***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Physical exercise has been shown to increase brain volume and improve cognition in r and omized trials of non-demented elderly . Although greater social engagement was found to reduce dementia risk in observational studies , r and omized trials of social interventions have not been reported . A representative sample of 120 elderly from Shanghai , China was r and omized to four groups ( Tai Chi , Walking , Social Interaction , No Intervention ) for 40 weeks . Two MRIs were obtained , one before the intervention period , the other after . A neuropsychological battery was administered at baseline , 20 weeks , and 40 weeks . Comparison of changes in brain volumes in intervention groups with the No Intervention group were assessed by t-tests . Time-intervention group interactions for neuropsychological measures were evaluated with repeated- measures mixed models . Compared to the No Intervention group , significant increases in brain volume were seen in the Tai Chi and Social Intervention groups ( p < 0.05 ) . Improvements also were observed in several neuropsychological measures in the Tai Chi group , including the Mattis Dementia Rating Scale score ( p = 0.004 ) , the Trailmaking Test A ( p = 0.002 ) and B ( p = 0.0002 ) , the Auditory Verbal Learning Test ( p = 0.009 ) , and verbal fluency for animals ( p = 0.01 ) . The Social Interaction group showed improvement on some , but fewer neuropsychological indices . No differences were observed between the Walking and No Intervention groups . The findings differ from previous clinical trials in showing increases in brain volume and improvements in cognition with a largely non-aerobic exercise ( Tai Chi ) . In addition , intellectual stimulation through social interaction was associated with increases in brain volume as well as with some cognitive improvements Physical exercise , particularly aerobic exercise , is documented as providing a low cost regimen to counter well-documented cognitive declines including memory , executive function , visuospatial skills , and processing speed in normally aging adults . Prior aging studies focused largely on the effects of medium to long term ( > 6 months ) exercise training ; however , the shorter term effects have not been studied . In the present study , we examined changes in brain blood flow , cognition , and fitness in 37 cognitively healthy sedentary adults ( 57–75 years of age ) who were r and omized into physical training or a wait-list control group .  The physical training group received supervised aerobic exercise for 3 sessions per week 1 h each for 12 weeks . Participants ' cognitive , cardiovascular fitness and resting cerebral blood flow ( CBF ) were assessed at baseline ( T1 ) , mid ( T2 ) , and post-training ( T3 ) . We found higher resting CBF in the anterior cingulate region in the physical training group as compared to the control group from T1 to T3 . Cognitive gains were manifested in the exercise group 's improved immediate and delayed memory performance from T1 to T3 which also showed a significant positive association with increases in both left and right hippocampal CBF identified earlier in the time course at T2 . Additionally , the two cardiovascular parameters , VO2 max and rating of perceived exertion ( RPE ) showed gains , compared to the control group . These data suggest that even shorter term aerobic exercise can facilitate neuroplasticity to reduce both the biological and cognitive consequences of aging to benefit brain health in sedentary adults Context How common is mild cognitive impairment in older adults ? Contribution This study of 856 individuals from the national Health and Retirement Study found that 22 % of adults age 71 or older had cognitive impairment that did not reach the threshold for dementia . Annually , about 8 % of those with cognitive impairment without dementia died and about 12 % progressed to dementia . Caution Criteria that differentiate mild impairment from dementia are imperfect . Only 856 of 1770 and 180 of 241 selected individuals completed baseline and follow-up  cognitive examinations , respectively . Implication Cognitive impairment without dementia probably affects a large segment of the elderly population . The Editors Cognitive impairment that does not reach the threshold for dementia diagnosis is associated with increased risk for progression to dementia in most studies , with progression rates of 10 % to 15 % per year compared with 1 % to 2.5 % among cognitively healthy older adults ( 13 ) . However , even among those without dementia , cognitive impairment contributes to decreased quality of life , increased neuropsychiatric symptoms , and increased disability ( 4 , 5 ) , as well as increased health care costs ( 6 , 7 ) . All of these negative outcomes make accurate national estimates of the prevalence of cognitive impairment without dementia essential for determining the