***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 Elevated plasma total homocysteine concentration may be a risk factor for cognitive decline and Alzheimer disease , but data from prospect i ve studies are limited . Further , high homocysteine levels are associated with low vitamin status , and it is unknown whether it is homocysteine toxicity or vitamin insufficiency that is responsible for the observed cognitive dysfunction . METHODS We performed cross-sectional and longitudinal analyses of a cohort of 499 high-functioning community-dwelling persons aged 70 to 79 years to determine the effect of homocysteine and related vitamin plasma concentrations on cognitive function and cognitive decline .  Nonfasting plasma concentrations of homocysteine , folate , vitamin B(6 ) , and vitamin B(12 ) were measured at baseline .  Summary measures of cognitive function were created from tests of multiple cognitive domains administered at baseline and again after 7 years . RESULTS In cross-sectional analyses investigating each variable separately , subjects with elevated homocysteine levels , or low levels of folate or vitamin B(6 ) , demonstrated worse baseline cognitive function . In longitudinal analyses , after adjusting for multiple covariates , including homocysteine , those in the bottom quartile of folate had a 1.6-fold increased risk ( 95 % confidence interval : 1.01 to 2.31 ; P = 0.04 ) of being in the worst quartile of 7-year cognitive decline . Low folate levels largely accounted for a trend towards greater cognitive decline with elevated homocysteine level . CONCLUSION In high-functioning older adults , low folate levels appear to be a risk factor for cognitive decline . The risk of developing cognitive decline might be reduced through dietary folate intake Based on research demonstrating associations between folate , B-12 and B-6 vitamins and cognition and mood , we investigated the effects of short-term supplementation in 211 healthy younger , middle-aged and older women who took either 750 microg of folate , 15 microg of vitamin B-12 , 75 mg of vitamin B-6 or a placebo daily for 35 d. In addition , we examined associations between dietary intake of these vitamins and cognition and mood . Usual dietary intake status was estimated using a retrospective , self-report , quantified food frequency question naire . Participants completed alternate forms of st and ardized tests of cognitive processing re sources , memory , executive function , verbal ability and self-report mood measures before and after supplementation . Supplementation had a significant positive effect on some measures of memory performance only , and no effect on mood . Dietary intake status was associated with speed of processing , recall and recognition and verbal ability BACKGROUND Deficiencies of vitamin B-12 , folic acid , and vitamin B-6-as defined by laboratory measures -occur in 10 - 20 % of elderly subjects . The clinical significance remains unresolved . OBJECTIVE The objective was to explore any association between vitamin status and vitamin treatment and movement and cognitive performance in elderly subjects . DESIGN Community-dwelling subjects ( n = 209 ) with a median age of 76 y were r and omly assigned to daily oral treatment with 0.5 mg cyanocobalamin , 0.8 mg folic acid , and 3 mg vitamin B-6 or placebo ( double blind ) for 4 mo . Movement and cognitive performance tests were performed before and after treatment . RESULTS A high plasma total homocysteine ( tHcy ) concentration ( > or = 16 micromol/L ) was found in 64 % of men and in 45 % of women , and a high serum methylmalonic acid ( MMA ) concentration ( > or = 0.34 micromol/L ) was found in 11 % of both sexes . Movement time , digit symbol , and block design ( adjusted for age , sex , smoking , and creatinine ) correlated independently with plasma tHcy ( P < 0.01 , < 0.05 , and < 0.01 , respectively ) ; the simultaneity index and block design correlated with serum MMA ( P < 0.05 for both ) . Vitamin therapy significantly decreased plasma tHcy ( 32 % ) and serum MMA ( 14 % ) . No improvements were found in the movement or cognitive tests compared with placebo . Neither vitamin therapy nor changes in plasma tHcy , serum MMA , serum vitamin B-12 , plasma folate , or whole-blood folate correlated with changes in movement or cognitive performance . CONCLUSIONS High plasma tHcy and serum MMA were prevalent and correlated inversely with movement and cognitive performance . Oral B vitamin