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Background: Depression is an established risk factor for dementia in later life, but it is unclear if this relationship is causal. This study aimed to determine if clinically significant depressive symptoms are likely to be causally related to cognitive impairment in later life., Methods: Observational cohort study of 4568 men aged 70-89 years living in Perth, Western Australia, who were free of cognitive impairment at the beginning of follow-up. Current clinically significant depressive symptoms were defined by a score of 7 or more on the Geriatric Depression Scale 15 items. Past depression was ascertained via electronic medical records, by self-report or use of antidepressants. A score of 27 or less on the Telephone Interview for Cognitive Status modified or a recorded diagnosis of dementia in electronic medical records established the presence of cognitive impairment., Results: During the 5-year follow-up, 534 men developed cognitive impairment, 811 died and 1455 were lost. The presence of clinically significant depressive symptoms at study entry was associated with increased risk rate (RR) of cognitive impairment (RR = 2.59, 95% confidence interval: 95%CI = 1.57-4.27), death (RR = 5.07, 95%CI = 3.32-7.75) and loss to follow-up (RR = 2.03, 95%CI = 1.32-3.13). These associations remained statistically significant after adjustment for age, country of birth, education, smoking history, and prevalence hypertension, diabetes, coronary heart disease and stroke. History of past clinically significant depressive symptoms was not associated with incident cognitive impairment (RR = 1.09, 95%CI = 0.78-1.52)., Conclusions: The lack of association between past depression and cognitive impairment suggests that the link between depression and cognitive impairment is not causal and that the presence of clinically significant depressive symptoms in later life may herald the onset of cognitive impairment in at least some people., (Copyright © 2015 John Wiley & Sons, Ltd.)

Introduction: Aboriginal Australians are reported to develop dementia earlier than the general population. The causes remain unknown., Methods: This was a longitudinal study of 363 participants aged ≥45 years. Consensus diagnoses were established for cognitive impairment or dementia., Results: At follow-up, 189 people (mean ± standard deviation age, 65.4 ± 10.3 years) participated, as 109 (30%) had died and 65 (18%) were unavailable. The incidence of cognitive impairment or dementia was 52.6 (95% confidence interval 33.9, 81.5) per 1000 person-years (380.3 total person-years) and for dementia was 21.0 (10.5, 42.1) per 1000 person-years (380.3 person-years total) over the age 60 years. Longitudinal risk factors associated with a decline from normal cognition to impairment were age and head injury. Other associations with cognitive decline were stroke, head injury, nonaspirin analgesics, lower BMI, and higher systolic BP., Discussion: Dementia incidence in Aboriginal Australians is among the highest in the world, and is associated with age and head injury., (Copyright © 2016 The Alzheimer's Association. Published by Elsevier Inc. All rights reserved.)

Background: A quality dementia-screening tool is required for older remote Aboriginal Australians who have high rates of dementia and limited access to appropriate medical equipment and clinicians. The Kimberley Indigenous Cognitive Assessment (KICA Cog) is a valid cognitive test for dementia in Aboriginal and Torres Strait Islander peoples. The KICA cognitive informant questionnaire (KICA Carer) had yet to be analyzed to determine validity alone or in combination with the KICA Cog., Methods: The KICA Carer was completed by nominated informants of 349 remote-living Aboriginal Australians in the Kimberley region, Western Australia. Validity was assessed by comparing KICA Carer with Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) and International Classification of Diseases (ICD-10) consensus diagnoses based on a blinded specialist review. KICA Carer and KICA Cog were then compared to determine joint validity., Results: A KICA Carer score of ≥3/16 gave optimum sensitivity (76.2%) and specificity (81.4%), area under curve (AUC) 0.89 (95% CI = 0.85, 0.94) with positive predictive value (PPV) of 35.8%, and negative predictive value (NPV) of 96.2%. A KICA Cog score of ≤33/39 gave a sensitivity of 92.9% and specificity of 89.9%, AUC 0.96 (95% CI = 0.94, 0.98), with PPV of 55.6% and NPV of 98.9%. Cut-off scores of KICA Cog ≤ 33/39 and KICA Carer ≥ 2/16 in series indicate possible dementia, with sensitivity of 90.5% and specificity of 93.5%. In this setting, PPV was 66.5% and NPV was 98.6%., Conclusions: The KICA Carer is an important tool to accurately screen dementia in remote Aboriginal Australians when the KICA Cog is unable to be used for a patient. It is readily accepted by caregivers., Key Points: • For the best practice in the cognitive assessment of an Aboriginal Australian aged over 45 years, KICA Cog should be utilized. • In cases where Aboriginal patients are not assessed directly, KICA Carer should be conducted with an informant. A cut-off score of ≥3/16 should be used (these tools can be downloaded from www.wacha.org.au/kica.html).

Background: The incidence of traumatic brain injury (TBI) is rising, as are its neuropsychiatric complications. This study aims to determine (1) the prevalence of TBI, (2) the association between history of past TBI and sociodemographic, lifestyle and clinical factors, and (3) the risk of depression and cognitive impairment in later life associated with exposure to TBI., Methods: Cross-sectional study of a community-derived sample of 5486 Australian men aged 70-89 years. Information on TBI was retrieved from the Western Australian Data Linkage System (WADLS) and via self-report. We used the WADLS and self-report to ascertain history of past depression, and the Geriatric Depression Scale 15-items to assess current clinically significant symptoms of depression, defined by score ≥7. We defined cognitive impairment by a mini-mental state examination score <24 or a WADLS diagnosis of dementia., Results: Nine hundred fifty-three men had history of TBI (17.4%). Factors associated with TBI included coronary heart disease, stroke, poor self-perceived physical health and falls. TBI increased the odds ratio of past (odds ratio (OR) = 1.55, 95% confidence interval (CI) = 1.21, 1.99) and current depression (OR = 1.77, 95% CI = 1.36, 2.32), as well as of cognitive impairment (OR = 1.23, 95% CI = 1.00, 1.51). The population fractions of depression and cognitive impairment attributable to TBI were 6.9% (95% CI = 3.3%, 10.3%) and 3.4% (95% CI = 0.0%, 6.9%)., Conclusions: History of TBI is common in older men, and is associated with increased risk of depression and cognitive impairment. If this association is truly causal, then the effective reduction of events leading to TBI (e.g., motor vehicle accidents and falls) may also decrease the prevalence of depression and cognitive impairment in later life., (Copyright © 2015 John Wiley & Sons, Ltd.)

