Publications
10 results found
Tunnicliffe L, Muzambi R, Bartlett JW, et al., 2024, Infection and telomere length: a systematic review protocol., BMJ Open, Vol: 14
INTRODUCTION: Telomeres are a measure of cellular ageing with potential links to diseases such as cardiovascular diseases and cancer. Studies have shown that some infections may be associated with telomere shortening, but whether an association exists across all types and severities of infections and in which populations is unclear. Therefore we aim to collate available evidence to enable comparison and to inform future research in this field. METHODS AND ANALYSIS: We will search for studies involving telomere length and infection in various databases including MEDLINE (Ovid interface), EMBASE (Ovid interface), Web of Science, Scopus, Global Health and the Cochrane Library. For grey literature, the British Library of electronic theses databases (ETHOS) will be explored. We will not limit by study type, geographical location, infection type or method of outcome measurement. Two researchers will independently carry out study selection, data extraction and risk of bias assessment using the ROB2 and ROBINS-E tools. The overall quality of the studies will be determined using the Grading of Recommendations Assessment, Development and Evaluation criteria. We will also evaluate study heterogeneity with respect to study design, exposure and outcome measurement and if there is sufficient homogeneity, a meta-analysis will be conducted. Otherwise, we will provide a narrative synthesis with results grouped by exposure category and study design. ETHICS AND DISSEMINATION: The present study does not require ethical approval. Results will be disseminated via publishing in a peer-reviewed journal and conference presentations. PROSPERO REGISTRATION NUMBER: CRD42023444854.
Doran W, Tunnicliffe L, Muzambi R, et al., 2024, Incident dementia risk among patients with type 2 diabetes receiving metformin versus alternative oral glucose-lowering therapy: an observational cohort study using UK primary healthcare records, BMJ Open Diabetes Research & Care, Vol: 12, ISSN: 2052-4897
Introduction 4.2 million individuals in the UK have type 2 diabetes, a known risk factor for dementia and mild cognitive impairment (MCI). Diabetes treatment may modify this association, but existing evidence is conflicting. We therefore aimed to assess the association between metformin therapy and risk of incident all-cause dementia or MCI compared with other oral glucose-lowering therapies (GLTs).Research design and methods We conducted an observational cohort study using the Clinical Practice Research Datalink among UK adults diagnosed with diabetes at ≥40 years between 1990 and 2019. We used an active comparator new user design to compare risks of dementia and MCI among individuals initially prescribed metformin versus an alternative oral GLT using Cox proportional hazards regression controlling for sociodemographic, lifestyle and clinical confounders. We assessed for interaction by age and sex. Sensitivity analyses included an as-treated analysis to mitigate potential exposure misclassification.Results We included 211 396 individuals (median age 63 years; 42.8% female), of whom 179 333 (84.8%) initiated on metformin therapy. Over median follow-up of 5.4 years, metformin use was associated with a lower risk of dementia (adjusted HR (aHR) 0.86 (95% CI 0.79 to 0.94)) and MCI (aHR 0.92 (95% CI 0.86 to 0.99)). Metformin users aged under 80 years had a lower dementia risk (aHR 0.77 (95% CI 0.68 to 0.85)), which was not observed for those aged ≥80 years (aHR 0.95 (95% CI 0.87 to 1.05)). There was no interaction with sex. The as-treated analysis showed a reduced effect size compared with the main analysis (aHR 0.90 (95% CI 0.83 to 0.98)).Conclusions Metformin use was associated with lower risks of incident dementia and MCI compared with alternative GLT among UK adults with diabetes. While our findings are consistent with a neuroprotective effect of metformin against dementia, further research is needed to reduce risks of confounding by indica
Muzambi R, Bhaskaran K, Rentsch CT, et al., 2022, Are infections associated with cognitive decline and neuroimaging outcomes? A historical cohort study using data from the UK Biobank study linked to electronic health records, Translational Psychiatry, Vol: 12
