***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: AIM To assess whether an intensive multifactorial treatment can reduce cognitive decrements and cognitive decline in screen-detected type 2 diabetes . METHODS The multinational ADDITION- study , a cluster-r and omized parallel group trial in patients with screen-detected type 2 diabetes , compared the effectiveness of intensive multifactorial treatment ( IT ; lifestyle advice and strict regulation of metabolic parameters ) with routine care ( RC ) on cardiovascular outcome . In The Netherl and s r and omization was stratified according to practice organization . Allocation was concealed from patients . The present study assessed the effect of IT on cognition through two  neuropsychological assessment s ( NPA ) on two occasions . The assessment s took place three and six years after the start of the intervention . Non-diabetic controls served as reference group . The first NPA was performed in 183 patients ( IT : 97 ; RC : 86 ) and 69 controls . The second NPA was performed in 135 patients ( IT : 71 ; RC : 64 ) and 55 controls . Primary outcome was a composite score , including the domains memory , information-processing speed and attention and executive function . Comparisons between the treatment groups were performed with multi-level analyses . RESULTS The first NPA showed no differences between the treatment groups ( mean difference composite z-score : 0.00 ; 95%-CI -0.16 to 0.16 ; IT vs RC ) . Over the next three years cognitive decline in the diabetic groups was within the range of the reference group and did not differ between the treatment arms ( difference decline between diabetic groups -0.12 ; -0.24 to 0.01 ; IT vs RC ) . CONCLUSIONS Six years of IT in screen-detected type 2 diabetes had no benefit on cognitive functioning over RC BACKGROUND The temporal relationship between the appearance of depressive symptoms and the clinical onset of dementia and Alzheimer disease was evaluated in a community sample . METHODS An original sample of 1366 subjects aged 65 years or older , selected r and omly from a rural Pennsylvania community , was cognitively screened at study entry and every 2 years thereafter . A subset of 954 survivors of this cohort without dementia was screened for depressive symptoms  at the second and subsequent data - collection waves . A " depression cluster " was identified by the presence of 5 or more depressive symptoms , including depressed mood , at the time of screening . Cognitively impaired subjects and a sample of unimpaired controls  underwent st and ardized clinical evaluation to determine the presence of incident dementia ( by DSM-III-R criteria ) and probable or possible Alzheimer disease ( by criteria of the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer 's Disease and Related Disorders Association ) and to estimate the clinical onset of dementia symptoms . RESULTS A highly increased probability of the depression cluster developing existed among subjects following the onset of dementia ( 15.4 % [ 6/39 ] ) and Alzheimer disease ( 17.6 % [ 6/34 ] ) compared with subjects without dementia ( 3.2 % [ 23/712 ] ) . The odds ratios , after adjustment for age , sex , education level , and self reported memory loss , for the development of depression were 6.5 ( 95 % confidence interval , 2.2 - 19.1 ) in subjects with Alzheimer disease and 5.2 ( 95 % confidence interval , 1.8 - 15.2 ) in subjects with overall dementia . Depressive symptoms did not confer a significantly increased relative risk of dementia ( 1.27 ; 95 % confidence interval , 0.55 - 2.93 ) or Alzheimer disease ( 1.28 ; 95 % confidence interval , 0.51 - 3.20 ) . CONCLUSION Depressive symptoms appeared to be early manifestations , rather than predictors , of Alzheimer disease in this community sample The relation between hypertension and cognitive function is not well established . Therefore , we examined cognitive function in a r and om sample of 744 nondiabetic elderly inhabitants of Kuopio , East Finl and . Five brief neuropsychological tests known to be sensitive to cognitive impairment due to dementia -- the Mini-Mental State Examination ( MMSE ) , the Trail Making Test ( TMT ) , the Buschke Selective Reminding Test ( BSR ) , Russell 's Adaptation of the Visual Reproduction Test ( HVR ) , and the Verbal Fluency Test (VFT)--were  used to evaluate cognitive function . The performance of the hypertensive group ( n = 378 ) was impaired in almost all test items compared with that of the normotensive group ( n = 366 ) , but the difference between these two groups was statistically significant in 5 of 19 test items only . Moreover , within the hypertensive group , hyperinsulinemic ( fasting plasma insulin > 17.9 mU/L ) hypertensive