Objective: To determine whether alcohol consumption is causally associated with cognitive impairment in older men as predicted by mendelian randomization., Methods: Retrospective analysis of a cohort study of 3,542 community-dwelling men aged 65 to 83 years followed for 6 years. Cognitive impairment was established by a Mini-Mental State Examination score of 23 or less. Participants provided detailed information about their use of alcohol during the preceding year and were classified as abstainers, occasional drinkers, and regular drinkers: mild (<15 drinks/wk), moderate (15-27 drinks/wk), heavy (28-34 drinks/wk), and abusers (≥35 drinks/wk). We genotyped the rs1229984 G→A variant of the alcohol dehydrogenase 1B (ADH1B) gene, which is associated with lower prevalence of alcohol abuse and dependence. Other measures included age, education, marital status, smoking and physical activity, body mass index, diabetes, hypertension, and cardiovascular diseases., Results: At study entry, rs1229984 G→A polymorphism was associated with lower prevalence of regular use of alcohol and decreased consumption among regular users. Six years later, 502 men (14.2%) showed evidence of cognitive impairment. Abstainers and irregular drinkers had higher odds of cognitive impairment than regular drinkers (odds ratio [OR] = 1.23, 95% confidence interval [CI] = 1.00-1.51, after adjustment for other measured factors). The rs1229984 G→A polymorphism did not decrease the odds of cognitive impairment (AA/GG OR = 1.35, 95% CI = 0.29-6.27; GA/GG OR = 1.05, 95% CI = 0.71-1.55)., Conclusions: Alcohol consumption, including heavy regular drinking and abuse, is not a direct cause of cognitive impairment in later life. Our results are consistent with the possibility, but do not prove, that regular moderate drinking decreases the risk of cognitive impairment in older men.

Reduced awareness of cognitive deficits in mild cognitive impairment (MCI) is associated with poorer outcomes although little is known about the anatomical correlates of this. We examined the association of insight and grey matter volume using a voxel-based morphometry approach in 65 volunteers with MCI and 55 healthy age-matched controls. Participants with MCI had multiple areas of subtle grey matter volume loss compared with controls, although these did not survive correction for multiple comparisons. These were predominantly in the temporal and anterior portions of the brain. Individuals with MCI did not differ from each other on a number of demographic and cognitive variables according to level of insight. Reduced awareness of cognitive deficits was associated with few differences in grey matter volume apart from a subtle loss of grey matter in the medial frontal gyri. Given the modest nature of these findings, the routine assessment of insight in non-clinical populations of individuals with MCI is therefore not supported. Prospective data in larger samples, however, would be helpful to clarify this further and determine if impaired insight predicts brain atrophy and cognitive decline.

Background: Depression and high total plasma homocysteine (tHcy) are independently associated with cognitive impairment in older adults. We designed this study to determine if high tHcy is a mediator of cognitive performance in older adults with major depression., Methods: We recruited 358 community-dwelling older adults experiencing depressive symptoms, 236 (65.9%) of who met DSM-IV-TR criteria for major depression. Assessment included the Montgomery Asberg Depression Rating Scale (MADRS), fasting tHcy and the Consortium to Establish a Registry for Alzheimer's Disease neuropsychological battery., Results: Individuals with major depression and high tHcy had significantly worse immediate verbal and delayed visual recall. Non-depressed participants with high tHcy had lower MMSE, immediate and delayed recall scores than those with normal tHcy. The odds of cognitive inefficiency for those with high tHcy was nearly doubled for the MMSE (OR 1.9, 95%CI 1.1-3.3), immediate (OR 1.9, 95%CI 1.1-3.5) and delayed (OR 1.9, 95%CI 1.1-3.4) word recall after adjusting for age, gender, IHD and MADRS score., Limitations: The presence of sub-syndromal depressive symptoms in our non-depressed group and exclusion of participants with established cognitive impairment may limit the generalizability of this study., Conclusions: Elevated tHcy was associated with weaker performance in tests of immediate and delayed memory and global cognitive performance when compared to those with normal tHcy independent of the presence of major depression or the severity of depressive symptoms. Homocysteine lowering B-vitamin supplementation may offer a potential therapeutic target to try and mitigate the often-disabling impact of cognitive deficits found in this population., (© 2013 Elsevier B.V. All rights reserved.)

Aims: Heart failure (HF) has been associated with cognitive dysfunction, a high prevalence of mood disorders, and a relative loss of grey matter in several brain regions. This study aimed to determine if, compared with controls with and without ischaemic heart disease (IHD), adults with HF show evidence of progressive loss of cerebral grey matter, and whether morphological changes are associated with changes in cognition, depression and anxiety symptoms over a follow-up period of 2 years., Methods and Results: This was a 24-month longitudinal study of 19 participants with systolic HF, 43 with IHD, and 45 controls. Subjects were older than 45 years and free of cognitive impairment at the start of follow-up. We acquired magnetic resonance images and used Statistical Parametric Mapping version 8 (SPM8) to investigate changes in the distribution of cerebral grey matter volume over time. We used the Cambridge Cognitive Examination of the Elderly (CAMCOG) and the Hospital Anxiety and Depression Scale (HADS) to assess 2-year changes in cognitive function and mood. Changes in total grey matter volume and cognitive function were similar across the three study groups, but participants with HF showed evidence of increasing severity of anxiety and depressive symptoms. HF was associated with subtle regional loss of grey matter in the right and left thalamus, left caudate, left and right posterior cingulate, left and right parahippocampal gyri, left superior and middle temporal gyri, and right inferior parietal lobule compared with controls and, to a lesser extent, participants with IHD., Conclusion: HF and IHD are not associated with a disproportional loss of cerebral grey matter or cognitive decline over 2 years compared with cardiologically healthy controls. Adults with HF experience increasing symptoms of anxiety and depression over 2 years compared with controls, and this increased vulnerability is associated with a relative loss of grey matter in brain regions that are important for the modulation of emotions.

