scholarly journals Kidney disease and risk of dementia: a Danish nationwide cohort study

BMJ Open ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. e052652
Author(s):  
Alisa D Kjaergaard ◽  
Benjamin R Johannesen ◽  
Henrik T Sørensen ◽  
Victor W Henderson ◽  
Christian F Christiansen

ObjectivesIt is unclear whether kidney disease is a risk factor for developing dementia. We examined the association between kidney disease and risk of future dementia.Design and settingNationwide historical registry-based cohort study in Denmark based on data from 1 January 1995 until 31 December 2016.ParticipantsAll patients diagnosed with kidney disease and matched general population cohort without kidney disease (matched 1:5 on age, sex and year of kidney disease diagnosis).Primary and secondary outcome measuresAll-cause dementia and its subtypes: Alzheimer’s disease, vascular dementia and other specified or unspecified dementia. We computed 5-year cumulative incidences (risk) and hazard ratios (HRs) for outcomes using Cox regression analyses.ResultsThe study cohort comprised 82 690 patients with kidney disease and 413 405 individuals from the general population. Five-year and ten-year mortality rates were twice as high in patients with kidney disease compared with the general population. The 5-year risk for all-cause dementia was 2.90% (95% confidence interval: 2.78% to 3.08%) in patients with kidney disease and 2.98% (2.92% to 3.04%) in the general population. Compared with the general population, the adjusted HRs for all-cause dementia in patients with kidney disease were 1.06 (1.00 to 1.12) for the 5-year follow-up and 1.08 (1.03 to 1.12) for the entire study period. Risk estimates for dementia subtypes differed substantially and were lower for Alzheimer’s disease and higher for vascular dementia.ConclusionsPatients diagnosed with kidney disease have a modestly increased rate of dementia, mainly driven by vascular dementia. Moreover, patients with kidney disease may be underdiagnosed with dementia due to high mortality and other comorbidities of higher priority.

BMJ Open ◽  
2018 ◽  
Vol 8 (9) ◽  
pp. e022404 ◽  
Author(s):  
Iain M Carey ◽  
H Ross Anderson ◽  
Richard W Atkinson ◽  
Sean D Beevers ◽  
Derek G Cook ◽  
...  

ObjectiveTo investigate whether the incidence of dementia is related to residential levels of air and noise pollution in London.DesignRetrospective cohort study using primary care data.Setting75 Greater London practices.Participants130 978 adults aged 50–79 years registered with their general practices on 1 January 2005, with no recorded history of dementia or care home residence.Primary and secondary outcome measuresA first recorded diagnosis of dementia and, where specified, subgroups of Alzheimer’s disease and vascular dementia during 2005–2013. The average annual concentrations during 2004 of nitrogen dioxide (NO2), particulate matter with a median aerodynamic diameter ≤2.5 µm (PM2.5) and ozone (O3) were estimated at 20×20 m resolution from dispersion models. Traffic intensity, distance from major road and night-time noise levels (Lnight) were estimated at the postcode level. All exposure measures were linked anonymously to clinical data via residential postcode. HRs from Cox models were adjusted for age, sex, ethnicity, smoking and body mass index, with further adjustments explored for area deprivation and comorbidity.Results2181 subjects (1.7%) received an incident diagnosis of dementia (39% mentioning Alzheimer’s disease, 29% vascular dementia). There was a positive exposure response relationship between dementia and all measures of air pollution except O3, which was not readily explained by further adjustment. Adults living in areas with the highest fifth of NO2concentration (>41.5 µg/m3) versus the lowest fifth (<31.9 µg/m3) were at a higher risk of dementia (HR=1.40, 95% CI 1.12 to 1.74). Increases in dementia risk were also observed with PM2.5, PM2.5specifically from primary traffic sources only and Lnight, but only NO2and PM2.5remained statistically significant in multipollutant models. Associations were more consistent for Alzheimer’s disease than vascular dementia.ConclusionsWe have found evidence of a positive association between residential levels of air pollution across London and being diagnosed with dementia, which is unexplained by known confounding factors.