treatment normalized plasma tHcy and serum MMA concentrations but did not affect movement or cognitive performance . This might have been due to irreversible or vitamin-independent neurocognitive decline or to an insufficient dose or duration of vitamins OBJECTIVE To explore the associations of low serum levels of vitamin B(12 ) and folate with  AD occurrence . METHODS A population -based longitudinal study in Sweden , the Kungsholmen PROJECT A r and om sample of 370 nondemented persons , aged 75 years and older and not treated with B(12 ) and folate  , was followed for 3 years to detect incident AD cases . Two cut-off points were used to define low levels of vitamin B(12 ) ( < or = 150 and < or = 250 pmol/L ) and folate ( < or = 10 and < or = 12 nmol/L ) , and all analyses were performed using both definitions . AD and other types of dementia were diagnosed by specialists according to DSM-III-R criteria . RESULTS When using B(12 ) < or = 150 pmol/L and folate < or = 10 nmol/L to define low levels , compared with people with normal levels of both vitamins , subjects with low levels of B(12 ) or folate had twice higher risks of developing AD ( relative risk [ RR ] = 2.1 , 95 % CI = 1.2 to 3.5 ) . These associations were even stronger in subjects with good baseline cognition ( RR = 3.1 , 95 % CI = 1.1 to 8.4 ) . Similar relative risks of AD were found in subjects with low levels of B(12 ) or folate and among those with both vitamins at low levels . A comparable pattern was detected when low vitamin levels were defined as B(12 ) < or = 250 pmol/L and folate < or = 12 nmol/L. CONCLUSIONS This study suggests that vitamin B(12 ) and folate may be involved in the development of AD . A clear association was detected only when both vitamins were taken into account , especially among the cognitively intact subjects . No interaction was found between the two vitamins . Monitoring serum B(12 ) and folate concentration in the elderly may be relevant for prevention of AD BACKGROUND Associations between vitamin B-12 deficiency and impaired cognitive function and depression have been reported . METHODS A r and omized placebo controlled study including 140 individuals with an increased plasma methylmalonic acid ( 0.40 - 2.00 micromol/l ) not previously treated with vitamin B-12 .  Cognitive function was assessed by the Cambridge Cognitive Examination  ( CAMCOG ) , Mini-Mental State Examination ( MMSE ) , and a 12-words learning test .  Symptoms of depression were evaluated by the Major Depression Inventory . The main outcome measure was change in cognitive function and depression score from baseline to follow-up 3 months later . RESULTS At baseline 78 ( 56 % ) individuals had cognitive impairment  judged from the CAMCOG score and 40 ( 29 % ) according to the MMSE ; 18 ( 13 % ) individuals had symptoms of depression . No improvement was found in cognitive function comparing the treatment and placebo group ( total CAMCOG score : P = 0.43 ) , nor among individuals with only slightly impaired cognitive function ( n = 44 , total CAMCOG score : P = 0.42 ) . The treatment group did not improve in depression score as compared to the placebo group ( P = 0.18 ) . LIMITATIONS The duration of impaired cognitive function was unknown . CONCLUSIONS A high proportion of individuals with an increased plasma methylmalonic acid had impaired cognitive function , and a rather high prevalence of depression was observed . However , vitamin B-12 treatment did not improve cognitive function or symptoms of depression within the 3-months study period Routine determination of serum vitamin B12 levels is generally recommended as part of the screening of demented patients , based on the notion that vitamin B12 deficiency is one of the causes of reversible dementia . We studied the effects of vitamin B12 replacement therapy in a prospect i ve longitudinal study at a memory clinic , with special emphasis on assessment of severity of dementia : not only cognitive deterioration , but also disability in the activities of daily life , behavioural problems , and the burden experienced by the caregiver were examined using instruments of proven validity . In a series of 170 consecutive patients with dementia , subnormal serum vitamin B12 levels were found in 26 cases ( 15 % ) ; all but one fulfilled diagnostic criteria for possible Alzheimer 's disease .  