In a previous study, we detected a 6p25-p24 region linked to schizophrenia in families with high composite cognitive deficit (CD) scores, a quantitative trait integrating multiple cognitive measures. Association mapping of a 10 Mb interval identified a 260 kb region with a cluster of single-nucleotide polymorphisms (SNPs) significantly associated with CD scores and memory performance. The region contains two colocalising genes, LYRM4 and FARS2, both encoding mitochondrial proteins. The two tagging SNPs with strongest evidence of association were located around the overlapping putative promoters, with rs2224391 predicted to alter a transcription factor binding site (TFBS). Sequencing the promoter region identified 22 SNPs, many predicted to affect TFBSs, in a tight linkage disequilibrium block. Luciferase reporter assays confirmed promoter activity in the predicted promoter region, and demonstrated marked downregulation of expression in the LYRM4 direction under the haplotype comprising the minor alleles of promoter SNPs, which however is not driven by rs2224391. Experimental evidence from LYRM4 expression in lymphoblasts, gel-shift assays and modelling of DNA breathing dynamics pointed to two adjacent promoter SNPs, rs7752203-rs4141761, as the functional variants affecting expression. Their C-G alleles were associated with higher transcriptional activity and preferential binding of nuclear proteins, whereas the G-A combination had opposite effects and was associated with poor memory and high CD scores. LYRM4 is a eukaryote-specific component of the mitochondrial biogenesis of Fe-S clusters, essential cofactors in multiple processes, including oxidative phosphorylation. LYRM4 downregulation may be one of the mechanisms involved in inefficient oxidative phosphorylation and oxidative stress, increasingly recognised as contributors to schizophrenia pathogenesis.

Aims: It is unclear whether the cognitive dysfunction associated with heart failure (HF) is due to HF or comorbid conditions such as ischaemic heart disease (IHD). This study aimed to determine whether, compared with controls with and without IHD, adults with systolic HF show evidence of cognitive impairment and cerebral grey matter (GM) loss., Methods and Results: Cross-sectional study of 35 participants with HF, 56 with IHD, and 64 controls without either HF or IHD. Subjects were older than 45 years and free of overt cognitive impairment. We acquired magnetic resonance images and used SPM8 to determine regional differences in cerebral GM volume. Participants with HF had lower scores than controls without IHD on immediate memory, long delay recall and digit coding, whereas those with IHD had lower long delay recall scores than controls without IHD. Compared with controls without IHD, participants with HF showed evidence of GM loss in the left cingulate, the right inferior frontal gyrus, the left middle and superior frontal gyri, the right middle temporal lobe, the right and left anterior cingulate, the right middle frontal gyrus, the inferior and pre-central frontal gyri, the right caudate, and occipital-parietal regions involving the left precuneus. The loss of GM followed a similar, less extensive, pattern when we compared participants with HF and IHD., Conclusion: Adults with HF have worse immediate and long-term memory and psychomotor speed than controls without IHD. Heart failure is associated with changes in brain regions that are important for demanding cognitive and emotional processing.

High total plasma homocysteine (tHcy) has been associated with cognitive impairment in later life, but it is unclear if this association is causal or is due to confounding. The C677T polymorphism of the 5,10 methylenetetrahydrofolate reductase gene (MTHFR) increases basal tHcy, but its contribution to cognitive impairment has not been established. We designed this study to determine if tHcy is causally related to cognitive impairment in later life by investigating its association with high tHcy and the MTHFR-C677T polymorphism. We recruited 1778 older men from the Health in Men Study cohort and established caseness on the basis of the participants' scores on a Telephone Interview for Cognitive Status score 27 in 2008. Exposure to tHcy, gene status and other variables of interest were obtained from assessments 4-7 years earlier. Multivariate logistic regression showed that the odds of cognitive impairment increased with a doubling of tHcy (adjusted odds ratio, OR 1.36; 95% confidence interval, 95% CI 1.02-1.82). Compared with the wild CC genotype, participants with the MTHFR-TT genotype had 46% greater odds of cognitive impairment (OR 1.46, 95% CI 1.01-2.11, P=0.043). The results of this study are consistent with, but do not prove the hypothesis that high tHcy causes cognitive impairment in later life.

Background: Elevated total plasma homocysteine (tHcy) has been associated with cognitive impairment, vascular disease and brain atrophy., Methods: We investigated 150 volunteers to determine if the association between high tHcy and cerebral grey matter volume and cognitive function is independent of cardiovascular disease., Results: Participants with high tHcy (≥15 µmol/L) showed a widespread relative loss of grey matter compared with people with normal tHcy, although differences between the groups were minimal once the analyses were adjusted for age, gender, diabetes, hypertension, smoking and prevalent cardiovascular disease. Individuals with high tHcy had worse cognitive scores across a range of domains and less total grey matter volume, although these differences were not significant in the adjusted models., Conclusions: Our results suggest that the association between high tHcy and loss of cerebral grey matter volume and decline in cognitive function is largely explained by increasing age and cardiovascular diseases and indicate that the relationship is not causal.

Background: Congestive heart failure (CHF) has been associated with impaired cognitive function, but it is unclear if these changes are specific to CHF and if they get worse with time. We designed this study to determine if adults with CHF show evidence of cognitive decline compared with adults with and without coronary artery disease (CAD)., Methods: A longitudinal study was carried out of 77 adults with CHF (ejection fraction, EF < 0.4), 73 adults with a clinical history of CAD and EF > 0.6, and 81 controls with no history of CAD. The Cambridge Cognitive Examination of the Elderly (CAMCOG) was the primary outcome measure. Secondary measures included the California Verbal Learning Test (CVLT), digit coding and copying, Hospital Anxiety and Depression Scale (HADS), and the short form health survey (SF36). Endpoints were collected at baseline and after 12 and 24 months., Results: The adjusted CAMCOG scores of CHF participants declined 0.9 points over two years (p = 0.022) compared with controls without CAD. There were no differences between the groups on other cognitive measures. Participants with CHF and with CAD experienced similar changes in cognitive function over two years. Left ventricular EF and six-minute walk test results could not explain the observed associations., Conclusions: The changes in cognitive function and mood associated with CHF over two years are subtle and not specific to CHF.

