In this cross-sectional study of 141 Aboriginal Australians aged ≥45 years living in the remote Kimberley region of Western Australia, we explored whether glycated haemoglobin (HbA1c) levels were associated with frailty. Sixty-four participants (45.4%) had a HbA1c level ≥6.5% and 84 participants (59.6%) were frail. A significant trend was observed with regard to HbA1c levels and frailty, with those having HbA1c levels ≥6.5% having the greatest prevalence of frailty (70.3%). In binary logistic regression analyses, having a HbA1c level ≥6.5% was associated with being frail after adjustment for age, sex, and education. This association was attenuated after further adjustment for body mass index (BMI). Poorer glycaemic control is very common and a potential risk factor for frailty in remote-living Aboriginal Australians, and appears to be partly mediated by BMI, a known risk factor for diabetes mellitus. Obesity and diabetes mellitus are potentially important modifiable risk factors for frailty.

OBJECTIVES:Frailty represents a loss of homeostasis, markedly increasing the risk of death and disability. Frailty has been measured in several ethnic groups, but not, to our knowledge, in Aboriginal Australians. We aimed to determine the prevalence and incidence of frailty, and associations with mortality and disability, in remote-living Aboriginal people.STUDY DESIGN:Between 2004 and 2006, we recruited 363 Aboriginal people aged ≥ 45 years from 6 remote communities and one town in the Kimberley region of Western Australia (wave 1). Between 2011 and 2013, 182 surviving participants were followed-up (wave 2). We assessed frailty with an index, comprising 20 health-related items. Participants with ≥ 4 deficits (frailty index ≥ 0.2) were considered frail. Disability was assessed by family/carer report. Those unable to do ≥ 2 of 6 key or instrumental activities of daily living were considered disabled. We investigated associations between frailty, and disability and mortality, with logistic regression and Cox proportional hazards models.RESULTS:At wave 1 (W1), 188 participants (65.3%) were frail, and of robust people at W1 who participated in wave 2, 38 (51.4%) had become frail. Frailty emerged at a younger age than expected. A total of 109 people died (30.0%), of whom 80 (73.4%) were frail at W1. Frailty at W1 was not associated with becoming disabled, but was associated with mortality (HR = 1.9; 95% CI 1.2, 3.0).CONCLUSIONS:Frailty in remote-living Aboriginal Australians is highly prevalent; substantially higher than in other populations. Research to understand the underlying causes of frailty in this population, and if possible, reverse frailty, is urgently needed.

OBJECTIVE:To describe the prevalence of falls and associated risk factors in older Indigenous Australians, and compare the accuracy of validated falls risk screening and assessment tools in this population in classifying fall status. METHOD:Cross-sectional study of 289 Indigenous Australians aged ≥45 years from the Kimberley region of Western Australia who had a detailed assessment including self-reported falls in the past year (n=289), the adapted Elderly Falls Screening Tool (EFST; n=255), and the Falls Risk for Older People-Community (FROP-Com) screening tool (3 items, n=74) and FROP-Com falls assessment tool (n=74). RESULTS:32% of participants had ≥1 fall in the preceding year, and 37.3% were classified high falls risk using the EFST (cut-off ≥2). In contrast, for the 74 participants assessed with the FROP-Com, only 14.9% were rated high risk, 35.8% moderate risk, and 49.3% low risk. The FROP-Com screen and assessment tools had the highest classification accuracy for identifying fallers in the preceding year (area under curve >0.85), with sensitivity/specificity highest for the FROP-Com assessment (cut-off ≥12), sensitivity=0.84 and specificity=0.73. CONCLUSIONS:Falls are common in older Indigenous Australians. The FROP-Com falls risk assessment tool appears useful in this population, and this research suggests changes that may improve its utility further.

We have previously demonstrated that Indigenous Australians have a very high prevalence rate of dementia, 5 times that of non-Indigenous Australians. We followed our original cohort to determine predictors of mortality in this population. Between 2004 and 2006, 363 Aboriginal people over the age of 45 years, living in remote Western Australia (WA) completed a comprehensive questionnaire and culturally appropriate diagnostic assessment for dementia. All participants were invited for reassessment between 2011 to 2013. We obtained mortality records for the cohort from the WA Data Linkage System and compared them to data for the general population. We used Cox proportional hazards regression to identify predictors of mortality over a 9-year follow-up period. The leading causes of mortality were diabetes, renal failure, and ischaemic heart disease. Of 40 participants with dementia at baseline, 31 (77%) had died. For the cohort as a whole diabetes and renal failure accounted for 28% of all deaths. This differed from both the Australian population as a whole, and the general Indigenous Australian population. The presence of chronic disease did not predict mortality, nor did behaviours such as smoking. Multivariate predictors of mortality included age (Hazard ratio (95% CI)), 1.03 (1.01, 1.05), male sex, 2.17 (1.39, 3.39), poor mobility, 2.11 (1.34, 3.30) and cognitive impairment 2.19 (1.31, 3.65). Cognitive impairment and dementia are major predictors of mortality in remote Indigenous Australians.