subjects ( n = 57 ) scored worse than normoinsulinemic hypertensive subjects ( n = 321 ) in 16 of 19 test items and worse than the normotensive subjects in the same 16 of 19 test items . The difference between the hyperinsulinemic hypertensive and normotensive groups was significant in 11 test items that reflected complex cognitive function such as calculation , language , semantic memory , and problem solving . This difference in neuropsychological tests among the three study groups ( normotensive , normoinsulinemic hypertensive , and hyperinsulinemic hypertensive subjects ) persisted after adjustment for fasting plasma glucose , age , sex , and education in 3 test items measuring calculation , copying , and semantic memory . Thus , essential hypertension in the elderly is associated with an impairment in complex cognitive function . ( ABSTRACT TRUNCATED AT 250 WORDS OBJECTIVE The effect of diabetes on  mild cognitive impairment ( MCI ) and its conversion to dementia remains controversial . We sought to examine whether diabetes and pre-diabetes are associated with MCI and accelerate the progression from MCI to dementia . RESEARCH DESIGN AND METHODS In the Kungsholmen Project , 963 cognitively intact participants and 302 subjects with MCI ( 120 with amnestic MCI [ aMCI ] and 182 with other cognitive impairment no dementia [ oCIND ] ) age ≥75 years were identified at baseline . The two cohorts were followed for 9 years to detect the incident MCI and dementia following international criteria . Diabetes was ascertained based on a medical examination , hypoglycemic medication use , and r and om blood glucose level ≥11.0 mmol/l . Pre-diabetes was defined as r and om blood glucose level of 7.8–11.0 mmol/l in diabetes-free participants . Data were analyzed using st and ard and time-dependent Cox proportional-hazards models . RESULTS During the follow-up period , in the cognitively intact cohort , 182 people developed MCI ( 42 aMCI and 140 oCIND ) , and 212 developed dementia . In the MCI cohort , 155 subjects progressed to dementia , the multi-adjusted hazard ratio ( 95 % CI ) of dementia was 2.87 ( 1.30–6.34 ) for diabetes , and 4.96 ( 2.27–10.84 ) for pre-diabetes . In a Kaplan-Meier survival analysis , diabetes and pre-diabetes accelerated the progression from MCI to dementia by 3.18 years . Diabetes and pre-diabetes were neither cross-sectionally nor longitudinally associated with  MCI . CONCLUSIONS Diabetes and pre-diabetes substantially accelerate the progression from MCI to dementia , and anticipate dementia occurrence by more than 3 years in people with MCI . The association of diabetes with the development of MCI is less evident in old people The incidence of brain damage in a r and om group of 100 insulin dependent diabetic patients below the age of 65 , compared with a matched control group , was investigated by means of the Walton-Black Modified New Word Learning Test .  Seventeen of the patients scored in the brain-damaged range of the test , but none of the control group . A significant relationship was found between low scores on the test and the apparent severity of past hypoglycaemic episodes . No relationship was found between brain damage and the age of the patient or duration of the illness . Vascular disease was not thought to be an important factor in the aetiology of the abnormal learning scores . The results support the view that mild dementia secondary to hypoglycaemia may be more common in diabetes than is usually supposed OBJECTIVE To determine whether elderly individuals with type 2 diabetes or impaired glucose tolerance are at increased risk for cognitive impairment compared with individuals with normal glucose tolerance . RESEARCH DESIGN AND METHODS Elderly Hispanic individuals ( n = 414 ) and non-Hispanic white individuals ( n = 469 ) aged > or = 65 years , r and omly selected from the Medicare rolls of Bernalillo County ( Albuquerque ) , NM , were recruited for an interview/examination that included an evaluation of glucose tolerance . Information on nine tests of cognitive function and two measures of depression allowed comparisons between diabetic status and these functions . Comparisons also were made between glycosolated hemoglobin concentrations and these cognitive tests in the 188 participants with diabetes . RESULTS None of the mean scores on the tests of cognitive function was significantly lower in the participants with diabetes compared with those participants with normal glucose tolerance after adjustments for ethnicity , sex , age , level of education , and presence of depression , with or without elimination of those with dementia ( Mini-Mental State Exam < 18 ) . Interestingly , participants with impaired glucose tolerance tended to