full societal impact of cognitive impairment on patients , families , and health care programs . However , previous estimates of the prevalence of this condition from regional and non-U.S. sample s have varied from 3 % to 29 % ( 810 ) , a range that is most likely due to differences in diagnostic criteria and sample characteristics . Estimates of the total number of people with cognitive impairment without dementia in the United States are not available . We conducted ADAMS ( Aging , Demographics , and Memory Study ) to determine the national prevalence of dementia and cognitive impairment without dementia in the United States . We previously ( 11 ) reported our estimates of the prevalence of dementia . In this article , we report prevalence rates from what we believe to be the first population -based study of cognitive impairment without dementia to include individuals from all regions of the country , as well as rates of progression from cognitive impairment without dementia to dementia and death . Methods Participants We drew the ADAMS sample from the larger HRS ( Health and Retirement Study ) , an ongoing nationally representative cohort study of individuals born before 1954 that was design ed to investigate the health , social , and economic implication s of aging in the U.S. population ( 1214 ) . The HRS began in 1992 , and the current sample includes approximately 22000 participants . The ADAMS sample began with a stratified r and om sub sample of 1770 individuals age 70 years or older from 5 cognitive strata based on participants ' scores on a self-reported or proxy-reported cognitive measure ( 15 ) from the most recent HRS interview ( either 2000 or 2002 ) . We further stratified the 3 highest cognitive strata by age ( age 70 to 79 years vs. 80 years ) and sex to ensure adequate numbers in each subgroup . Full details of the ADAMS sample design and selection procedures are described elsewhere ( 16 , 17 ) . The ADAMS initial assessment s occurred between July 2001 and December 2003 , on average , 13.3 months ( SD , 6.9 ) after the HRS interview . Thus , participants were 71 years of age or older at the initial assessment . As part of the ADAMS assessment , proxies ( usually a spouse or adult child ) provided information about the participant 's cognitive and functional decline , neuropsychiatric symptoms , and medical history . Use of proxies to collect this information is preferred , because self-reporting of this type of information may not be reliable , particularly among cognitively impaired individuals . The Figure summarizes the number of participants at each phase of the study ; additional details on participation rates are reported elsewhere ( 17 ) . A total of 856 individuals , 56 % of the nondeceased target sample , participated in all phases of the dementia assessment . A major concern in ADAMS , as in similar population -based studies , is the potential for selective nonparticipation to bias prevalence estimates . However , because the ADAMS sample was derived from the HRS sample , a wide range of health and social information was available to assess and correct for potential selection bias due to nonparticipation in our sample . Using logistic regression , we modeled the probability that a sample individual participated in the ADAMS assessment as a function of covariates , such as age , sex , education , marital status , HRS cognition scores , nursing home residency , and indicators of past or existing major health conditions . We used the results of this response propensity analysis to develop nonresponse adjustments to the ADAMS sample selection weights ( 18 ) . We then constructed population sample weights to take into account the probabilities of selection in the stratified sample design and to adjust for differential nonparticipation in ADAMS ( 16 ) . Figure . Study flow diagram . ADAMS = Aging , Demographics , and Memory Study . The ADAMS data are publicly available and can be obtained from the HRS Web site ( hrsonline.isr.umich.edu ) . The institutional review boards at Duke University Medical Center and the University of Michigan approved all study procedures , and study participants or their surrogates provided informed consent . Measurements A nurse and a neuropsychology technician assessed all participants at their residence for cognitive impairment . The full details of the assessment and diagnostic procedures are described elsewhere ( 17 ) . In brief , the following information about the participant was collected from a knowledgeable informant : chronological history of cognitive symptoms , medical history , current medications , current neuropsychiatric symptoms , measures of severity of cognitive and functional impairment , and family history of memory problems . During the assessment , the participant completed a battery of  neuropsychological measures  ; a  self-reported depression measure ; a st and ardized neurologic examination ; a blood