Background: Observational studies investigating the association between smoking, cognitive decline and dementia have produced conflicting results. We completed this trial to determine if smoking cessation decreases the progression of cognitive decline in later life., Methods: We recruited older smokers (n=229) and never smokers (n=98) and invited smokers to join a smoking cessation trial. The primary outcome of interest was change in Alzheimer's Disease Assessment Scale cognitive subscale (ADAS-cog) scores over 24 months. Secondary measures included the Logical Memory test and changes in gray matter density. Successful smoking cessation was defined as a minimum of 547 smoking free days during follow up., Results: The ADAS-cog scores of unsuccessful quitters (UQ) increased (i.e., became worse) 1.1±0.3 and 1.2±0.4 points more than the scores of never smokers (NS) (p=0.001) and successful quitters (SQ) (p=0.006) respectively over the 24 months of follow up. Similarly, the scores of UQ declined (i.e., became worse) relative to NS on measures of immediate (p=0.004) and delayed recall (p=0.029). All analyses were adjusted for age, years of education, baseline cognitive performance, alcohol use, depression scores, and the presence of chronic respiratory disease. Thirty-six NS, 18 SQ and 48 UQ completed the imaging substudy. Compared with NS, UQ showed a disproportional loss of gray matter density in the right thalamus, right and left inferior semi-lunar lobule, as well as left superior and inferior parietal lobule over 24 months. SQ showed loss of gray matter compared with NS in the right middle and inferior occipital gyri, right and left culmen, and the left superior frontal gyrus. We did not find any brain regions in which UQ had lost more gray matter than SQ over 2 years., Conclusion: These results are consistent with the hypothesis that smoking causes cognitive decline and loss of gray matter tissue in the brain over time., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Impaired awareness of cognitive deficits is a common symptom of dementia, but its prognostic importance in people with cognitive impairment-no dementia (CIND) is uncertain. In this study, we examined whether community volunteers with CIND and reduced awareness had worse cognitive performance and cognitive decline over 18 months than CIND participants with intact awareness or healthy controls. We recruited 92 participants with CIND and 91 healthy controls with their respective informants. We used discrepancy scores (informant minus participant) on the Anosognosia Questionnaire for Dementia and Dysexecutive Questionnaire to ascertain participants' awareness of their cognitive performance. The main cognitive outcome variable was the Alzheimer Disease Assessment Scale: Cognitive Section. Bivariate correlations showed no relationship between the awareness measures and cognitive performance or decline. Overall, CIND participants' ratings of cognitive deficits correlated significantly with their Alzheimer Disease Assessment Scale: Cognitive Section score after 18-months (for Anosognosia Questionnaire for Dementia, r=0.45, P <0.001) and showed a stronger relationship with cognitive performance than informant ratings. These results indicate that reduced awareness of deficit may be uncommon in community volunteer samples with CIND. In addition, self-report of cognitive complaints may be at least as useful as informant report when screening community-dwelling older adults at risk of cognitive decline and dementia., (Copyright © 2011 by Lippincott Williams & Wilkins)

Background/aims: The nature and extent of adverse cognitive effects due to the prescription of anticholinergic drugs in older people with and without dementia is unclear., Methods: We calculated the anticholinergic load (ACL) of medications taken by participants of the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of ageing, a cohort of 211 Alzheimer's disease (AD) patients, 133 mild cognitive impairment (MCI) patients and 768 healthy controls (HC) all aged over 60 years. The association between ACL and cognitive function was examined for each diagnostic group (HC, MCI, AD)., Results: A high ACL within the HC group was associated with significantly slower response speeds for the Stroop color and incongruent trials. No other significant relationships between ACL and cognition were noted., Conclusion: In this large cohort, prescribed anticholinergic drugs appeared to have modest effects upon psychomotor speed and executive function, but not on other areas of cognition in healthy older adults., (Copyright © 2011 S. Karger AG, Basel.)

Cardiovascular risk factors have been associated with 2 common manifestation of unhealthy brain in older people, cognitive impairment and depression. The evidence for these effects is almost entirely observational, but links hypertension, smoking, hypercholesterolemia, diabetes mellitus, and hyperhomocysteinemia with cognitive impairment and depression. Unfortunately randomized trials evaluating interventions for these risk factors on the outcomes of cognition or mood have either been inconclusive or negative. However, as there are considerable other health benefits from targeting cardiovascular risk factors, these interventions should be more widely adopted, which would also probably result in positive outcomes for the brain.

Background: Research evidence from observational studies suggests that cognitive activity reduces the risk of cognitive impairment in later life as well as the rate of cognitive decline of people with dementia. The Promoting Healthy Ageing with Cognitive Exercise (PACE) study has been designed to determine whether a cognitive activity intervention decreases the rate of cognitive decline amongst older adults with mild cognitive impairment (MCI)., Methods/design: The study will recruit 160 community-dwelling men and women aged 65 years of age or over with mild cognitive impairment (MCI). Participants will be randomly allocated to two treatment groups: non-specific education and cognitive activity. The intervention will consist of ten 90-minute sessions delivered twice per week over a period of five weeks. The primary outcome measure of the study is the change from baseline in the total score on the Cambridge Cognitive Score (CAMCOG). Secondary outcomes of interest include changes in memory, attention, executive functions, mood and quality of life. Primary endpoints will be collected 12, 52 and 104 weeks after the baseline assessment., Discussion: The proposed project will produce the best available evidence on the merits of increased cognitive activity as a strategy to prevent cognitive decline among older adults with MCI. We anticipate that the results of this study will have implications for the development of evidence-based preventive strategies to reduce the rate of cognitive decline amongst older people at risk of dementia., Trial Registration: ACTRN12608000556347.

Background: Cognitive impairment and heart failure are both serious health problems related to population ageing. Impaired cognitive function is an important but underrecognized complication of congestive heart failure (CHF). The aim of the study was to examine the sociodemographic, clinical, neuroimaging and biochemical parameters affecting cognition in CHF., Methods: Thirty-one patients with CHF (left-ventricular ejection fraction < 40%) and 24 controls without CHF, all free of clinically significant cognitive impairment, participating in a case-control study were assessed using a cognitive battery (CAMCOG), a depression scale, 6-min-walk test, left-ventricular ejection fraction, semi-quantitative magnetic resonance imaging, and cortisol, aldosterone and renin concentrations., Results: The CHF patients had lower CAMCOG scores than controls (93.5 +/- 6.1 vs 99.9 +/- 2.4, P < 0.001) and had significantly lower scores on visuospatial, executive function, visual memory and verbal learning tasks. Concentrations of renin and aldosterone were higher in patients with CHF (5.4 +/- 6.0 vs 0.8 +/- 0.7 mU/L, P < 0.001 and 598.2 +/- 306.2 vs 346.0 +/- 201.5, P= 0.003). Right medial temporal lobe atrophy was more prominent in CHF (P= 0.030). Left medial temporal lobe atrophy and deep white matter hyperintensities showed moderate association with cognitive scores in CHF, whereas functional capacity and biochemical parameters were fairly correlated to cognition., Conclusion: Congestive heart failure is associated with a pattern of generalized cognitive decline. Structural brain changes, functional capacity and biochemical parameters are associated with the cognitive performance of patients with CHF, but their contribution appears modest. The design of a definitive case-control study is described.