score higher than those with normal glucose tolerance . No significant associations were found between glycosolated hemoglobin concentrations and cognitive test scores in participants with diabetes . CONCLUSIONS We could not show any increased risk for cognitive impairment in participants with diabetes compared with those with normal glucose tolerance after adjustments for ethnicity , sex , age , education , and presence of depression , before or after elimination of dementia in this r and om sample from a biethnic population of predominantly community-dwelling elders Objective : To determine whether the rate of decline in performance on a memory test is more rapid in AD patients with higher versus lower educational and occupational attainment . Background : Epidemiologic and imaging studies have suggested that , given comparable clinical severity of dementia , AD pathology is more advanced in patients with higher educational and occupational attainment . Because educational and occupational attainment should not influence the progression of AD pathology , and because severe AD pathology will eventually produce a mortality-causing condition , people with higher attainment might experience clinical AD for a shorter time and have a more rapid clinical progression . Methods : A total of 177 AD patients were tested yearly for up to four study visits with the Selective Reminding Test ( a memory test ) . Analysis of prospect i ve change in the total recall score was performed by applying generalized estimating equations to regression analyses with repeated measures . Results : At the initial visit , scores were comparable in the high- and low-education and the high- and low-occupation groups . Overall , memory scores declined by approximately 1 point yearly ( p < 0.01 ) . There was a more rapid decline in memory scores in patients with higher educational ( p < 0.057 ) and higher occupational attainment ( p < 0.02 ) . The authors then stratified patients based on their initial memory scores . The more rapid decline in memory scores associated with higher educational and occupational attainment was noted only in the group with low initial scores ( p < 0.05 for both ) . The full group and stratified group analyses were also repeated controlling for other potentially relevant variables including age , gender , race , ethnicity , and the presence of extrapyramidal signs , stroke , or at least one apolipoprotein E-ε4 allele . The results remained unchanged . Conclusions : Memory declined more rapidly in AD patients with higher educational and occupational attainment . This adds support to the idea that the discontinuity between the degree of AD pathology and the observed clinical severity of AD is mediated through some form of reserve Background Many patients with type 2 diabetes fail to achieve good glycaemic control . Poor control is associated with complications including coronary heart disease ( CHD ) . Effective self-management and engagement in health behaviours can reduce risks of complications . However , patients often struggle to adopt and maintain these behaviours . Self-management interventions have been found to be effective in improving glycaemic control . Recent developments in the field of genetics mean that patients can be given personalised information about genetic- and lifestyle-associated risk of developing CHD . Such information may increase patients ’ motivation to engage in self-management . The Coronary Risk in Diabetes ( CoRDia ) trial will compare the effectiveness of a self-management intervention , with and without provision of personalised genetic- and lifestyle-associated risk information , with usual care , on clinical and behavioural outcomes , the cognitive predictors of behaviour , and psychological wellbeing . Methods / Design Participants will be adults aged 25–74 years registered with general practice s in the East of Engl and , diagnosed with type 2 diabetes , with no history of heart disease , and with a glycated haemoglobin level of ≥6.45 % ( 47 mmol/mol ) . Consenting participants will be r and omised to one of three arms : usual care control , group self-management only , group self-management plus personalised genetic- and lifestyle-associated risk information . The self-management groups will receive four weekly 2 
    Output:
    
AUTHORS ' CONCLUSIONS We found no good evidence that any specific treatment or treatment strategy for Type 2 diabetes can prevent or delay cognitive impairment .
The best available evidence related to the comparison of intensive with st and ard glycaemic control strategies .
Here there was moderate- quality evidence that the strategies do not differ in their effect on global cognitive functioning over 40 to 60 months