***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 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Cognitive impairment and depression often co-occur in older adults , but it is not clear whether depression is a risk factor for cognitive decline , a psychological reaction to cognitive decline , or whether changes in depressive symptoms correlate with changes in cognitive performance over time . The co-morbid manifestation of depression and cognitive impairment may reflect either a causal effect or a common cause , depending on the specific symptoms experienced and the cognitive functions affected . Method The study sample comprised 1506 community-dwelling older adults aged ⩾65 years from the Longitudinal Aging Study Amsterdam ( LASA ) . We conducted cross-domain latent growth curve analyses to examine longitudinal associations between late-life depression dimensions ( i.e. depressed affect , positive affect , and somatic symptoms ) and specific domains of cognitive functioning ( i.e. processing speed , inductive reasoning , immediate recall , and delayed recall ) . Results Poorer delayed recall performance at baseline predicted a steeper increase in depressed affect over time . Steeper decline in processing speed correlated with a steeper increase in somatic symptoms of depression over time . Conclusions Our findings suggest a prospect i ve association between memory function and depressed affect , whereby older adults may experience an increase in depressed affect in reaction to poor memory function . Somatic symptoms of depression increased concurrently with declining processing speed , which may reflect common neurodegenerative processes . Our findings do not support the hypothesis that depression symptoms may be a risk factor for cognitive decline in the general population . These findings have potential implication s for the treatment of late-life depression and for the prognosis of cognitive outcomes Indices of functional connectivity in the default mode network ( DMN ) are promising neural markers of treatment response in late-life depression . We examined the differences in DMN functional connectivity between treatment-responsive and treatment-resistant depressed older adults . Forty-seven depressed older adults underwent MRI scanning pre- and post-pharmacotherapy . Forty-six never depressed older adults underwent MR scanning as comparison subjects . Treatment response was defined as achieving a Hamilton Depression Rating Scale of 10 or less post-treatment . We analyzed resting state functional connectivity using the posterior cingulate cortex as the seed region-of-interest . The result ing correlation maps were employed to investigate between-group differences . Additionally we examined the association between white matter hyperintensity burden and functional connectivity results . Comparison of pre- and post-treatment scans of depressed participants revealed greater post-treatment functional connectivity in the frontal pre central gyrus . Relative to treatment-responsive participants , treatment-resistant participants had increased functional connectivity in the left striatum . When adjusting for white matter hyperintensity burden , the observed differences lost significance for the PCC-prefrontal functional connectivity , but not for the PCC-striatum functional connectivity . The post-treatment " frontalization " of the DMN connectivity suggests a normalizing effect of antidepressant treatment . Moreover , our study confirms the central role of white matter lesions in disrupting brain functional connectivity Kendall 's coefficient concordance ( KCC ) can measure the similarity of a number of time series . It has been used for purifying a given cluster in functional MRI ( fMRI ) . In the present study , a new method was developed based on the regional homogeneity ( ReHo ) , in which KCC was used to measure the similarity of the time series of a given voxel to those of its nearest neighbors in a voxel-wise way . Six healthy subjects performed left and right finger movement tasks  in event-related design ; five of them were additionally scanned in a rest condition .  KCC was compared among the three conditions ( left finger movement , right finger movement , and the rest ) . Results show that bilateral primary motor cortex ( M1 ) had higher KCC in either left or right finger movement condition than in rest condition . Contrary to prediction and to activation pattern , KCC of ipsilateral M1 is significantly higher than contralateral M1 in unilateral finger movement conditions . These results support the previous electrophysiologic findings of increasing ipsilateral M1 excitation during unilateral movement . ReHo can consider as a complementary method to model-driven method , and it could help reveal the complexity of the human brain function . More work is needed to underst and the neural mechanism underlying ReHo BACKGROUND Mild cognitive impairment is increasingly recognized as an important public health problem associated with increased risk of developing dementia . Annual conversion rates , however , vary across different studies with clinic sample s showing higher rates of conversion than community-based sample s. OBJECTIVES To establish whether the rates of conversion from mild cognitive impairment to dementia differed according to recruitment source and , if so , to investigate factors that might explain this discrepancy . DESIGN Rates and predictors of conversion were examined in a prospect i ve longitudinal study at a single center . SETTING Among the participants , 46 % were recruited from a clinical setting and 54 % were recruited directly through community outreach .  