Objectives: To determine the prevalence of dementia and cognitive impairment among older Indigenous Australians., Methods: A total of 363 Indigenous Australians aged over 45 years from the Kimberley region in the far north of Western Australia were assessed with the Kimberley Indigenous Cognitive Assessment (KICA). All those scoring less than 37 on the KICA and a percentage of those scoring 37 or more were reviewed by specialist clinicians and DSM-IV consensus diagnoses were obtained from two other specialists blinded to KICA results., Results: The prevalence of dementia was 12.4%, substantially higher than in the Australian general population. The prevalence of cognitive impairment not dementia was 8.0%., Conclusions: The prevalence of dementia among Indigenous Australians is substantially higher than that found in non-Indigenous Australians and all other studied populations.

A common T-->C polymorphism of the KIBRA gene has been recently associated with worse performance on tests of episodic memory. This should aimed to determine whether older adults with the KIBRA CC genotype (1) have worse episodic memory than T-allele carriers and, (2) are more likely to express the phenotype of amnestic mild cognitive impairment (MCI). Our Cross-sectional investigation of 312 adults aged 50-89 years free of dementia included genotyping of the KIBRA rs17070145 gene and the assessment of episodic memory to Establish a Registry for Alzheimer's Disease (CERAD). Participants were considered to have MCI if their memory scores were 1.5 standard deviations below the mean norm for the population. 138/312 participants carried the KIBRA CC genotype. Their immediate and delayed recall scores were significantly lower than the scores of carriers of the T allele (P < 0.05; adjusted for age, gender and pre-morbid IQ), although the effect size of the CC genotype was weak (0.2). Amongst our volunteers, 133 had MCI, of whom 63 (47.4%) had the CC genotype. There was no association between KIBRA genotype and MCI phenotype (TT/CT versus CC; adjusted odds ratio = 1.70, 95%CI = 0.74, 3.90). We concluded that the KIBRA T-->C polymorphism contributes to modulate episodic memory amongst community-dwelling older adults free of dementia, but plays no obvious role in the phenotypic expression of MCI. Future studies should aim to clarify the long term implications of this polymorphism on cognitive function and to identify other genes involved in the modulation of memory that might confer greater risk of MCI in later life.

Background: Plasma amyloid beta-peptide (Abeta) can compromise the blood-brain barrier, contributing to cerebrovascular alterations and amyloid angiopathy in Alzheimer's disease (AD). The objectives of this study were to investigate the distribution of lipoprotein-bound plasma-Abeta isoforms., Methods: This involved a case-control study of subjects with AD or amnestic mild cognitive impairment (MCI) versus controls. Lipoprotein Abeta distribution was determined in fasted plasma. For assessment of chylomicron homeostasis in the postabsorptive state, subjects were bled 4 h after a low-fat meal. The main outcome measures were plasma lipoprotein Abeta isoform distribution and lipid homeostasis., Results: We found the majority of plasma Abeta to be associated with triglyceride-rich lipoproteins (TRLs) encompassing chylomicrons, VLDL and IDL. For all lipoprotein groups, Abeta1-40 was the predominant isoform, accounting for approximately 50% of the total. Thereafter, equivalent amounts of the isoforms 1-42, 2-40, 1-38, 1-37 and 1-39 were found. Abeta1-37, Abeta1-38 and Abeta2-40 isoforms were significantly enriched within the TRL fraction of AD/MCI subjects and similar trends were observed for isoforms Abeta1-39, Abeta1-40 and Abeta1-42. Lipoprotein-Abeta was inversely associated with plasma total- and LDL cholesterol. AD/MCI subjects were not dyslipidaemic, however, there was evidence of accumulation of chylomicrons in the postabsorptive state., Conclusions: Our data show that Abeta was found to be associated with plasma lipoproteins, especially those enriched with triglyceride. We find that Abeta may be increased in normolipidaemic AD subjects, commensurate with possible disturbances in postprandial lipoprotein homeostasis.

Cognitive impairment of any severity associated with cerebrovascular damage is defined as vascular cognitive impairment as proposed by O'Brien. This is a heterogeneous syndrome with many subtypes, the most prevalent being vascular cognitive impairment without dementia. Neuropathological studies confirm that cerebrovascular disease and Alzheimer's disease frequently coexist. Diagnosis depends on criteria for dementia and vascular pathologies. Brain imaging is an important diagnostic tool. Although there is no approved intervention specifically for vascular cognitive impairment, general treatments (such as antiplatelet and antihypertensives) aimed at the prevention and management of stroke are used. Evidence from randomised, placebo-controlled studies of cholinesterase inhibitors for vascular dementia suggests that there may be beneficial effects for cognitive function, and clinical global impression is more favourable for the cholinesterase inhibitors compared with placebo. The effect of memantine also seems to be modest and similar to the effect that is demonstrated in patients with Alzheimer's disease. The accumulated evidence is not as comprehensive as that which exists for Alzheimer's disease. The cholinesterase inhibitors and memantine have not been extensively studied in vascular cognitive impairment without dementia. For the purposes of this review, the authors focus on interventions that have been evaluated by randomised controlled trials.

We developed a telemedicine protocol for diagnosis of Alzheimer's Disease (AD). Assessments by video-conferencing (remote) were compared with face to face (direct) assessments. Eight physicians performed direct assessments and two physicians conducted remote assessments. There was alternate allocation of direct or remote initial assessment. The participants were 20 subjects over 65 years living in a rural area and referred by general practitioners (GPs) because of cognitive impairment. Each assessment included a Standardised Mini Mental State Examination, Geriatric Depression Scale, Katz assessment of Activities of Daily Living, Instrumental ADL assessment, and the Informant Questionnaire for Cognitive Decline in the Elderly. Laboratory results and radiological imaging were available from referring GPs. There was good agreement for diagnosing Alzheimer's disease between telemedicine and direct assessment, kappa = 0.8 (P<0.0001). However, because of the small sample size, the presence of systematic bias could not be completely excluded. We conclude that it is possible to diagnose AD at a distance using telemedicine, but this requires validation with a larger study.

Background: Indigenous Australians have a unique cultural heritage dating back many thousands of years. Unfortunately, there is no validated tool to assess cognition in older indigenous Australians. This study was designed to address this deficiency. The Kimberley Indigenous Cognitive Assessment (KICA) was developed with Indigenous health and aged care organizations, and comprises cognitive, informant and functional sections. The psychometric properties of the cognitive assessment section (KICA-Cog) are described in this paper., Methods: The KICA-Cog was tested in 70 indigenous subjects, of varying cognitive abilities and diagnoses, over 45 years of age. Subjects were interviewed using the KICA-Cog and then independently assessed by expert clinical raters using DSM-IV and ICD-10 criteria. Interrater and internal reliability were determined., Results: The KICA-Cog score showed no systematic interrater difference; the mean was -0.07 (SD = 1.83). Interrater reliability for 16 individual questions from the cognitive section revealed a kappa-value > or = 0.6 and intraclass correlations for 12 questions. Internal consistency, as assessed by Cronbach's alpha, was 0.88. Three items on the cognitive score (pension week, recall and free recall) effectively discriminated 85-7% of dementia cases. Sensitivity and specificity were 90.6% and 92.6%, respectively, using a cut-off score of 31/32., Conclusions: The KICA-Cog appears to be a reliable assessment tool for cognitive impairment in an Australian older traditionally living indigenous population.

