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      Physical Activity: A Viable Way to Reduce the Risks of Mild Cognitive Impairment, Alzheimer’s Disease, and Vascular Dementia in Older Adults

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          Abstract

          A recent alarming rise of neurodegenerative diseases in the developed world is one of the major medical issues affecting older adults. In this review, we provide information about the associations of physical activity (PA) with major age-related neurodegenerative diseases and syndromes, including Alzheimer’s disease, vascular dementia, and mild cognitive impairment. We also provide evidence of PA’s role in reducing the risks of these diseases and helping to improve cognitive outcomes in older adults. Finally, we describe some potential mechanisms by which this protective effect occurs, providing guidelines for future research.

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          Most cited references70

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          The diagnosis and management of mild cognitive impairment: a clinical review.

          Cognitive decline is a common and feared aspect of aging. Mild cognitive impairment (MCI) is defined as the symptomatic predementia stage on the continuum of cognitive decline, characterized by objective impairment in cognition that is not severe enough to require help with usual activities of daily living.
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            Validity of the MoCA and MMSE in the detection of MCI and dementia in Parkinson disease.

            Due to the high prevalence of mild cognitive impairment (MCI) and dementia in Parkinson disease (PD), routine cognitive screening is important for the optimal management of patients with PD. The Montreal Cognitive Assessment (MoCA) is more sensitive than the commonly used Mini-Mental State Examination (MMSE) in detecting MCI and dementia in patients without PD, but its validity in PD has not been established. A representative sample of 132 patients with PD at 2 movement disorders centers was administered the MoCA, MMSE, and a neuropsychological battery with operationalized criteria for deficits. MCI and PD dementia (PDD) criteria were applied by an investigator blinded to the MoCA and MMSE results. The discriminant validity of the MoCA and MMSE as screening and diagnostic instruments was ascertained. Approximately one third of the sample met diagnostic criteria for a cognitive disorder (12.9% PDD and 17.4% MCI). Mean (SD) MoCA and MMSE scores were 25.0 (3.8) and 28.1 (2.0). The overall discriminant validity for detection of any cognitive disorder was similar for the MoCA and the MMSE (receiver operating characteristic area under the curve [95% confidence interval]): MoCA (0.79 [0.72, 0.87]) and MMSE (0.76 [0.67, 0.85]), but as a screening instrument the MoCA (optimal cutoff point = 26/27, 64% correctly diagnosed, lack of ceiling effect) was superior to the MMSE (optimal cutoff point = 29/30, 54% correctly diagnosed, presence of ceiling effect). The Montreal Cognitive Assessment, but not the Mini-Mental State Examination, has adequate psychometric properties as a screening instrument for the detection of mild cognitive impairment or dementia in Parkinson disease. However, a positive screen using either instrument requires additional assessment due to suboptimal specificity at the recommended screening cutoff point.
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              The metabolic syndrome, inflammation, and risk of cognitive decline.

              Several studies have reported an association between the metabolic syndrome and cardiovascular disease. Despite an increasing awareness that cardiovascular risk factors increase risk of cognitive decline and dementia, there are few data on the metabolic syndrome and cognition. To determine if the metabolic syndrome is a risk factor for cognitive decline and if this association is modified by inflammation. A 5-year prospective observational study conducted from 1997 to 2002 at community clinics at 2 sites. A total of 2632 black and white elders (mean age, 74 years). Association of the metabolic syndrome (measured using National Cholesterol Education Program guidelines) and high inflammation (defined as above median serum level of interleukin 6 and C-reactive protein) with change in cognition (Modified Mini-Mental State Examination [3MS]) at 3 and 5 years. Cognitive impairment was defined as at least a 5-point decline. Compared with those without the metabolic syndrome (n = 1616), elders with the metabolic syndrome (n = 1016) were more likely to have cognitive impairment (26% vs 21%, multivariate adjusted relative risk [RR], 1.20; 95% confidence interval [CI], 1.02-1.41). There was a statistically significant interaction with inflammation and the metabolic syndrome (P = .03) on cognitive impairment. After stratifying for inflammation, those with the metabolic syndrome and high inflammation (n = 348) had an increased likelihood of cognitive impairment compared with those without the metabolic syndrome (multivariate adjusted RR, 1.66; 95% CI, 1.19-2.32). Those with the metabolic syndrome and low inflammation (n = 668) did not exhibit an increased likelihood of impairment (multivariate adjusted RR, 1.08; 95% CI, 0.89-1.30). Stratified multivariate random-effects models demonstrated that participants with the metabolic syndrome and high inflammation had greater 4-year decline on 3MS (P = .04) compared with those without the metabolic syndrome, whereas those with the metabolic syndrome and low inflammation did not (P = .44). These findings support the hypothesis that the metabolic syndrome contributes to cognitive impairment in elders, but primarily in those with high level of inflammation.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Brain Sci
                Brain Sci
                brainsci
                Brain Sciences
                MDPI
                2076-3425
                20 February 2017
                February 2017
                : 7
                : 2
                : 22
                Affiliations
                [1 ]Department of Nutritional Sciences, The University of Arizona, Tucson, AZ 85721-0038, USA; gallaway@ 123456email.arizona.edu (P.J.G.); ask1@ 123456email.arizona.edu (A.S.K.)
                [2 ]Nishinomiya Kyoritsu Neurosurgical Hospital, Hyogo 663-8211, Japan; miyake@ 123456nk-hospital.or.jp
                [3 ]Department of Medicine, Vanderbilt University, Nashville, TN 37232-5280, USA; maciej.buchowski@ 123456vanderbilt.edu
                [4 ]Chiba Prefectural University of Health Sciences, Chiba 261-0014, Japan; mieko.shimada@ 123456cpuhs.ac.jp
                [5 ]National Institute of Fitness & Sport in Kanoya, Kagoshima 891-2311, Japan; yositake@ 123456nifs-k.ac.jp
                Author notes
                [* ]Correspondence: hongu@ 123456email.arizona.edu ; Tel.: +1-520-626-2085; Fax: +1-520-621-9446
                Article
                brainsci-07-00022
                10.3390/brainsci7020022
                5332965
                28230730
                7977230a-179c-47ab-bf34-459aa8717234
                © 2017 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 30 November 2016
                : 03 February 2017
                Categories
                Review

                aging,alzheimer’s disease,cognitive decline,dementia,health,mild cognitive impairment,physical activity

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