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      Incidence and Risk Factors for Mild Cognitive Impairment: A Population-Based Three-Year Follow-Up Study of Cognitively Healthy Elderly Subjects

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          Abstract

          Background: Mild cognitive impairment (MCI) has attracted considerable interest as a potential predictor of Alzheimer’s disease (AD). Both the apolipoprotein E (ApoE) Ε4 allele and vascular factors have been associated with a higher risk for AD, recently they have also been linked to the risk of MCI. Objectives: To estimate the incidence of MCI among cognitively healthy elderly subjects during a 3-year follow-up, and to evaluate the impact of demographic and vascular factors as well as the ApoE Ε4 allele on the conversion to MCI. Methods: At baseline, the cognitive abilities of 806 out of 1,150 eligible subjects (aged 60–76 years) from a population-based sample were examined. Cognitively intact subjects (n = 747) were followed for an average of 3 years. Results: 66 subjects (8.8%) had converted to MCI. The global incidence rate of MCI was 25.94/1,000 person-years. Persons with higher age (OR 1.08, 95% CI 1.01–1.16), ApoE Ε4 allele carriers (OR 2.04, 95% CI 1.15–3.64) and persons with medicated hypertension (OR 1.86, 95% CI 1.05–3.29) were more likely to convert to MCI than those individuals of lower age and without an ApoE Ε4 allele or medicated hypertension. Persons with high education (OR 0.79, 95% CI 0.70–0.89) were less likely to convert to MCI than persons with low or no education. In subjects with both the ApoE Ε4 allele and medicated hypertension, the crude OR for conversion was 3.92 (95% CI 1.81–8.49). In subjects with cardiovascular disease, the crude OR for conversion was 2.13 (95% CI 1.26–3.60). Gender, elevated blood pressure, diabetes or cerebrovascular disease had no significant effect on the conversion to MCI. Conclusion: Higher age, the presence of at least one ApoE Ε4 allele and medicated hypertension are independent risk factors, but high education is a protective factor for MCI. The results suggest that vascular factors may have an important role in the pathogenesis of MCI.

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          Cerebral microvascular pathology in aging and Alzheimer's disease.

          E Farkas, P G Luiten (2001)
          The aging of the central nervous system and the development of incapacitating neurological diseases like Alzheimer's disease (AD) are generally associated with a wide range of histological and pathophysiological changes eventually leading to a compromised cognitive status. Although the diverse triggers of the neurodegenerative processes and their interactions are still the topic of extensive debate, the possible contribution of cerebrovascular deficiencies has been vigorously promoted in recent years. Various forms of cerebrovascular insufficiency such as reduced blood supply to the brain or disrupted microvascular integrity in cortical regions may occupy an initiating or intermediate position in the chain of events ending with cognitive failure. When, for example, vasoconstriction takes over a dominating role in the cerebral vessels, the perfusion rate of the brain can considerably decrease causing directly or through structural vascular damage a drop in cerebral glucose utilization. Consequently, cerebral metabolism can suffer a setback leading to neuronal damage and a concomitant suboptimal cognitive capacity. The present review focuses on the microvascular aspects of neurodegenerative processes in aging and AD with special attention to cerebral blood flow, neural metabolic changes and the abnormalities in microvascular ultrastructure. In this context, a few of the specific triggers leading to the prominent cerebrovascular pathology, as well as the potential neurological outcome of the compromised cerebral microvascular system are also going to be touched upon to a certain extent, without aiming at total comprehensiveness. Finally, a set of animal models are going to be presented that are frequently used to uncover the functional relationship between cerebrovascular factors and the damage to neural networks.
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            15-year longitudinal study of blood pressure and dementia

            I Skoog, L. Nilsson, G. Persson … (1996)
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              The association between midlife blood pressure levels and late-life cognitive function. The Honolulu-Asia Aging Study.

              Andrea L. Launer, H Petrovitch, D. Foley … (1995)
              To assess the long-term relationship of midlife blood pressure levels to late-life cognitive function. The 4678 surviving cohort members of the prospective Honolulu Heart Program (baseline, 1965-1968) were examined a fourth time in 1991 through 1993 and given a cognitive test. The subjects were 3735 Japanese-American men living in Hawaii in the community or in institutions, with an average age of 78 years at the fourth examination. Cognitive function, measured by the 100-point Cognitive Abilities Screening Instrument (CASI), was categorized into good (reference: a CASI score of 92 to 100), intermediate ( or = 160 mm Hg; and for DBP, or = 95 mm Hg. When we controlled for age and education, the risk for intermediate and poor cognitive function increased progressively with increasing level of midlife SBP category (P for trend < .03 and < .001, respectively). For every 10-mm Hg increase in SBP there was an increase in risk for intermediate cognitive function of 7% (95% confidence interval [CI], 3% to 11%) and for poor cognitive function of 9% (95% CI, 3% to 16%). Adjustment for prevalent stroke, coronary heart disease, and subclinical atherosclerosis reduced the strength of the relationship between midlife SBP and poor cognitive function to 5% (95% CI, 0% to 12%). The level of cognitive function was not associated with midlife DBP. Midlife SBP is a significant predictor of reduced cognitive function in later life. Early control of SBP levels may reduce the risk for cognitive impairment in old age.
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                Author and article information

                Journal
                Journal ID (publisher-id): DEM
                Journal ID (nlm-ta): Dement Geriatr Cogn Disord
                Journal ID (doi): 10.1159/issn.1420-8008
                Title: Dementia and Geriatric Cognitive Disorders
                Publisher: S. Karger AG
                ISSN (Print): 1420-8008
                ISSN (Electronic): 1421-9824
                Publication date Subscription-year: 2004
                Publication date (Print): March 2004
                Publication date (Electronic): 17 March 2004
                Volume: 17
                Issue: 3
                Pages: 196-203
                Affiliations
                aDepartment of Neuroscience and Neurology, Brain Research Unit, Clinical Research Centre, Mediteknia, University of Kuopio; bDepartment of Neurology, Kuopio University Hospital and cDepartment of Pathology, University of Kuopio, Kuopio, Finland and dAging Research Center, Division of Geriatric Epidemiology, Neurotec, Karolinska Institutet, Stockholm, Sweden
                Article
                Publisher ID: 76356 Other ID: Dement Geriatr Cogn Disord 2004;17:196–203
                DOI: 10.1159/000076356
                PubMed ID: 14739544
                SO-VID: 7b5a058a-d423-443d-b3b7-1b6003b4ca84
                Copyright © © 2004 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 13 August 2003
                Page count
                Figures: 1, Tables: 3, References: 62, Pages: 8
                Categories
                Subject: Original Research Article

                ScienceOpen disciplines: Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Keywords: Mild cognitive impairment,Cognitive impairment, mild,Risk factors
                Data availability:
                ScienceOpen disciplines: Geriatric medicine, Neurology, Cardiovascular Medicine, Neurosciences, Clinical Psychology & Psychiatry, Public health
                Keywords: Mild cognitive impairment, Cognitive impairment, mild, Risk factors

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