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Objectives: To explore the strength of the association between cognitive functioning and depression and anxiety in older people without dementia. Methods: An exploratory, cross‐sectional analysis of Wave 1 (2004–2007) data from the Lothian Birth Cohort 1936 dataset. Three subgroups were based on Hospital Anxiety and Depression Scale (HADS) subscales: no probable anxiety or depression (N = 592), probable anxiety no depression (N = 122), probable depression with/without anxiety (depression) (N = 30). Regression analyses determined relationships between subgroups and identified cognitive test variables. Results: Participants were 744 individuals (male = 385 [51.5%]; mean [M] age = 69.5 years [Standard deviation = 0.83]); characteristics for subgroups were similar. Participants with probable depression had slower simple reaction time scores than those with no anxiety or depression (regression slope [β] on the log10 scale = 0.05, 95% Confidence Interval [0.03, 0.08], p ≤ 0.001). Those with probable anxiety had significantly worse scores on other tests: Spatial span (β = −0.80 [−1.36, −0.25], p ≤ 0.005), Symbol Search (β = −1.67 [−2.90, −0.45], p ≤ 0.01), Matrix Reasoning (β = −1.58 [−2.55, −0.60], p ≤ 0.005) and Block Design (β = −3.33 [−5.29, −1.37], p ≤ 0.001), than those without probable anxiety or depression. Conclusion: Probable depression and anxiety were found to be associated with lower cognitive function in those without evidence of dementia. People with probable anxiety showed poorer performance in tests that concerned making decisions. People with probable depression showed slower processing speed. [ABSTRACT FROM AUTHOR]

Background: Multimorbidity (the co-occurrence of multiple chronic conditions) is increasingly common, especially among people with dementia. Few neuroimaging studies have explored amyloid biomarkers in people with multimorbidity.Objective: We aimed to conduct the first study of the association between multimorbidity and cerebrospinal fluid amyloid-β42 (CSF Aβ).Method: The European Prevention of Alzheimer's Dementia (EPAD) Longitudinal Cohort Study V500.0 dataset includes volunteers aged ≥50 years from 12 sites. Participants undergo detailed phenotyping, including CSF measures and a self-reported medical history. Using logistic and linear regression analyses, we explored the association between multimorbidity and continuous chronic condition count with CSF Aβ positivity (Aβ42 <1000pg/ml) and continuous CSF Aβ concentration. All models were adjusted for age, sex, APOE status, education, and family history of dementia.Results: Among 447 eligible participants without dementia, the mean (SD) age was 66.6 (6.6) years, 234 (52.3%) were women, and 157 (35.1%) were amyloid positive. With chronic conditions regarded as pseudo-continuous, each additional condition carried a decreased likelihood of amyloid positivity (OR = 0.82, 95% CI: 0.68-0.97; p = 0.026). With CSF Aβ as a continuous variable, each additional condition was associated with an increase of 54.2 pg/ml (95% CI: 9.9-98.5, p = 0.017). Having ≥2 conditions was inversely associated with amyloid positivity (OR 0.59, 95% CI: 0.37-0.95, p = 0.030) compared to one or none.Conclusion: Our findings suggest that the established association between multimorbidity and dementia may be due to a pathway other than amyloid. However, this cross-sectional study does not allow us to make causal inferences. Longitudinal work is required to confirm the inverse association found. [ABSTRACT FROM AUTHOR]

ABSTRACTBackground:Smoking is a well-established risk factor for dementia, but the effects of passive smoking are unclear. We aimed to examine links between passive smoking and dementia or cognitive impairment.Methods: We searched seven medical research databases: MEDLINE, Web of Science (Core Collection), Cochrane, EMBASE, PsycINFO, Scopus, and CINAHL Plus. Studies were included if they examined measures of passive smoking and either cognitive impairment or dementia.Results: Of 1,425 records found, nine papers of varying methodologies were included after screening against inclusion criteria. Eight papers reported weak associations between passive smoking and either cognitive impairment or dementia. One paper only found this association alongside carotid artery stenosis. The papers' quality was variable, with only two deemed high quality.Conclusion: There is limited weak observational evidence linking passive smoking with an increased risk of cognitive impairment or dementia. However, the studies were methodologically diverse and of inconsistent quality, preventing firm conclusions. [ABSTRACT FROM AUTHOR]

Background: Polypharmacy, the concurrent use of multiple medicines, is increasing. Population‐wide studies of its association with dementia are lacking. We examined this relationship longitudinally, at a national level. Method: We used National Health Service community prescribing data from all adults in Scotland aged ≥50 years who received at least one drug in the first quarter of 2009. These data were linked to death records, including cause of death. We used Cox proportional hazards models to assess associations between the number of unique medicines dispensed in one quarter and mortality with any subtype of dementia over 8.5 years, in the whole sample and stratified by age. Result: The sample contained 1,225,894 people aged ≥50 years (mean age 67.4 (SD = 10.8) years, 56.1% female, 3.8% care home residents). The mean number of drugs dispensed at baseline was 5.0 (SD = 3.7). Over 8.5 years, there were 336,244 deaths, of which 58,358 had any subtype of dementia on the death certificate. Among the whole sample, the hazard ratio (HR) for dementia mortality with each additional medicine was 1.027 (95% CI 1.024‐1.028). In people aged 50‐64 years, the HR was 1.075 (1.061‐1.089); for 65‐79 year‐olds, HR = 1.043 (1.040‐1.047) and for those aged ≥80 years, HR = 1.009 (1.006‐1.012). All models were adjusted for baseline age, gender, care home residence status and deprivation index based on postcode. Conclusion: There was higher mortality with dementia as the number of dispensed medicines increased. Age‐stratified analyses showed that the association was stronger in younger age groups, perhaps reflecting that younger people taking medication for more comorbidities had an increased risk of dying with dementia. These analyses did not allow adjustment for multimorbidity or the consideration of individual drug classes. [ABSTRACT FROM AUTHOR]