Send to

Choose Destination
Biochim Biophys Acta. 2016 May;1862(5):945-51. doi: 10.1016/j.bbadis.2015.08.019. Epub 2015 Aug 28.

Clinical-pathologic correlations in vascular cognitive impairment and dementia.

Author information

Department of Pathology, University of Washington, Seattle, WA, United States.
Group Health Research Institute, Seattle, WA, United States.
Department of Psychiatry & Behavioral Sciences, University of Washington, Seattle, WA, United States.
Department of Medicine, University of Washington, Seattle, WA, United States.
Pacific Health Research and Education Institute, Honolulu, HI, United States; Department of Geriatric Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, HI, United States.
Department of Pathology, University of Washington, Seattle, WA, United States. Electronic address:


The most common causes of cognitive impairment and dementia are Alzheimer's disease (AD) and vascular brain injury (VBI), either independently, in combination, or in conjunction with other neurodegenerative disorders. The contribution of VBI to cognitive impairment and dementia, particularly in the context of AD pathology, has been examined extensively yet remains difficult to characterize due to conflicting results. Describing the relative contribution and mechanisms of VBI in dementia is important because of the profound impact of dementia on individuals, caregivers, families, and society, particularly the stability of health care systems with the rapidly increasing age of our population. Here we discuss relationships between pathologic processes of VBI and clinical expression of dementia, specific subtypes of VBI including microvascular brain injury, and what is currently known regarding contributions of VBI to the development and pathogenesis of the dementia syndrome. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center