Cobalamin supplementation was given to all patients and the effect was evaluated after 6 months . When the size and pattern of individual change scores , and the mean change scores on all instruments were taken into account , functioning after replacement therapy was not improved . When change scores of treated patients were compared with those of patients with Alzheimer 's disease ( n = 69 ) , vitamin B12 replacement did not result in slowing of the progression of dementia . Contrary to widely accepted beliefs , subnormal serum vitamin B12 levels are not a ( quantitatively ) important cause of reversible dementia BACKGROUND Associations between low levels of folate and vitamin B12 and cognitive impairment in patients with dementia have been reported . Some studies revealed correlations between low levels of vitamin B12  and behavioural and psychological signs and symptoms of dementia ( BPSD ) in Alzheimer 's disease ( AD ) patients . Given the lack of studies in frontotemporal dementia ( FTD ) and on folate and given the method ological shortcomings of former publications , we set up a prospect i ve study . METHODS At inclusion , AD ( n=152 ) and FTD ( n=28 ) patients underwent a neuropsychological examination . Behaviour  was assessed using a battery of behavioural assessment scales . Determination of serum vitamin B12 and red cell folate levels  were performed within a time frame of two weeks of inclusion . RESULTS In both patient groups , significantly negative correlations between levels of serum vitamin B12 and red cell folate and the degree of cognitive deterioration were found . No correlations with BPSD were found in the AD patient group . In FTD patients , levels of vitamin B12 were negatively correlated with both hallucinations ( p=0.022 ) and diurnal rhythm disturbances ( p=0.036 ) . CONCLUSIONS The observed negative correlations between levels of vitamin B12 and folate and cognitive impairment in both AD and FTD patients , raise the possibility of a non-specific etiological role . Although levels of vitamin B12 and folate did not correlate with BPSD in AD patients , negative correlations between serum vitamin B12 levels and BPSD in FTD patients were revealed . Decreased serum vitamin B12 levels may predispose FTD patients to develop hallucinations and diurnal rhythm disturbances BACKGROUND Mild cobalamin ( Cbl ) deficiency is frequently found in older persons and is associated with cognitive and cerebral abnormalities . The effects of Cbl supplementation on these abnormalities are largely unknown . METHODS In a single-blind , placebo-controlled intervention study , 16 healthy community-dwelling elderly subjects with low plasma Cbl concentration and no cognitive impairments were studied . Subjects underwent 1 month of treatment with placebo , followed by 5 months of treatment with intramuscular injections of hydroxycobalamin . Before and after measurements of plasma cobalamin , total homocysteine ( tHcy ) , methylmalonic acid ( MMA ) , quantitative electroencephalograph ( qEEG ) , and psychometric tests were taken . RESULTS After Cbl supplementation , plasma Cbl concentrations increased , and plasma MMA and tHcy concentrations decreased . The performance on the Verbal Word Learning Test , Verbal Fluency and Similarities improved . qEEG showed more fast activity and less slow activity . Lower plasma tHcy concentrations were related to increased fast activity on qEEG on the one h and and improved performance on the Verbal Word Learning Test and Similarities on the other . Increased fast or decreased slow activity on qEEG was associated with improved performance on the Verbal Word Learning Test , Similarities and Verbal Fluency . CONCLUSIONS Electrographic signs of improved cerebral function and improved cognitive function were found after Cbl supplementation in older subjects with low plasma Cbl concentrations who were free of significant cognitive impairment . These improvements were related to a reduction of plasma tHcy concentration OBJECTIVES To investigate the effect of cobalamin/folate supplementation on cognitive function in elderly patients with dementia . METHOD The cobalamin/folate status of the patients was evaluated by measuring plasma homocysteine , serum methylmalonic acid , serum cobalamin and blood folate .  Thirty-three patients were studied and repeatedly assessed with the  Mini-Mental State Examination ( MMSE )  and  ' A short cognitive performance test for assessing memory and attention ' ( SKT )  
    Output:
    
Association of dietary intake levels of B vitamins  with age-related neurodegenerative diseases and cognitive