Institution
Danube University Krems
Education•Krems, Niederösterreich, Austria•
About: Danube University Krems is a education organization based out in Krems, Niederösterreich, Austria. It is known for research contribution in the topics: Stroke & Population. The organization has 498 authors who have published 1572 publications receiving 68797 citations.
Papers published on a yearly basis
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TL;DR: The use of ROBINS-I in GRADE assessments may allow for a better comparison of evidence from randomized controlled trials (RCTs) and nonrandomized studies (NRSs) because they are placed on a common metric for risk of bias.
406 citations
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TL;DR: This review discusses how executive deficits relate to pathology in specific territories of the basal ganglia, consider the impact of dopaminergic treatment on executive function (EF) in this context, and review the changes in EFs with disease progression.
Abstract: Executive dysfunction can be present from the early stages of Parkinson's disease (PD). It is characterized by deficits in internal control of attention, set shifting, planning, inhibitory control, dual task performance, and on a range of decision-making and social cognition tasks. Treatment with dopaminergic medication has variable effects on executive deficits, improving some, leaving some unchanged, and worsening others. In this review, we start by defining the specific nature of executive dysfunction in PD and describe suitable neuropsychological tests. We then discuss how executive deficits relate to pathology in specific territories of the basal ganglia, consider the impact of dopaminergic treatment on executive function (EF) in this context, and review the changes in EFs with disease progression. In later sections, we summarize correlates of executive dysfunction in PD with motor performance (e.g., postural instability, freezing of gait) and a variety of psychiatric (e.g., depression, apathy) and other clinical symptoms, and finally discuss the implications of these for the patients' daily life.
399 citations
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Broad Institute1, Harvard University2, deCODE genetics3, University of Oxford4, University of Copenhagen5, University of Michigan6, Yeshiva University7, Texas Biomedical Research Institute8, Wake Forest University9, University of Southern Denmark10, Pfizer11, Imperial College London12, Ealing Hospital13, National Health Service14, Hallym University15, Lund University16, University of Helsinki17, University of Texas Health Science Center at Houston18, Norwegian University of Science and Technology19, Uppsala University20, University of Bergen21, Aalborg University22, Novo Nordisk23, University of Eastern Finland24, Technische Universität München25, University of North Carolina at Chapel Hill26, University of Liverpool27, National Institute for Health and Welfare28, National University of Singapore29, Agency for Science, Technology and Research30, University of Iceland31, Danube University Krems32, King Abdulaziz University33, University of Pennsylvania34, University of Mississippi35, Churchill Hospital36, Massachusetts Institute of Technology37
TL;DR: In this article, the authors identified 12 rare protein-truncating variants in SLC30A8, which encodes an islet zinc transporter (ZnT8) and harbors a common variant (p.Trp325Arg) associated with T2D risk and glucose and proinsulin levels.
Abstract: Loss-of-function mutations protective against human disease provide in vivo validation of therapeutic targets, but none have yet been described for type 2 diabetes (T2D). Through sequencing or genotyping of ~150,000 individuals across 5 ancestry groups, we identified 12 rare protein-truncating variants in SLC30A8, which encodes an islet zinc transporter (ZnT8) and harbors a common variant (p.Trp325Arg) associated with T2D risk and glucose and proinsulin levels. Collectively, carriers of protein-truncating variants had 65% reduced T2D risk (P = 1.7 × 10(-6)), and non-diabetic Icelandic carriers of a frameshift variant (p.Lys34Serfs*50) demonstrated reduced glucose levels (-0.17 s.d., P = 4.6 × 10(-4)). The two most common protein-truncating variants (p.Arg138* and p.Lys34Serfs*50) individually associate with T2D protection and encode unstable ZnT8 proteins. Previous functional study of SLC30A8 suggested that reduced zinc transport increases T2D risk, and phenotypic heterogeneity was observed in mouse Slc30a8 knockouts. In contrast, loss-of-function mutations in humans provide strong evidence that SLC30A8 haploinsufficiency protects against T2D, suggesting ZnT8 inhibition as a therapeutic strategy in T2D prevention.
394 citations
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University of Belgrade1, Danube University Krems2, Max Planck Society3, University of Glasgow4, Vestre Viken Hospital Trust5, University Hospital Bonn6, Shaare Zedek Medical Center7, Radboud University Nijmegen8, Jewish General Hospital9, Pusan National University10, Samsung Medical Center11, Inha University12, Hallym University13, Gachon University14, University of Tuzla15, University of Michigan16, Rambam Health Care Campus17, Technion – Israel Institute of Technology18, University of Edinburgh19, university of lille20, Tel Aviv University21
TL;DR: PSD is proposed as a label for any dementia following stroke in temporal relation and no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD.
Abstract: Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing.
359 citations
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TL;DR: New, interim guidance to support the conduct of rapid reviews (RRs) produced within Cochrane and beyond is offered in response to requests for timely evidence syntheses for decision-making purposes including urgent health issues of high priority.
359 citations
Authors
Showing all 514 results
Name | H-index | Papers | Citations |
---|---|---|---|
Jaakko Tuomilehto | 115 | 1285 | 210682 |
Massimo Zeviani | 104 | 478 | 39743 |
J. Tuomilehto | 69 | 197 | 19801 |
Manfred Reichert | 67 | 695 | 19569 |
Roland W. Scholz | 64 | 289 | 15387 |
Michael Brainin | 55 | 215 | 44194 |
Gerald Gartlehner | 54 | 295 | 15320 |
Thomas Schrefl | 50 | 403 | 10867 |
Charity G. Moore | 50 | 179 | 11040 |
Josef Finsterer | 48 | 1479 | 13836 |
Silvia Miksch | 44 | 264 | 7790 |
J. Tuomilehto | 44 | 107 | 11425 |
Heinrich Schima | 43 | 249 | 5973 |
Reinhard Bauer | 40 | 228 | 5435 |
Thomas Groth | 38 | 186 | 5191 |