Urayama Rodney M. Ritzel Rodney M. Ritzel |
| author_sort | Romeesa Khan |
| collection | DOAJ |
| description | Stroke is a leading cause of death and disability globally, with significant long-term impacts such as post-stroke cognitive impairment (PSCI). PSCI affects up to one-third of stroke survivors, substantially increasing their risk of dementia, especially after recurrent strokes. Despite advances in acute stroke treatments, the mechanisms underlying PSCI remain poorly understood. Emerging evidence highlights that PSCI arises from a complex interplay of vascular damage, neurodegenerative pathologies, and chronic inflammation. This review explores the epidemiology and clinical characteristics of PSCI, emphasizing the role of age, education, vascular integrity, and comorbidities such as diabetes. Additionally, we examine experimental findings that utilize rodent models to elucidate the time course and biological mechanisms of PSCI. Notable contributions include insights from transgenic Alzheimer's disease (AD) mouse models, revealing how vascular and amyloid pathologies accelerate cognitive decline post-stroke. Moreover, studies on neuroinflammation and immune responses, such as those involving TREM2, underscore the significance of inflammatory pathways in PSCI. By integrating clinical and experimental findings, this literature review provides a comprehensive understanding of PSCI mechanisms, offering a foundation for developing targeted diagnostic tools and therapeutic interventions to mitigate the long-term cognitive effects of stroke. |
| format | Article |
| id | doaj-art-069b3e27087945bba35d9cc6d0d04f1b |
| institution | OA Journals |
| issn | 2813-3056 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Stroke |
| spelling | doaj-art-069b3e27087945bba35d9cc6d0d04f1b2025-08-20T02:28:20ZengFrontiers Media S.A.Frontiers in Stroke2813-30562025-05-01410.3389/fstro.2025.15639241563924Models and mechanisms of post-stroke dementia and cognitive impairmentRomeesa Khan0Romeesa Khan1Patrick Devlin2Akihiko Urayama3Rodney M. Ritzel4Rodney M. Ritzel5Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, United StatesUniversity of Texas MD Anderson Cancer Center GSBS, Houston, TX, United StatesDepartment of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, United StatesDepartment of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, United StatesDepartment of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, United StatesUniversity of Texas MD Anderson Cancer Center GSBS, Houston, TX, United StatesStroke is a leading cause of death and disability globally, with significant long-term impacts such as post-stroke cognitive impairment (PSCI). PSCI affects up to one-third of stroke survivors, substantially increasing their risk of dementia, especially after recurrent strokes. Despite advances in acute stroke treatments, the mechanisms underlying PSCI remain poorly understood. Emerging evidence highlights that PSCI arises from a complex interplay of vascular damage, neurodegenerative pathologies, and chronic inflammation. This review explores the epidemiology and clinical characteristics of PSCI, emphasizing the role of age, education, vascular integrity, and comorbidities such as diabetes. Additionally, we examine experimental findings that utilize rodent models to elucidate the time course and biological mechanisms of PSCI. Notable contributions include insights from transgenic Alzheimer's disease (AD) mouse models, revealing how vascular and amyloid pathologies accelerate cognitive decline post-stroke. Moreover, studies on neuroinflammation and immune responses, such as those involving TREM2, underscore the significance of inflammatory pathways in PSCI. By integrating clinical and experimental findings, this literature review provides a comprehensive understanding of PSCI mechanisms, offering a foundation for developing targeted diagnostic tools and therapeutic interventions to mitigate the long-term cognitive effects of stroke.https://www.frontiersin.org/articles/10.3389/fstro.2025.1563924/fullpost-stroke cognitive impairmentdementiachronic hypoperfusionischemic strokeneurodegeneration |
| spellingShingle | Romeesa Khan Romeesa Khan Patrick Devlin Akihiko Urayama Rodney M. Ritzel Rodney M. Ritzel Models and mechanisms of post-stroke dementia and cognitive impairment Frontiers in Stroke post-stroke cognitive impairment dementia chronic hypoperfusion ischemic stroke neurodegeneration |
| title | Models and mechanisms of post-stroke dementia and cognitive impairment |
| title_full | Models and mechanisms of post-stroke dementia and cognitive impairment |
| title_fullStr | Models and mechanisms of post-stroke dementia and cognitive impairment |
| title_full_unstemmed | Models and mechanisms of post-stroke dementia and cognitive impairment |
| title_short | Models and mechanisms of post-stroke dementia and cognitive impairment |
| title_sort | models and mechanisms of post stroke dementia and cognitive impairment |
| topic | post-stroke cognitive impairment dementia chronic hypoperfusion ischemic stroke neurodegeneration |
| url | https://www.frontiersin.org/articles/10.3389/fstro.2025.1563924/full |
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