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   Vascular Contributions to Cognitive Impa   
   26 Jul 15 20:00:30   
   
   From: hounddog23x@gmail.com   
      
   Vascular Contributions to Cognitive Impairment and Dementia    
      
      
   A Statement for Healthcare Professionals From the American Heart   
   Association/American Stroke Association    
   Philip B. Gorelick, MD, MPH, FAHA, Co-Chair;    
   Angelo Scuteri, MD, PhD, Co-Chair;    
   Sandra E. Black, MD, FRCPC, FAHA*;    
   Charles DeCarli, MD*;    
   Steven M. Greenberg, MD, PhD, FAHA*;    
   Costantino Iadecola, MD, FAHA*;    
   Lenore J. Launer, MD*;    
   Stephane Laurent, MD*;    
   Oscar L. Lopez, MD*;    
   David Nyenhuis, PhD, ABPP-Cn*;    
   Ronald C. Petersen, MD, PhD*;    
   Julie A. Schneider, MD, MS*;    
   Christophe Tzourio, MD, PhD*;    
   Donna K. Arnett, PhD, MSPH, FAHA;    
   David A. Bennett, MD;    
   Helena C. Chui, MD, FAHA;    
   Randall T. Higashida, MD, FAHA;    
   Ruth Lindquist, PhD, RN, ACNS-BC, FAHA;    
   Peter M. Nilsson, MD, PhD;    
   Gustavo C. Roman, MD;    
   Frank W. Sellke, MD, FAHA;    
   Sudha Seshadri, MD on behalf of the American Heart Association Stroke Council,   
   Council on Epidemiology and Prevention, Council on Cardiovascular Nursing,   
   Council on Cardiovascular Radiology and Intervention, and Council on   
   Cardiovascular Surgery and    
   Anesthesia    
   Abstract    
   Background and Purpose--This scientific statement provides an overview of the   
   evidence on vascular contributions to cognitive impairment and dementia.   
   Vascular contributions to cognitive impairment and dementia of later life are   
   common. Definitions of    
   vascular cognitive impairment (VCI), neuropathology, basic science and   
   pathophysiological aspects, role of neuroimaging and vascular and other   
   associated risk factors, and potential opportunities for prevention and   
   treatment are reviewed. This statement    
   serves as an overall guide for practitioners to gain a better understanding of   
   VCI and dementia, prevention, and treatment.    
      
   Methods--Writing group members were nominated by the writing group co-chairs   
   on the basis of their previous work in relevant topic areas and were approved   
   by the American Heart Association Stroke Council Scientific Statement   
   Oversight Committee, the    
   Council on Epidemiology and Prevention, and the Manuscript Oversight   
   Committee. The writing group used systematic literature reviews (primarily   
   covering publications from 1990 to May 1, 2010), previously published   
   guidelines, personal files, and expert    
   opinion to summarize existing evidence, indicate gaps in current knowledge,   
   and, when appropriate, formulate recommendations using standard American Heart   
   Association criteria. All members of the writing group had the opportunity to   
   comment on the    
   recommendations and approved the final version of this document. After peer   
   review by the American Heart Association, as well as review by the Stroke   
   Council leadership, Council on Epidemiology and Prevention Council, and   
   Scientific Statements Oversight    
   Committee, the statement was approved by the American Heart Association   
   Science Advisory and Coordinating Committee.    
      
   Results--The construct of VCI has been introduced to capture the entire   
   spectrum of cognitive disorders associated with all forms of cerebral vascular   
   brain injury--not solely stroke--ranging from mild cognitive impairment   
   through fully developed    
   dementia. Dysfunction of the neurovascular unit and mechanisms regulating   
   cerebral blood flow are likely to be important components of the   
   pathophysiological processes underlying VCI. Cerebral amyloid angiopathy is   
   emerging as an important marker of risk    
   for Alzheimer disease, microinfarction, microhemorrhage and macrohemorrhage of   
   the brain, and VCI. The neuropathology of cognitive impairment in later life   
   is often a mixture of Alzheimer disease and microvascular brain damage, which   
   may overlap and    
   synergize to heighten the risk of cognitive impairment. In this regard,   
   magnetic resonance imaging and other neuroimaging techniques play an important   
   role in the definition and detection of VCI and provide evidence that   
   subcortical forms of VCI with    
   white matter hyperintensities and small deep infarcts are common. In many   
   cases, risk markers for VCI are the same as traditional risk factors for   
   stroke. These risks may include but are not limited to atrial fibrillation,   
   hypertension, diabetes mellitus,   
    and hypercholesterolemia. Furthermore, these same vascular risk factors may   
   be risk markers for Alzheimer disease. Carotid intimal-medial thickness and   
   arterial stiffness are emerging as markers of arterial aging and may serve as   
   risk markers for VCI.    
   Currently, no specific treatments for VCI have been approved by the US Food   
   and Drug Administration. However, detection and control of the traditional   
   risk factors for stroke and cardiovascular disease may be effective in the   
   prevention of VCI, even in    
   older people.    
      
   Conclusions--Vascular contributions to cognitive impairment and dementia are   
   important. Understanding of VCI has evolved substantially in recent years,   
   based on preclinical, neuropathologic, neuroimaging, physiological, and   
   epidemiological studies.    
   Transdisciplinary, translational, and transactional approaches are recommended   
   to further our understanding of this entity and to better characterize its   
   neuropsychological profile. There is a need for prospective, quantitative,   
   clinical-pathological-   
   neuroimaging studies to improve knowledge of the pathological basis of   
   neuroimaging change and the complex interplay between vascular and Alzheimer   
   disease pathologies in the evolution of clinical VCI and Alzheimer disease.   
   Long-term vascular risk marker    
   interventional studies beginning as early as midlife may be required to   
   prevent or postpone the onset of VCI and Alzheimer disease. Studies of   
   intensive reduction of vascular risk factors in high-risk groups are another   
   important avenue of research.    
      
   Key Words: AHA Scientific Statements vascular dementia Alzheimer disease risk   
   factors prevention treatment    
   (c) 2011 American Heart Association, Inc.    
   Stroke. 2011; 42: 2672-2713 Published online before print July 21, 2011, doi:   
   10.1161/STR.0b013e3182299496    
   >> AbstractFree    
   Full TextFree    
   PDFFree    
   Japanese Translation    
   All Versions of this Article:    
   STR.0b013e3182299496v1    
   42/9/2672 most recent    
   Email me this article    
   Copyright (c) 2015 by American Heart Association, Inc. All righs reserved.   
   Unauthorized use probihited | Contact AHA | Help Pages | Full Site    
      
      
      
   http://m.stroke.ahajournals.org/content/42/9/2672   
      
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