55
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Physical activity reduces hippocampal atrophy in elders at genetic risk for Alzheimer's disease

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          We examined the impact of physical activity (PA) on longitudinal change in hippocampal volume in cognitively intact older adults at varying genetic risk for the sporadic form of Alzheimer's disease (AD). Hippocampal volume was measured from structural magnetic resonance imaging (MRI) scans administered at baseline and at an 18-month follow-up in 97 healthy, cognitively intact older adults. Participants were classified as High or Low PA based on a self-report questionnaire of frequency and intensity of exercise. Risk status was defined by the presence or absence of the apolipoprotein E-epsilon 4 (APOE-ε4) allele. Four subgroups were studied: Low Risk/High PA ( n = 24), Low Risk/Low PA ( n = 34), High Risk/High PA ( n = 22), and High Risk/Low PA ( n = 17). Over the 18 month follow-up interval, hippocampal volume decreased by 3% in the High Risk/Low PA group, but remained stable in the three remaining groups. No main effects or interactions between genetic risk and PA were observed in control brain regions, including the caudate, amygdala, thalamus, pre-central gyrus, caudal middle frontal gyrus, cortical white matter (WM), and total gray matter (GM). These findings suggest that PA may help to preserve hippocampal volume in individuals at increased genetic risk for AD. The protective effects of PA on hippocampal atrophy were not observed in individuals at low risk for AD. These data suggest that individuals at genetic risk for AD should be targeted for increased levels of PA as a means of reducing atrophy in a brain region critical for the formation of episodic memories.

          Related collections

          Most cited references27

          • Record: found
          • Abstract: not found
          • Article: not found

          Geriatric Depression Scale.

          J Yesavage (1988)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Risk factors for Alzheimer's disease: a prospective analysis from the Canadian Study of Health and Aging.

            J. Lindsay (2002)
            A prospective analysis of risk factors for Alzheimer's disease was a major objective of the Canadian Study of Health and Aging, a nationwide, population-based study. Of 6,434 eligible subjects aged 65 years or older in 1991, 4,615 were alive in 1996 and participated in the follow-up study. All participants were cognitively normal in 1991 when they completed a risk factor questionnaire. Their cognitive status was reassessed 5 years later by using a similar two-phase procedure, including a screening interview, followed by a clinical examination when indicated. The analysis included 194 Alzheimer's disease cases and 3,894 cognitively normal controls. Increasing age, fewer years of education, and the apolipoprotein E epsilon4 allele were significantly associated with increased risk of Alzheimer's disease. Use of nonsteroidal anti-inflammatory drugs, wine consumption, coffee consumption, and regular physical activity were associated with a reduced risk of Alzheimer's disease. No statistically significant association was found for family history of dementia, sex, history of depression, estrogen replacement therapy, head trauma, antiperspirant or antacid use, smoking, high blood pressure, heart disease, or stroke. The protective associations warrant further study. In particular, regular physical activity could be an important component of a preventive strategy against Alzheimer's disease and many other conditions.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Circulating insulin-like growth factor I mediates exercise-induced increases in the number of new neurons in the adult hippocampus.

              Although the physiological significance of continued formation of new neurons in the adult mammalian brain is still uncertain, therapeutic strategies aimed to potentiate this process show great promise. Several external factors, including physical exercise, increase the number of new neurons in the adult hippocampus, but underlying mechanisms are not yet known. We recently found that exercise stimulates uptake of the neurotrophic factor insulin-like growth factor I (IGF-I) from the bloodstream into specific brain areas, including the hippocampus. In addition, IGF-I participates in the effects of exercise on hippocampal c-fos expression and mimics several other effects of exercise on brain function. Because subcutaneous administration of IGF-I to sedentary adult rats markedly increases the number of new neurons in the hippocampus, we hypothesized that exercise-induced brain uptake of blood-borne IGF-I could mediate the stimulatory effects of exercise on the adult hippocampus. Thus, we blocked the entrance of circulating IGF-I into the brain by subcutaneous infusion of a blocking IGF-I antiserum to rats undergoing exercise training. The resulting inhibition of brain uptake of IGF-I was paralleled by complete inhibition of exercise-induced increases in the number of new neurons in the hippocampus. Exercising rats receiving an infusion of nonblocking serum showed normal increases in the number of new hippocampal neurons after exercise. Thus, increased uptake of blood-borne IGF-I is necessary for the stimulatory effects of exercise on the number of new granule cells in the adult hippocampus. Taken together with previous results, we conclude that circulating IGF-I is an important determinant of exercise-induced changes in the adult brain.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Aging Neurosci
                Front Aging Neurosci
                Front. Aging Neurosci.
                Frontiers in Aging Neuroscience
                Frontiers Media S.A.
                1663-4365
                23 April 2014
                2014
                : 6
                : 61
                Affiliations
                [1] 1Department of Kinesiology, School of Public Health, University of Maryland College Park, MD, USA
                [2] 2Department of Psychology, Marquette University Milwaukee, WI, USA
                [3] 3Department of Neurology, Medical College of Wisconsin Milwaukee, WI, USA
                [4] 4Department of Psychology, Wayne State University Detroit, MI, USA
                [5] 5Department of Psychology, Rosalind Franklin University of Medicine and Science North Chicago, IL, USA
                [6] 6Cleveland Clinic, Schey Center for Cognitive Neuroimaging, Neurological Institute Cleveland, OH, USA
                Author notes

                Edited by: Emil C. Toescu, Birmingham University, UK

                Reviewed by: José M. Delgado-García, University Pablo de Olavide, Seville, Spain; Diego Ruano, University of Sevilla, Spain; Kirk I. Erickson, University of Pittsburgh, USA

                *Correspondence: Stephen M. Rao, Cleveland Clinic, Schey Center for Cognitive Neuroimaging, Neurological Institute, 9500 Euclid Ave./U10, Cleveland, OH 44195, USA e-mail: raos2@ 123456ccf.org

                This article was submitted to the journal Frontiers in Aging Neuroscience.

                Article
                10.3389/fnagi.2014.00061
                4005962
                24795624
                806dcc83-3407-4101-8706-b2fa8d00920b
                Copyright © 2014 Smith, Nielson, Woodard, Seidenberg, Durgerian, Hazlett, Figueroa, Kandah, Kay, Matthews and Rao.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 22 January 2014
                : 20 March 2014
                Page count
                Figures: 1, Tables: 3, Equations: 0, References: 41, Pages: 7, Words: 5841
                Categories
                Neuroscience
                Original Research Article

                Neurosciences
                cognitive aging,alzheimer's disease,volumetric mri,association studies in genetics,physical activity,exercise

                Comments

                Comment on this article