The aim of this study was to examine inspection time (IT) performance in older adults with mild cognitive impairment (MCI), who are at higher risk of developing further cognitive decline or dementia. IT is described as an index of speed of informational intake. IT correlates with measures of fluid intelligence and is possibly a marker for the integrity of the cholinergic system of the brain. IT may therefore be useful in aiding the diagnosis of early-stage progressive cognitive impairment. The current study compares IT in 28 people with MCI to 28 age, gender and education-matched controls. The computer-based, visual IT task required participants to discriminate between two visual stimuli that were presented for brief periods. Participants' IT performance was compared to their performance on cognitive and memory tasks. Group comparison showed that participants with MCI performed significantly worse on IT than controls and was not affected by years of education. In combination with other clinical, neuropsychological and biological tests, IT may be a useful assessment tool for improving the identification of older adults at risk for clinically relevant cognitive decline.

Objective: The authors investigated the frequency distribution of well-established risk factors for dementia--high plasma homocysteine and the apolipoprotein E epsilon4 allele (APOE epsilon4)--among older women with subjective memory complaints (SMC) but no cognitive impairment, and with mild cognitive impairment (MCI)., Methods: This was a cross-sectional, community-based study., Results: Women with MCI had higher total plasma homocysteine than healthy-comparison subjects. There was also a nonsignificant excess of APOE epsilon4 carriers in the MCI than in the healthy group. Participants with SMC had higher depression and anxiety scores than healthy-comparison subjects, but did not differ from subjects in the healthy-comparison group in relation to their total plasma homocysteine and APOE epsilon4 distribution., Conclusions: MCI seems to be more closely related to well-established risk factors for dementia than is SMC.

Objective: The authors investigated the association between physiological levels of estrogen and mood/cognitive functioning among older postmenopausal women., Methods: This was a cross-sectional study of 265 postmenopausal women (mean age: 74.6 years), who were given a semistructured psychiatric interview (CAMDEX-R) and self-rated their health with the Beck Depression and Anxiety Inventories (BDI and BAI) and the SF-36 Health Survey. Cognitive abilities were assessed with the cognitive subsection of the CAMDEX (CAMCOG), the Word Lists subtest of the Wechsler Memory Scale, and the Block Design and Verbal Fluency subtests of the Wechsler Adult Intelligence Scale. Estradiol- and estrone-sensitive immunoassays were used to measure serum estradiol and estrone., Results: Women in the lowest 50th percentile of serum estradiol were more likely than women in the highest 50th percentile to have BDI scores suggestive of clinically significant or severe depression. Women in the lowest 50th percentile of serum estrone had higher BAI scores. There was no significant association between serum estradiol/estrone and cognitive functioning., Conclusions: Physiological serum concentrations of estradiol and estrone are inversely associated with depression and anxiety scores in older postmenopausal women. The association between serum estradiol and depression ratings is not linear and seems to be subject to a threshold effect.

Homocysteine (Hcy) is harmful to neurons and blood vessels, including the cerebral microvasculature. It is possible that such effects contribute to the cascade of events that leads to cognitive decline, dementia, and depression in later life. Hcy is produced during the metabolism of the essential amino-acid methionine, which also involves a methyl group transfer derived from folate and choline metabolism. Its plasma level can be influenced by factors such as age, vitamin deficiency, renal function, and a common mutation in the methylenetetrahydrofolate reductase (MTHFR) gene, where cytosine is replaced by thymidine (C-->T) at nucleotide position 677. Subjects with the TT genotype have higher homocysteine levels and may be particularly prone to experiencing depression as a result of high plasma Hcy and dysfunction of methylation metabolic pathways critical to the synthesis of noradrenaline and serotonin. We designed the present study to investigate whether older women with the TT genotype would have higher depression and lower cognitive scores than women with CT and CC genotypes. A total of 240 community-dwelling women aged 70 years or over volunteered to take part in the study - 29 carried the TT genotype, 113 the CT and 98 the CC genotype. The Beck Depression Inventory (BDI) score for subjects with the TT genotype was statistically similar to the other groups (P = 0.609). Plasma Hcy showed a modest and significant correlation with BDI scores (r = 0.21) that was independent from age, B12 and folate levels. There was no association between beck anxiety inventory (BAI) scores and MTHFR genotype or homocysteine levels. The cognitive assessment of participants included measures of verbal memory, memory for faces, verbal fluency, visuo-spatial abilities and the cognitive section of the Cambridge Examination For Mental Disorders Of The Elderly (CAMCOG)-MTHFR genotype had no clear association with cognitive scores. These results indicate that, in isolation, the MTHFR C677T gene variation does not play an important role in the modulation of mood and cognitive performance in later life.

The epsilon4 allele of apolipoprotein E (APOE), and the plasma levels of APOE, amyloid beta-protein precursor, amyloid beta1-40 (Abeta40) and homocysteine (Hcy) have all been correlated with the presence of dementia. Mutations in the methylnetetrahydrofolate reductase enzyme (MTHFR) have been associated with elevated levels of Hcy. This study explored the association of these factors with cognition and depression in community dwelling older men. Two hundred and ninety-nine men, mean age 78.9 years (SD 2.8), were studied in this cross-sectional survey. Mean plasma Hcy was 13.5 (SD 5.3) micromol/L. The MTHFR genotype had no obvious impact on Hcy levels. Ln Hcy and Ln Abeta40 were both inversely correlated with calculated glomerular filtration rate (cGFR), r = -0.41 (p < 0.001) and r = -0.28 (p < 0.001), respectively. There was a positive correlation between Ln Hcy and Ln Abeta40, r = 0.19 (p < 0.001), which remained significant after adjusting for cGFR, with a doubling of Hcy associated with a 24% increase of Abeta40. The e4 allele was associated with increased depressive symptoms as measured by the Geriatric Depression Scale-15, Odds ratio (OR) = 2.59 (95%CI 1.06-6.34) and poorer performance on the Clock Drawing Test, OR = 2.32 (95% CI: 1.25-4.29). There was a positive association between Abeta40 and Hcy, even after adjustment for cGFR in this sample of well, community dwelling older men. This association may help elucidate the link between elevated levels of Hcy and Alzheimer's disease.