<jats:title>Abstract</jats:title><jats:p>While there is growing evidence of associations between infections and dementia risk, associations with cognitive impairment and potential structural correlates of cognitive decline remain underexplored. Here we aimed to investigate the presence and nature of any associations between common infections, cognitive decline and neuroimaging parameters. The UK Biobank is a large volunteer cohort (over 500,000 participants recruited aged 40–69) with linkage to primary and secondary care records. Using linear mixed effects models, we compared participants with and without a history of infections for changes in cognitive function during follow-up. Linear regression models were used to investigate the association of infections with hippocampal and white matter hyperintensity (WMH) volume. 16,728 participants (median age 56.0 years [IQR 50.0–61.0]; 51.3% women) had baseline and follow-up cognitive measures. We found no evidence of an association between the presence of infection diagnoses and cognitive decline for mean correct response time (slope difference [infections versus no infections] = 0.40 ms, 95% CI: −0.17–0.96 per year), visual memory (slope difference 0.0004 log errors per year, 95% CI: −0.003–0.004, fluid intelligence (slope difference 0.007, 95% CI: −0.010–0.023) and prospective memory (OR 0.88, 95% CI: 0.68–1.14). No evidence of an association was found between infection site, setting or frequency and cognitive decline except for small associations on the visual memory test. We found no association between infections and hippocampal or WMH volume. Limitations of our study include selection bias, potential practice effects and the relatively young age of our cohort. Our findings do not support a major role for common midlife infections in contributing to cognitive decline for this cohort. Further research is warranted in in
Beran M, Muzambi R, Geraets A, et al., 2022, The bidirectional longitudinal association between depressive symptoms and HbA<sub>1c</sub>: A systematic review and meta‐analysis, Diabetic Medicine, Vol: 39, ISSN: 0742-3071
<jats:title>Abstract</jats:title><jats:sec><jats:title>Aim</jats:title><jats:p>To investigate whether there is a bidirectional longitudinal association of depression with HbA<jats:sub>1c</jats:sub>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We conducted a systematic literature search in PubMed, PsycINFO, CINAHL and EMBASE for observational, longitudinal studies published from January 2000 to September 2020, assessing the association between depression and HbA<jats:sub>1c</jats:sub> in adults. We assessed study quality with the Newcastle‐Ottawa‐Scale. Pooled effect estimates were reported as partial correlation coefficients (r<jats:sub>p</jats:sub>) or odds ratios (OR).</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We retrieved 1642 studies; 26 studies were included in the systematic review and eleven in the meta‐analysis. Most studies (16/26) focused on type 2 diabetes. Study quality was rated as good (n = 19), fair (n = 2) and poor (n = 5). Of the meta‐analysed studies, six investigated the longitudinal association between self‐reported depressive symptoms and HbA<jats:sub>1c</jats:sub> and five the reverse longitudinal association, with a combined sample size of n = 48,793 and a mean follow‐up of 2 years. Higher levels of baseline depressive symptoms were associated with subsequent higher levels of HbA<jats:sub>1c</jats:sub> (partial r = 0.07; [95% CI 0.03, 0.12]; I<jats:sup>2</jats:sup>38%). Higher baseline HbA<jats:sub>1c</jats:sub> values were also associated with 18% increased risk of (probable) depression (OR = 1.18; [95% CI 1.12,1.25]; I<jats:sup>2</jats:sup>0.0%).</jats:p></jats:sec><jats:sec><jats:title>Conclu
Muzambi R, Bhaskaran K, Smeeth L, et al., 2021, Assessment of common infections and incident dementia using UK primary and secondary care data: a historical cohort study, The Lancet Healthy Longevity, Vol: 2, Pages: e426-e435, ISSN: 2666-7568
Geraets AFJ, Köhler S, Muzambi R, et al., 2020, The association of hyperglycaemia and insulin resistance with incident depressive symptoms over 4 years of follow-up: The Maastricht Study, Diabetologia, Vol: 63, Pages: 2315-2328, ISSN: 0012-186X
<jats:title>Abstract</jats:title><jats:sec><jats:title>Aims/hypothesis</jats:title><jats:p>Depression is twice as common in individuals with type 2 diabetes as in the general population. However, it remains unclear whether hyperglycaemia and insulin resistance are directly involved in the aetiology of depression. Therefore, we investigated the association of markers of hyperglycaemia and insulin resistance, measured as continuous variables, with incident depressive symptoms over 4 years of follow-up.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We used data from the longitudinal population-based Maastricht Study (<jats:italic>n</jats:italic> = 2848; mean age 59.9 ± 8.1 years, 48.8% women, 265 incident depression cases, 10,932 person-years of follow-up). We assessed hyperglycaemia by fasting and 2 h post-load OGTT glucose levels, HbA<jats:sub>1c</jats:sub> and skin autofluorescence (reflecting AGEs) at baseline. We used the Matsuda insulin sensitivity index and HOMA-IR to calculate insulin resistance at baseline. Depressive symptoms (nine-item Patient Health Questionnaire score ≥10) were assessed at baseline and annually over 4 years. We used Cox regression analyses, and adjusted for demographic, cardiovascular and lifestyle risk factors.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Fasting plasma glucose, 2 h post-load glucose and HbA<jats:sub>1c</jats:sub> levels were associated with an increased risk for incident depressive symptoms after full adjustment (HR 1.20 [95% CI 1.08, 1.33]; HR 1.25 [1.08, 1.44]; and HR 1.22 [1.09, 1.37] per SD, respectively), while skin autofluorescence, insulin sensitivity index and HOMA-IR were not (HR 0.99 [0.86, 1.13]; HR 1.02 [0.85, 1.25]; and HR 0.93 [0.81, 1.08], per SD, respectiv
