Digital screening tool for the assessment of cognitive impairment in unsupervised setting–digiDEM-SCREEN: study protocol for a validation study

Introduction
Dementia is one of the most relevant widespread diseases, with a prevalence of currently 55 million people with dementia worldwide. However, about 60–75% of people with dementia have not yet received a formal diagnosis. Asymptomatic screening of cognitive impairments using neuropsychiatric tests has been proven to efficiently enhance diagnosis rates. Digital screening tools, in particular, provide the advantage of being accessible without spatial or time restrictions. The study aims to validate a digital cognitive screening test (digiDEM-SCREEN) as an app in the German language.

Methods and analysis
This is a multicentre study in Bavaria. Participants are people with mild cognitive impairment, people with dementia in an early stage and cognitively healthy people. Recruitment will take place in specialised diagnostic facilities (memory outpatient clinics). 135 participants are aimed based on a power analysis. Sociodemographic data, diagnosis and results of neuropsychiatric tests (Consortium to Establish a Registry for Alzheimer’s Disease, Montreal Cognitive Assessment, digiDEM-SCREEN) will be collected at one point per person via electronic data capturing. The sensitivity, specificity and corresponding cut-off values will be determined based on receiver-operating-characteristic curves. The correlation of the digiDEM-SCREEN test with existing cognitive screening/testing procedures will be analysed.

Ethics and dissemination
The study obtained ethical approval from the Ethics Committee of the Julius-Maximilians-Universität of Würzburg (JMU) (application number: 177/23-sc). The test will give feedback about the current cognitive status and possible cognitive impairments that should lead to the users seeking further diagnostic measures by medical professionals. It will be accessible free of charge in established app stores. The results of the validation study will be published in peer-reviewed journals.

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Effects of aerobic exercise on cognitive function and quality of life in patients with Alzheimers disease: a systematic review and meta-analysis

Objectives
Numerous studies have examined the effects of physical activity on cognitive performance and executive function in people with Alzheimer’s disease (AD), although the findings are not entirely consistent. There are also insufficient study reviews for specific workout and assessment tool types. Therefore, the purpose of this study was to systematically investigate the effects of aerobic exercise on the quality of life, cognitive performance and depressive symptoms in people with AD.

Design
Risk of bias was assessed using the Cochrane risk of bias tool, systematic reviews and meta-analyses using random-effects modelling, and certainty of evidence using the Grading of Recommendations Assessment, Development and Evaluation tool.

Data sources
PubMed, Web of Science, Cochrane Library, EMBASE, Scopus, CINAHL and CNKI through 12 March 2024.

Eligibility criteria
The analysis includes all randomised controlled trials (RCTs) that used aerobic exercise as an intervention for individuals with AD.

Data extraction and synthesis
Two writers selected and searched for data using defined techniques. To investigate possible sources of heterogeneity between studies, meta-regression was carried out using Stata MP V.18.0 and V.14.0 software, standardised mean differences (SMDs) and 95% CIs were computed, and data were reviewed using Review Manager V.5.4 software, which was made available by the Cochrane Collaboration. Sensitivity analyses were employed to ascertain the stability and reliability of the results, and funnel plots and Egger’s test were employed to check for publication bias. Correction and assessment of publication bias was done using Duval and Tweedie clipping methods.

Results
Aerobic exercise enhanced cognitive function. For the Minimum Mental State Examination (MMSE) (SMD=0.95, 95% CI 0.58 to 1.32, Z=5.06, p

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Endometriosis and Ovarian Cancer

To the Editor As noted by Dr Barnard and colleagues, existing evidence confirms that endometriosis is associated with an elevated risk of ovarian cancer with differences by histotype. However, despite the varying presentations of endometriosis—most notably 3 macrosurgically visualized subphenotypes (endometriomas, superficial peritoneal, and/or deep lesions)—identifying women with endometriosis who are at high risk remains elusive. To address this question, the investigators leveraged data from the Utah Population Database and defined endometriosis subphenotypes by International Classification of Diseases (ICD) codes documented from 1992 to 2019 in more than 450 000 women. A consistent challenge in registry-based studies has been the selection of a comparison group. As demonstrated by Hermens et al in the Dutch nationwide registry, women diagnosed with ovarian cancer may be concurrently diagnosed with endometriosis, biasing estimated risk compared with members of the general population, who typically have not had pelvic surgery and whose endometriosis is more likely to remain undetected, leading to an observed 29 (95% CI, 20.7-40.9) times greater risk of endometrioid ovarian cancer (incident rate per 100 000 person-years, 29.7) when they included concurrent endometriosis diagnosis, but a much lower 2.6 (95% CI, 1.5-4.5)–fold greater risk when they excluded endometriosis diagnosed within 1 year of a diagnosis of ovarian cancer (incident rate per 100 000 person-years, 4.1). Unfortunately, Barnard and colleagues did not exclude concurrent diagnoses of ovarian cancer and endometriosis (17% of endometriosis and ovarian cancer diagnoses were within 5 mm under the peritoneal surface). Furthermore, since deep lesions were combined with endometriomas, the reader is unable to distinguish the true ovarian cancer risk for women with endometriomas vs deep lesions. Ultimately, the results may encourage clinicians to advise women with endometriomas or deep endometriosis toward prophylactic bilateral oophorectomy based on an overestimation of the true risk. Such an approach disregards the growing evidence of harm caused by inducing early menopause unnecessarily, including elevated risk of cardiovascular disease, bone fracture, and Alzheimer disease. As this is an essential question for women’s health, a reanalysis of the data are needed to guide women and clinicians in understanding a realistic estimation of their ovarian cancer risk and valid attribution to an accurately defined endometriosis subtype.

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Vascular Neurology Considerations for Antiamyloid Immunotherapy: A Science Advisory From the American Heart Association

Stroke, Ahead of Print. Antibodies directed at the amyloid-β peptide offer the prospect of disease-modifying therapy for early-stage Alzheimer disease but also carry the risk of brain edema or bleeding events, collectively designated amyloid-related imaging abnormalities. Introduction of the antiamyloid immunotherapies into practice is therefore likely to present a new set of questions for clinicians treating patients with cerebrovascular disease: Which manifestations of cerebrovascular disease should preclude, or permit, antibody treatment? Is it safe to prescribe amyloid immunotherapies to individuals who require antithrombotic treatment, or to administer thrombolysis to antibody-treated individuals with acute stroke? How should severe amyloid-related imaging abnormalities be managed? This science advisory summarizes the data and key considerations to guide these challenging decisions as the medical community collects further data and experience with these groundbreaking agents.

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Gastrointestinal syndromes in Parkinsons disease: risk factors or comorbidities?

With great interest, we read the article by Konings et al,1 in which the authors conducted a combined case–control and cohort study and found that dysphagia, gastroparesis, irritable bowel syndrome (IBS) without diarrhoea and constipation specifically predict subsequent newly onset idiopathic Parkinson’s disease (PD) through comparing patients with PD with matched negative controls and patients with Alzheimer’s disease (AD) and cerebrovascular diseases (CVDs). However, several methodological concerns should be carefully addressed before concluding that those gastrointestinal (GI) syndromes can predict the development of PD. First, reverse causation from the diagnostic delay of neurodegenerative diseases is a big concern,2 3 and not considering it in the analysis might lead to spurious associations (eg, the short-term increased PD risk after Clostridium difficile infection4). Given this diagnostic delay, the temporal relationship between GI syndromes and neurodegenerative disease in Konings et al’s study1…

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