Background: Telehealth could be a medium for the provision of cognitive assessments to distant sites., Aims: The aims of the present study were to determine the interrater reliability of the Standardized Mini Mental State Exam (SMMSE) and the Geriatric Depression Scale (GDS) through Telehealth as compared to face-to-face administration., Methods: Duplicate interviews of subjects with crossover of interview modality were carried out. Twenty patients were interviewed between two sites 11 km apart. Subjects were persons older than 65 years (mean age 82 years) who consented to Telehealth assessments. The outcome measures were the differences in assessment scores between the two media., Results: The average SMMSE score by remote assessment was 24.0 (range 11.0-30.0) and by direct assessment was 24.3 (range 9.0-30.0). The correlation between direct and remote SMMSE scores was 0.90. The mean difference between direct and remote SMMSE scores was -0.3 (95% confidence interval (CI): -4.6 to 4.0). In 8 of 20 participants (40%) the difference between Telehealth and direct assessments was two points or more on the SMMSE. The average GDS by remote assessment was 6.1 (range 1.0-14.0) and by direct assessment was 5.8 (range 2.0-13.0). The correlation between direct and remote GDS scores was 0.78. The mean difference between direct and remote GDS assessment was 0.3 (95% CI: -3.8 to 4.4)., Conclusion: Remote assessments with SMMSE and GDS using Telehealth methods yielded similar results to direct assessments. However, there was a moderate difference between face-to-face and Telehealth assessments in some subjects, which could influence clinical decision-making.

Background: Alzheimer's disease sufferers have been found to have a lack of the enzyme responsible for converting choline into acetylcholine within the brain. Lecithin is a major dietary source of choline, so extra consumption may reduce the progression of dementia., Objectives: To determine the efficacy of lecithin in the treatment of dementia or cognitive impairment., Search Strategy: The Cochrane Dementia and Cognitive Improvement Group's Specialized Register was searched on 15 May 2002 using the terms lecithin and phosphaditylcholine. This contains records from all major databases and many trials databases. Reference lists and relevant books have been examined., Selection Criteria: All unconfounded, randomized trials comparing lecithin with placebo in a treatment period longer than one day, in patients with dementia of the Alzheimer type, vascular dementia, mixed vascular and Alzheimer's disease, unclassified or other dementia or unclassified cognitive impairment not fulfilling the criteria for dementia are eligible for inclusion., Data Collection and Analysis: Data were extracted by two independent reviewers and cross-checked. Meta-analyses were performed when more than one trial provided data on a comparable outcome on sufficiently similar patients. Random effects analyses were performed whenever heterogeneity between results appeared to be present. Standardised differences in mean outcome measures were used due do the use of different scales and periods of treatment. Odds ratios for dichotomous data were pooled using the Mantel-Haenszel or DerSimonian and Laird methods., Main Results: Twelve randomized trials have been identified involving patients with Alzheimer's disease (265 patients), Parkinsonian dementia (21 patients) and subjective memory problems (90 patients). No trials reported any clear clinical benefit of lecithin for Alzheimer's disease or Parkinsonian dementia. Few trials contributed data to meta-analyses. The only statistically significant result was in favour of placebo for adverse events, based on one trial, which appears likely to be a spurious result. A dramatic result in favour of lecithin was obtained in a trial of subjects with subjective memory problems., Reviewer's Conclusions: Evidence from randomized trials does not support the use of lecithin in the treatment of patients with dementia. A moderate effect cannot be ruled out, but results from the small trials to date do not indicate priority for a large randomized trial.

The aim of this study was to compare traditional methods of scoring the Logical Memory test of the Wechsler Memory Scale-III with a new method based on Latent Semantic Analysis (LSA). LSA represents texts as vectors in a high-dimensional semantic space and the similarity of any two texts is measured by the cosine of the angle between their respective vectors. The Logical Memory test was administered to a sample of 72 elderly individuals, 14 of whom were classified as cognitively impaired by the Mini-Mental State Examination (MMSE). The results showed that LSA was at least as valid and sensitive as traditional measures. Partial correlations between prose recall measures and measures of cognitive function indicated that LSA explained all the relationship between Logical Memory and general cognitive function. This suggests that LSA may serve as an improved measure of prose recall.