2018 ◽  
Vol 31 (04) ◽  
pp. 571-577 ◽  
Author(s):  
Margaret Miller ◽  
Dennis Orwat ◽  
Gelareh Rahimi ◽  
Jacobo Mintzer

ABSTRACTIntroduction:The relationship between Alzheimer’s Disease (AD) and alcohol addiction is poorly characterized. Arrests for driving under the influence (DUI) can serve as a proxy for alcohol addiction. Therefore, the potential association between DUI and AD could be helpful in understanding the relationship between alcohol abuse and AD.Materials and methods:A retrospective, population-based cohort study using state health and law enforcement data was performed. The study cross-referenced 141,281 South Carolina Alzheimer’s Disease Registry cases with state law enforcement data.Results:Of the 2,882 registry cases (1.4%) found to have a history of at least one DUI arrest, cases were predominantly White (58.7%) and male (77.4%). Results showed a correlation coefficient of 0.7 (p &lt; 0.0001) between the age of first DUI arrest and the age of AD diagnosis. A dose-response relationship between the number of DUIs and age of AD onset was found to exist, where those with a history of DUI arrest were diagnosed an average of 9.1 years earlier, with a further 1.8 years earlier age at diagnosis in those with two or more arrests for DUI. A history of DUI arrest was also found to be negatively associated with survival after diagnosis, with a 10% decreased life expectancy in those with a DUI arrest history.Conclusions:Driving under the influence, a potential indicator of alcohol addiction, is associated with an earlier onset of AD registry diagnosis and shortened survival after diagnosis. This study contributes to the growing body of evidence suggesting that some cases of AD are alcohol related and, possibly, postponable or preventable.


Drugs & Aging ◽  
2018 ◽  
Vol 35 (11) ◽  
pp. 985-992
Author(s):  
Anna-Maija Tolppanen ◽  
Miia Tiihonen ◽  
Heidi Taipale ◽  
Marjaana Koponen ◽  
Antti Tanskanen ◽  
...  

2020 ◽  
Vol 16 (S10) ◽  
Author(s):  
Saima Basit ◽  
Mette Brimnes Damholt ◽  
Jan Wohlfahrt ◽  
Heather A Boyd

2022 ◽  
Vol 14 (1) ◽  
Author(s):  
Peter Hermann ◽  
Anna Villar-Piqué ◽  
Matthias Schmitz ◽  
Christian Schmidt ◽  
Daniela Varges ◽  
...  

Abstract Background Lipocalin-2 is a glycoprotein that is involved in various physiological and pathophysiological processes. In the brain, it is expressed in response to vascular and other brain injury, as well as in Alzheimer’s disease in reactive microglia and astrocytes. Plasma Lipocalin-2 has been proposed as a biomarker for Alzheimer’s disease but available data is scarce and inconsistent. Thus, we evaluated plasma Lipocalin-2 in the context of Alzheimer’s disease, differential diagnoses, other biomarkers, and clinical data. Methods For this two-center case-control study, we analyzed Lipocalin-2 concentrations in plasma samples from a cohort of n = 407 individuals. The diagnostic groups comprised Alzheimer’s disease (n = 74), vascular dementia (n = 28), other important differential diagnoses (n = 221), and healthy controls (n = 84). Main results were validated in an independent cohort with patients with Alzheimer’s disease (n = 19), mild cognitive impairment (n = 27), and healthy individuals (n = 28). Results Plasma Lipocalin-2 was significantly lower in Alzheimer’s disease compared to healthy controls (p < 0.001) and all other groups (p < 0.01) except for mixed dementia (vascular and Alzheimer’s pathologic changes). Areas under the curve from receiver operation characteristics for the discrimination of Alzheimer’s disease and healthy controls were 0.783 (95%CI: 0.712–0.855) in the study cohort and 0.766 (95%CI: 0.627–0.905) in the validation cohort. The area under the curve for Alzheimer’s disease versus vascular dementia was 0.778 (95%CI: 0.667–0.890) in the study cohort. In Alzheimer’s disease patients, plasma Lipocalin2 did not show significant correlation with cerebrospinal fluid biomarkers of neurodegeneration and AD-related pathology (total-tau, phosphorylated tau protein, and beta-amyloid 1-42), cognitive status (Mini Mental Status Examination scores), APOE genotype, or presence of white matter hyperintensities. Interestingly, Lipocalin 2 was lower in patients with rapid disease course compared to patients with non-rapidly progressive Alzheimer’s disease (p = 0.013). Conclusions Plasma Lipocalin-2 has potential as a diagnostic biomarker for Alzheimer’s disease and seems to be independent from currently employed biomarkers.


BMJ Open ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. e019684 ◽  
Author(s):  
Grazia Dell’Agnello ◽  
Urvi Desai ◽  
Noam Y Kirson ◽  
Jody Wen ◽  
Mark K Meiselbach ◽  
...  

