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    Activation of hemostasis and decline in cognitive function in older people.

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    Authors
    Stott, David J
    Robertson, Michele
    Rumley, Ann
    Welsh, Paul
    Sattar, Naveed
    Packard, Christopher J
    Shepherd, James
    Trompet, Stella
    Westendorp, Rudi G J
    de Craen, Anton J M
    Jukema, J Wouter
    Buckley, Brendan
    Ford, Ian
    Lowe, Gordon D O
    Show allShow less
    Affiliation
    Academic Section of Geriatric Medicine, 3 Floor Queen Elizabeth Building, Royal Infirmary, Glasgow G31 2ER. d.j.stott@clinmed.gla.ac.uk
    Issue Date
    2010-03
    MeSH
    Activities of Daily Living
    Age Factors
    Aged
    Aged, 80 and over
    Biological Markers
    Cognition
    Cognition Disorders
    Dementia, Vascular
    Female
    Fibrin Fibrinogen Degradation Products
    Fibrinogen
    Follow-Up Studies
    Hemostasis
    Humans
    Male
    Prothrombin
    Risk Factors
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    Citation
    Activation of hemostasis and decline in cognitive function in older people. 2010, 30 (3):605-11 Arterioscler. Thromb. Vasc. Biol.
    Journal
    Arteriosclerosis, thrombosis, and vascular biology
    URI
    http://hdl.handle.net/10147/200316
    DOI
    10.1161/ATVBAHA.109.199448
    PubMed ID
    20032290
    Additional Links
    http://atvb.ahajournals.org/content/30/3/605.full.pdf+html
    Abstract
    To determine whether activation of hemostatic function (thrombosis and fibrinolysis) is associated with cognitive decline in older people.
    We studied 5804 people (age, 70-82 years) in the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER). Mean follow-up was 3.2 years, including annual measurement of speed of information processing (letter, digit coding, and Stroop), verbal memory (picture-word naming), and basic and instrumental activities of daily living. Raised levels of markers of thrombin generation (d-dimer and prothrombin fragment 1+2) were associated independently with increased rate of cognitive decline (eg, Stroop increased by 4.44 s [SEM, 0.68] in bottom tertile of d-dimer compared to 5.46 [SEM, 0.71] in highest tertile; P<0.05) and deterioration in activities of daily living. This increased rate of decline was attenuated but not removed when subjects with incident nonfatal stroke were omitted from the analysis. It also persisted when adjustments were made for inflammation (C-reactive protein and IL-6).
    Older patients with increased markers of thrombin generation (d-dimer and prothrombin fragment 1+2) are at increased risk for cognitive decline and deterioration in ability to perform activities of daily living. This is likely attributable to increased risk of cerebral ischemic damage (including covert disease) associated with prothrombotic states.
    Item Type
    Article
    Language
    en
    ISSN
    1524-4636
    ae974a485f413a2113503eed53cd6c53
    10.1161/ATVBAHA.109.199448
    Scopus Count
    Collections
    Cork University Hospital

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