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.

Objective This study aimed to develop a culturally acceptable and valid scale to assess depressive symptoms in older Indigenous Australians, to determine the prevalence of depressive disorders in the older Kimberley community, and to investigate the sociodemographic, lifestyle and clinical factors associated with depression in this population. Methods Cross-sectional survey of adults aged 45 years or over from six remote Indigenous communities in the Kimberley and 30% of those living in Derby, Western Australia. The 11 linguistic and culturally sensitive items of the Kimberley Indigenous Cognitive Assessment of Depression (KICA-dep) scale were derived from the signs and symptoms required to establish the diagnosis of a depressive episode according to the DSM-IV-TR and ICD-10 criteria, and their frequency was rated on a 4-point scale ranging from ‘never’ to ‘all the time’ (range of scores: 0 to 33). The diagnosis of depressive disorder was established after a face-to-face assessment with a consultant psychiatrist. Other measures included sociodemographic and lifestyle factors, and clinical history. Results The study included 250 participants aged 46 to 89 years (mean±SD = 60.9±10.7), of whom 143 (57.2%) were women. The internal reliability of the KICA-dep was 0.88 and the cut-point 7/8 (non-case/case) was associated with 78% sensitivity and 82% specificity for the diagnosis of a depressive disorder. The point-prevalence of a depressive disorder in this population was 7.7%; 4.0% for men and 10.4% for women. Heart problems were associated with increased odds of depression (odds ratio = 3.3, 95% confidence interval = 1.2,8.8). Conclusions The KICA-dep has robust psychometric properties and can be used with confidence as a screening tool for depression among older Indigenous Australians. Depressive disorders are common in this population, possibly because of increased stressors and health morbidities.

Abstract Background Depression is a leading cause of disability worldwide and depressive symptoms are common in later life. Observational evidence suggests that depression is more prevalent among people with high plasma homocysteine (tHcy), but the results of randomized trials to date have been unable to show that lowering tHcy through the supplementation of vitamins B6, B12 and folate benefits depressive symptoms. We designed the B-VITAGE trial to determine whether adjunctive treatment with vitamins B6, B12 and folate increases the efficacy of standard antidepressant treatment. Methods/Design The B-VITAGE trial is a 12-month randomized, double-blind, placebo-controlled trial of daily citalopram (20 to 40 mg) plus B12(0.4 mg), B6 (25 mg) and folic acid (2 mg) or citalopram (20 to 40 mg) plus placebo for the treatment of depression in later life. The trial aims to recruit over 300 older adults with major depression (DSM-IV) and has been powered to detect the impact of an intervention associated with moderate effect size. Depressive symptoms will be rated with the Montgomery-Åsberg Depression Rating Scale (MADRS). The trial has two main outcomes of interest: a reduction of 50% or more in the MADRS total score between baseline and week 12 and the remission of the depressive episode at weeks 12, 26 and 52 according to DSM-IV criteria. We hypothesize that subjects randomly allocated to the vitamin arm of the study will be more likely to show a clinically significant improvement and achieve and maintain remission of symptoms at 12, 26 and 52 weeks. Secondary outcomes of interest include compliance with treatment, reduction in the severity of depressive symptoms, switching to different antidepressants, the use of non-pharmacological antidepressant treatments, response to treatment according to MTHFRC677T genotype, and changes in cognitive function over 52 weeks. Conclusions The results of this trial will clarify whether the systematic use of B-vitamins improves the response of older adults to standard antidepressant treatment. We anticipate that our findings will have implications for clinical practice and health policy development. Trial Registration The trial is registered with the Australian Clinical Trials Registry, trial number (())ACTRN12609000256279.

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.

OBJECTIVE:To review the effect of cholinesterase inhibitors on the behavioural and neuropsychiatric symptoms of dementia and discuss the current clinical guidelines for the prescription of cholinesterase inhibitors in Australia.METHOD:This paper reports the case of a patient with clinical diagnosis of dementia with lewy bodies (DLB) who was referred to an old age psychiatry service for the treatment of severe visual hallucinations and behavioural problems.RESULTS:Pharmacological treatment with olanzapine produced marked parkinsonism, agitation and confusion. A cholinesterase inhibitor, donepezil, was introduced. The introduction of donepezil was associated with cognitive improvement (mini-mental state examination [MMSE] increased from 23 to 27) and complete remission of behavioural symptoms.CONCLUSION:That cholinesterase inhibitors may have a role in the management of behavioural symptoms of dementia and the current Australian PBS guidelines for prescribing cholinesterase inhibitors are clinically restrictive. This has clinical and ethical implications that need to be addressed by consumers, the medical community and regulating authorities.