Background: Nicergoline is an ergot derivative currently in use in over fifty countries for more than three decades, for the treatment of cognitive, affective, and behavioral disorders of older people. It was initially considered as a vasoactive drug and mainly prescribed for cerebrovascular disorders. Recent findings suggest other actions which has provided a rationale for the use of nicergoline for the treatment of various forms of dementia, including Alzheimer's Disease., Objectives: To determine whether there is evidence of efficacy of nicergoline in the treatment of dementia and other age-associated forms of cognitive decline,and to assess the safety and tolerability of the drug., Search Strategy: 1. Electronic databases search. The Cochrane Controlled Trials Register (which contains citations from the MEDLINE, EMBASE, Psych LIT, and hand searches of geriatric, dementia, psychogeriatric journals, and conference abstracts) was searched using the following terms: 'Nicergoline', 'Sermion'. 2. Reference search. The reference lists of all obtained studies was checked. 3. Pharmaceutical company Pharmacia & Upjohn, owners of the rights to produce and market nicergoline in various different countries, was asked to provide data and reports of clinical trials. In case of unavailability of numerical data in published studies, the authors of each paper, were asked for any published or unpublished data., Selection Criteria: - All unconfounded, double-blind, randomized, placebo-controlled, published and unpublished trials were sought. Non-randomized trials were excluded. Open trials were considered for inclusion if patients were randomized to the different treatment groups. - All patients diagnosed as having dementia or other cognitive disorder defined according to classification criteria accepted at the time of each study. - Nicergoline given at any dose for more than one day with placebo control. Type of outcome variables: 1. Cognitive function (as measured by psychometric tests). 2. Clinical impression (such as CIBIC or other clinical global measures of change). 3. Functional performance including dependency. 4. Behavioural disturbance. 5. Safety and acceptability as measured by the incidence of adverse effects (including side-effects) leading to withdrawal. 6. Death 7. Effect on carer 8. Use of services 9. Quality of life., Data Collection and Analysis: A comprehensive search of the international literature and the producing company archives has been performed to identify all possible sources of data for this review. Only those trials fulfilling the inclusion criteria of belonging to either category A or B of allocation concealment, as defined by the Cochrane Organisation, were examined for data extraction by one reviewer. If there was doubt then the other reviewer was consulted. Data availability restricted analyses to 'completers' analyses for the outcome measures. Outcomes able to be assessed included: Behaviour, Cognition, Clinical Judgment, Tolerability, EEG., Main Results: The Sandoz Clinical Assessment Geriatric Scale (SCAG) was the outcome used in the largest number of patients (814 patients). The results from these studies were homogeneous in nature despite including patients observed for periods of time ranging from 2 months to 12 months. There was a difference in favour of the active treatment in reducing the behavioural symptoms described by this scale, -5.18 points [-8.03, -2.33]. This scale has a maximum of 133 points. The therapeutic effects of nicergoline seem to be evident by 2 months of treatment and maintained for 6 months. In general other behavioural outcome measures which include the GRS, the IADL, and the MACC and were episodically used in few studies, failed to demonstrate statistically significant results although there was a trend favouring treatment. Cognitive assessment has been performed in a moderate number of patients with the MMSE (261 patients) and the ADAS-Cog (342 patients). No significant heterogeneity was found for these trials, despite the trials extending over periods of treatment of 3 to 12 months. There was a difference between treatment and control groups on the MMSE favouring nicergoline treatment. At 12 months the effect size was 2.86 [0.98, 4.74] The effect size for the ADAS-Cog, used exclusively with Alzheimer's disease patients, did not reveal a significant benefit. At 12 months the trend favoured treatment (-1.64 [-4.62, 1.34]). The other results from various cognitive measures tended to favour nicergoline but this was based on a small number of cases. The clinical impression of change obtained from a total of 921 patients was homogeneous across the studies, despite reflecting changes over periods of time ranging from 2 to 12 months. The Peto odd ratio for improvement in the subjects treated with nicergoline over these varying time periods was 3.33 [2.50, 4.43]. Tolerability assessed in 1427 patients was homogeneous across all studies and demonstrated a mildly increased risk of adverse events on treatment, OR 1.51[1.10, 2.07]., Reviewer's Conclusions: The clinical studies on nicergoline were carried out with diverse criteria and modalities of evaluation. Despite this, the 14 studies included in this review, have presented generally consistent results. Results of this meta-analysis provide some evidence of positive effects of nicergoline on cognition and behaviour and these effects are supported by an effect on clinical global impression. There was some evidence that there were increased risk of adverse effects associated with nicergoline. These results were obtained on older patients with mild to moderate cognitive and behavioural impairment of various clinical origins, including chronic cerebrovascular disorders and Alzheimer's dementia. The few studies specifically performed on patients with Alzheimer's disease were performed with too few people to give a definitive answer to the questions concerning the use of nicergoline for this form of dementia. This drug has not been evaluated using current diagnostic categories such as MCI or in association with therapeutic agents of different nature such as cholinesterase or antioxidant drugs.

Objectives: To determine the clinical efficacy of piracetam for the features of dementia or cognitive impairment, classified according to the major subtypes of dementia: vascular, Alzheimer's disease or mixed vascular and Alzheimer's disease, or unclassified dementia, or cognitive impairment not fulfilling the criteria for dementia., Search Strategy: The trials were identified from a search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 10 November 2000 using the term spiracetam, nootropic and 2-Oxo-1-pyrrolidine. In addition the pharmaceutical company responsible for marketing most of the piracetam worldwide, UCB Pharma, provided a comprehensive list of abstracts, which included many unpublished studies. As many of these unpublished, placebo-controlled studies will be reviewed as possible., Selection Criteria: All unconfounded trials specified as randomized in which treatment with piracetam was administered for more than a day and compared with placebo in patients with dementia of Alzheimer type, vascular dementia,or mixed vascular and Alzheimer's disease, or unclassified dementia, or cognitive impairment not fulfilling the criteria for dementia., Data Collection and Analysis: Data were extracted independently by two reviewers. Each study was independently verified as fulfilling the inclusion criteria. Studies were rated for methodological quality by assessment of blinding and loss before analysis as described by Jadad et al. (1996). Studies were pooled if appropriate and possible, and the pooled odds ratios (95%CI) or the average differences (95%CI) were estimated. Where possible, intention-to-treat analyses were undertaken. Sensitivity analyses were performed to determine if successive elimination of those studies performing most poorly on these quality criteria changed the effect estimate., Main Results: Unfortunately, many of the studies were of cross-over design and first-phase data were unavailable, or could not be extracted. Global Impression of Change was the only outcoeme for which there was a significant volume of evidence from the pooled data. There was evidence of heterogeneity in the results from the individual studies, chi-square test = 20.8 (df=5). Using a fixed effects model the odds ratio for improvement in the piracetam group compared with the placebo group was 3.55, [95% CI][2.45, 5.16]. If a random effects model was used the odds ratio was 3.47 [1.29, 9.30]. If one single-blind study was excluded, the fixed effects model yielded an odds ratio of 3.36 [2.29, 4.99] and if a random effects model was applied then the odds ratio was 2.89 [1.01, 8.24]. The evidence of effects on cognition and other measures, was inconclusive., Reviewer's Conclusions: At this stage the evidence available from the published literature does not support the use of piracetam in the treatment of people with dementia or cognitive impairment. Although effects were found on global impression of change, no benefit was shown by any of the more specific measures. There is a need for further evaluation of piracetam by : 1) Obtaining the data from the identified studies for an individual patient database review, 2) Performing a randomized trial of piracetam in patients with diagnoses made by currently accepted diagnostic criteria. The trial should extend over for a period of at least 6 months and preferably longer. Specific cognitive instruments which are sensitive to change, Clinician Global Impression of Change, levels of dependency and caregiver quality of life scales should also be incorporated in such a study.

The aim of this study was to determine the effect cognitive impairment has on direct and indirect costs to elderly people, their carers and the community over one year, by following prospectively a cohort of elderly people referred to an aged care assessment team. The 78 subjects were drawn from a random sample of people referred to the NorthWest Hospital team, and validated tools were used to assess their cognitive state. Outcome measures included total costs of community services, residential care, hospital bed use, carer burden and psychological morbidity. A comparison of outcome measures was made between those with cognitive impairment and those without. Use of community services and hospital beds was high overall. Those with cognitive impairment were substantially greater users of residential care, accounting for the higher expenditure in this group. Psychological morbidity and burden remain high in carers of those with cognitive impairment despite a high rate of institutionalisation in this group. The total costs for those referred to aged care assessment teams with cognitive impairment are double those seen for those with normal cognition.