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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              --- SoupGate-Win32 v1.05        * Origin: you cannot sedate... all the things you hate (1:229/2)    |
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