Davidson J, Banerjee A, Muzambi R, et al., 2020, <p>Validity of Acute Cardiovascular Outcome Diagnoses Recorded in European Electronic Health Records: A Systematic Review</p>, Clinical Epidemiology, Vol: Volume 12, Pages: 1095-1111
Muzambi R, Bhaskaran K, Brayne C, et al., 2020, Common Bacterial Infections and Risk of Dementia or Cognitive Decline: A Systematic Review, Journal of Alzheimer's Disease, Vol: 76, Pages: 1609-1626, ISSN: 1387-2877
Davidson JA, Banerjee A, Muzambi R, et al., 2019, Validity of acute cardiovascular outcome diagnoses in European electronic health records: a systematic review protocol, BMJ Open, Vol: 9, Pages: e031373-e031373, ISSN: 2044-6055
<jats:sec><jats:title>Introduction</jats:title><jats:p>Cardiovascular diseases (CVDs) are among the leading causes of death globally. Electronic health records (EHRs) provide a rich data source for research on CVD risk factors, treatments and outcomes. Researchers must be confident in the validity of diagnoses in EHRs, particularly when diagnosis definitions and use of EHRs change over time. Our systematic review provides an up-to-date appraisal of the validity of stroke, acute coronary syndrome (ACS) and heart failure (HF) diagnoses in European primary and secondary care EHRs.</jats:p></jats:sec><jats:sec><jats:title>Methods and analysis</jats:title><jats:p>We will systematically review the published and grey literature to identify studies validating diagnoses of stroke, ACS and HF in European EHRs. MEDLINE, EMBASE, SCOPUS, Web of Science, Cochrane Library, OpenGrey and EThOS will be searched from the dates of inception to April 2019. A prespecified search strategy of subject headings and free-text terms in the title and abstract will be used. Two reviewers will independently screen titles and abstracts to identify eligible studies, followed by full-text review. We require studies to compare clinical codes with a suitable reference standard. Additionally, at least one validation measure (sensitivity, specificity, positive predictive value or negative predictive value) or raw data, for the calculation of a validation measure, is necessary. We will then extract data from the eligible studies using standardised tables and assess risk of bias in individual studies using the Quality Assessment of Diagnostic Accuracy Studies 2 tool. Data will be synthesised into a narrative format and heterogeneity assessed. Meta-analysis will be considered when a sufficient number of homogeneous studies are available. The overall quality of evidence will be assessed using the Grading of Recommendations, Assessment, Development
Muzambi R, Bhaskaran K, Brayne C, et al., 2019, Common bacterial infections and risk of incident cognitive decline or dementia: a systematic review protocol, BMJ Open, Vol: 9, Pages: e030874-e030874, ISSN: 2044-6055
<jats:sec><jats:title>Introduction</jats:title><jats:p>The global burden of dementia is rising, emphasising the urgent need to develop effective approaches to risk reduction. Recent evidence suggests that common bacterial infections may increase the risk of dementia, however the magnitude and timing of the association as well as the patient groups affected remains unclear. We will review existing evidence of the association between common bacterial infections and incident cognitive decline or dementia.</jats:p></jats:sec><jats:sec><jats:title>Methods and analysis</jats:title><jats:p>We will conduct a comprehensive search of published and grey literature from inception to 18 March 2019. The following electronic databases will be searched; MEDLINE, EMBASE, Global health, PsycINFO, Web of Science, Scopus, Cochrane Library, the Cumulative Index to Nursing and Allied Health Literature, Open Grey and the British Library of Electronic Theses databases. There will be no restrictions on the date, language or geographical location of the studies. We will include longitudinal studies with a common clinically symptomatic bacterial infection as an exposure and incident cognitive decline or dementia as an outcome. Study selection, data extraction and risk of bias will be performed independently by two researchers. We will assess the risk of bias using the Cochrane collaboration approach. The overall quality of the studies will be assessed using the Grading of Recommendations, Assessment, Development and Evaluations criteria. We will explore the heterogeneity of relevant studies and, if feasible, a meta-analysis will be performed, otherwise we will present a narrative synthesis. We will group the results by exposure and outcome definitions and differences will be described by subgroups and outcomes.</jats:p></jats:sec><jats:sec><jats:title>Ethics and dissemination</jats:title><jats:p>Et
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