ObjectivesEvaluate the reliability of using diagnosis codes and prescription data to identify the timing of symptomatic onset, cognitive assessment and diagnosis of Alzheimer’s disease (AD) among patients diagnosed with AD.MethodsThis was a retrospective cohort study using the UK Clinical Practice Research Datalink (CPRD). The study cohort consisted of a random sample of 50 patients with first AD diagnosis in 2010–2013. Additionally, patients were required to have a valid text-field code and a hospital episode or a referral in the 3 years before the first AD diagnosis. The earliest indications of cognitive impairment, cognitive assessment and AD diagnosis were identified using two approaches: (1) using an algorithm based on diagnostic codes and prescription drug information and (2) using information compiled from manual review of both text-based and coded data. The reliability of the code-based algorithm for identifying the earliest dates of the three measures described earlier was evaluated relative to the comprehensive second approach. Additionally, common cognitive assessments (with and without results) were described for both approaches.ResultsThe two approaches identified the same first dates of cognitive symptoms in 33 (66%) of the 50 patients, first cognitive assessment in 29 (58%) patients and first AD diagnosis in 43 (86%) patients. Allowing for the dates from the two approaches to be within 30 days, the code-based algorithm’s success rates increased to 74%, 70% and 94%, respectively. Mini-Mental State Examination was the most commonly observed cognitive assessment in both approaches; however, of the 53 tests performed, only 19 results were observed in the coded data.ConclusionsThe code-based algorithm shows promise for identifying the first AD diagnosis. However, the reliability of using coded data to identify earliest indications of cognitive impairment and cognitive assessments is questionable. Additionally, CPRD is not a recommended data source to identify results of cognitive assessments.


2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Márcia L. Chaves ◽  
Ana L. Camozzato ◽  
Cristiano Köhler ◽  
Jeffrey Kaye

Introduction. This study evaluates the progression of dementia and identifies prognostic risk factors for dementia.Methods. A group of 80 Brazilian community residents with dementia (34 with Alzheimer's disease and 46 with vascular dementia) was assessed over the course of 2 years. Data were analyzed with Cox regression survival analysis.Results. The data showed that education predicted cognitive decline (HR=1.2;P<.05) when analyzed without controlling for vascular risk factors. After the inclusion of vascular risk factors, education (HR=1.32;P<.05) and hypertension were predictive for cognitive decline (HR=38;P<.05), and Alzheimer's disease diagnosis was borderline predictive (P=.055).Conclusion.Vascular risk factors interacted with the diagnosis of vascular dementia. Education was a strong predictor of decline.


BMJ ◽  
2021 ◽  
pp. n1954 ◽  
Author(s):  
Manuella Lech Cantuaria ◽  
Frans Boch Waldorff ◽  
Lene Wermuth ◽  
Ellen Raben Pedersen ◽  
Aslak Harbo Poulsen ◽  
...  

Abstract Objective To investigate the association between long term residential exposure to road traffic and railway noise and risk of incident dementia. Design Nationwide prospective register based cohort study. Setting Denmark. Participants 1 938 994 adults aged ≥60 years living in Denmark between 1 January 2004 and 31 December 2017. Main outcome measures Incident cases of all cause dementia and dementia subtypes (Alzheimer’s disease, vascular dementia, and Parkinson’s disease related dementia), identified from national hospital and prescription registries. Results The study population included 103 500 participants with incident dementia, and of those, 31 219 received a diagnosis of Alzheimer’s disease, 8664 of vascular dementia, and 2192 of Parkinson’s disease related dementia. Using Cox regression models, 10 year mean exposure to road traffic and railway noise at the most (L den max) and least (L den min) exposed façades of buildings were associated with a higher risk of all cause dementia. These associations showed a general pattern of higher hazard ratios with higher noise exposure, but with a levelling off or even small declines in risk at higher noise levels. In subtype analyses, both road traffic noise and railway noise were associated with a higher risk of Alzheimer’s disease, with hazard ratios of 1.16 (95% confidence interval 1.11 to 1.22) for road L den max ≥65 dB compared with <45 dB, 1.27 (1.22 to 1.34) for road L den min ≥55 dB compared with <40 dB, 1.16 (1.10 to 1.23) for railway L den max ≥60 dB compared with <40 dB, and 1.24 (1.17 to 1.30) for railway L den min ≥50 dB compared with <40 dB. Road traffic, but not railway, noise was associated with an increased risk of vascular dementia. Results indicated associations between road traffic L den min and Parkinson’s disease related dementia. Conclusions This nationwide cohort study found transportation noise to be associated with a higher risk of all cause dementia and dementia subtypes, especially Alzheimer’s disease.


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