pressure measurement  ; collection of buccal DNA sample s for apolipoprotein E ( APOE ) genotyping ; and a 7-minute , videotaped segment covering portions of the cognitive status and neurologic examinations . Specific assessment measures reported here are the  Mini-Mental State Examination  ( 19 ) and the  Dementia Severity Rating Scale ( 20 ) . The Dementia Severity Rating Scale is completed by an informant and assesses the presence and severity of impairment in 12 cognitive and functional domains . Scores range from 0 to 54 , with higher scores reflecting more impairment . We also sought medical record releases to obtain relevant neuroimaging and laboratory results from participants ' physicians . A consensus expert panel of neuropsychologists , neurologists , geropsychiatrists , and internists review ed all information collected during the in-home assessment and assigned final diagnoses . The consensus panel review ed each case and assigned a diagnosis in 2 stages , first without and then with medical records . For most cases , the consensus panel reached agreement with little discussion ; however , diagnostic agreement was more challenging for participants with little or no education or with substantial sensory or physical impairment . The medical records often provided the necessary neuroimaging results to change a diagnosis from possible Alzheimer disease or vascular dementia to probable Alzheimer disease or vascular dementia . Except for these situations , the diagnoses seldom changed after the consensus panel review ed the additional information in the medical records . Diagnoses were divided within the 3 general categories : normal cognitive function , cognitive impairment without dementia , and dementia . The consensus panel used clinical judgment to assign the final diagnosis , based on the following criteria . Dementia diagnosis was based on guidelines from the Diagnostic and Statistical Manual of Mental Disorders , Revised Third Edition ( 21 ) , and the Diagnostic and Statistical Manual of Mental Disorders , Fourth Edition ( 22 ) ; diagnoses of Alzheimer disease and other types of dementia were based on currently accepted criteria ( 2326 ) . The definition of cognitive impairment without dementia and its subtypes has been developed over 17 years , primarily on the basis of the accumulated clinical experience of a group of research ers common to ADAMS and 3 other epidemiologic studies of dementia ( 2729 ) . Before ADAMS , we operationalized the definition for cognitive impairment without dementia on the basis of analyses of both neuropsychological data and an objective measure of daily function from participants with this diagnosis in our other studies ( 27 , 28 ) . We defined cognitive impairment without dementia as mild cognitive or functional impairment , reported by the participant or informant , that did not meet criteria for dementia ( that is , Dementia Severity Rating Scale score of 6 to 11 ) , or performance on neuropsychological measures that was both below expectation and at least 1.5 SDs below published norms on any test . To reflect the variation in clinical presentation and potential differences in the cause of the impairment we used 12 diagnostic subcategories for cognitive impairment without dementia , unspecified cognitive impairment without dementia : prodromal Alzheimer disease , amnestic mild cognitive impairment ( 30 , 31 ) , vascular cognitive impairment without dementia , stroke , medical conditions or sensory impairment , neurologic conditions , depression , other psychiatric disorders , low baseline intellect or learning disorder , past alcohol abuse , and current alcohol abuse ( Appendix Table 1 ) . In population -based sample s , few individuals meet the criteria typically used for  amnestic mild cognitive impairment  ( 30 , 31 ) . For this reason , we used the additional category of The hippocampus shrinks in late adulthood , leading to impaired memory and increased risk for dementia . Hippocampal and medial temporal lobe volumes are larger in higher-fit adults , and physical activity training increases hippocampal perfusion , but the extent to which aerobic exercise training can modify hippocampal volume in late adulthood remains unknown . Here we show , in a r and omized controlled trial with 120 older adults , that aerobic exercise training increases the size of the anterior hippocampus , leading to improvements in spatial memory .  Exercise training increased hippocampal volume by 2 % , effectively reversing age-related loss in volume by 1 to 2 y. We also demonstrate that increased hippocampal volume is associated with greater serum levels of BDNF , a mediator of neurogenesis in the dentate gyrus . Hippocampal volume declined in the control group , but higher preintervention 
    Output:
    
Findings of the individual studies suggest that MRI measures may be more sensitive to the effects of physical activity than neurocognitive measures .