PARTICIPANTS One hundred eleven individuals with mild cognitive impairment were followed up longitudinally for an average of 2.4 years ( range , 0.5 - 4.0 years ) . MAIN OUTCOME MEASURES Conversion from mild cognitive impairment to dementia . RESULTS During the follow-up period , 28 individuals progressed to dementia with a mean ( SD ) time to conversion of 2.19 ( 0.72 ) years . The clinic sample had an annual conversion rate of 13 % , whereas the community sample had an annual conversion rate of 3 % . In a Cox proportional hazards model , clinic recruitment source alone was associated with an increased hazard of incident dementia ( hazard ratio = 3.50 ; 95 % confidence interval , 1.31 - 9.18 ; P = .01 ) . When other variables were added to the model , only baseline functional impairment as measured by the Clinical Dementia Rating Scale ( and no demographic , cognitive , or neuroimaging variables or mild cognitive impairment subtype ) accounted for the differences in conversion rates across the 2 cohorts . CONCLUSIONS These findings add to the growing literature to suggest that the degree of functional impairment at baseline is an important predictor of conversion to dementia and may help explain differences in findings between epidemiological and clinic-based studies Objectives : To provide up date d estimates of Alzheimer disease ( AD ) dementia prevalence in the United States from 2010 through 2050 . Methods : Probabilities of AD dementia incidence were calculated from a longitudinal , population -based study including substantial numbers of both black and white participants . Incidence probabilities for single year of age , race , and level of education were calculated using weighted logistic regression and AD dementia diagnosis from 2,577 detailed clinical evaluations of 1,913 people obtained from stratified r and om sample s of previously disease-free individuals in a population of 10,800 . These were combined with US mortality , education , and new US Census Bureau estimates of current and future population to estimate current and future numbers of people with AD dementia in the United States . Results : We estimated that in 2010 , there were 4.7 million individuals aged 65 years or older with AD dementia ( 95 % confidence interval [ CI ] = 4.0–5.5 ) . Of these , 0.7 million ( 95 % CI = 0.4–0.9 ) were between 65 and 74 years , 2.3 million were between 75 and 84 years ( 95 % CI = 1.7–2.9 ) , and 1.8 million were 85 years or older ( 95 % CI = 1.4–2.2 ) . The total number of people with AD dementia in 2050 is projected to be 13.8 million , with 7.0 million aged 85 years or older . Conclusion : The number of people in the United States with AD dementia will increase dramatically in the next 40 years unless preventive measures are developed There is scarce information about the pathophysiological processes underlying Late-Life Depression ( LLD ) . We aim ed to determine the neurobiological abnormalities related to LLD through a multi-modal biomarker approach combining a large , unbiased peripheral proteomic panel and structural brain imaging . We examined data from 44 LLD and 31 control participants .  Plasma proteomic analysis was performed using a multiplex immunoassay . We evaluated the differential protein expression between groups with r and om intercept models . We carried out enrichment pathway analyses ( EPA ) to uncover biological pathways and processes related to LLD . Machine learning analysis was applied to the combined data set to determine the accuracy with which specific proteins could correctly discriminate LLD versus control participants . Sixty-one proteins were differentially expressed in LLD ( p < 0.05 and FDR < 0.01 ) . EPA showed that these proteins were related to abnormal immune-inflammatory control , cell survival and proliferation , proteostasis control , lipid metabolism , intracellular signaling . Machine learning analysis showed that a panel of three proteins ( C-peptide , FABP-liver , ApoA-IV ) discriminated LLD and control participants with 100 % accuracy . The plasma proteomic profile in LLD revealed dysregulation in biological processes essential to the maintenance of homeostasis at cellular and systemic levels . These abnormalities increase brain and systemic allostatic load leading to the downstream negative outcomes of LLD , including increased risk of medical comorbidities and dementia . The peripheral biosignature of LLD has predictive power and may suggest novel putative therapeutic targets for prevention , treatment , and neuroprotection in LLD 
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Further , posterior midline regions ( posterior cingulate cortex and precuneus ) appeared to have the most structural and functional alterations in all patient groups .