Ran Lu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Ran Lu has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Monique M. B. Breteler
Population Health Sciences, German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany
3 shared publications - Tony Stöcker
German Center for Neurodegenerative Diseases, Bonn, Germany
3 shared publications - Kersten Diers
Image Analysis German Center for Neurodegenerative Diseases (DZNE) Bonn Germany
2 shared publications - Martin Reuter
German Center for Neurodegenerative Diseases (DZNE)
2 shared publications - Nasir Ahmad Aziz
Population Health Sciences, German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany
2 shared publications - Elke Hattingen
Institute for Neuroradiology, University Hospital Frankfurt, Frankfurt am Main, 60528, Germany
1 shared publication
Latest Publications
- Open Access
- 29 November 2021
- Published by Springer Nature in Neuroradiology
- Vol. 64 (3) , 503-512
Incidental findings on 3 T neuroimaging: cross-sectional observations from the population-based Rhineland Study
Purpose: Development of best practices for dealing with incidental findings on neuroimaging requires insight in their frequency and clinical relevance. Methods: Here, we delineate prevalence estimates with 95% confidence intervals and clinical management of incidental findings, based on the first 3589 participants of the population-based Rhineland Study (age range 30–95 years) who underwent 3 Tesla structural neuroimaging (3D, 0.8 mm3 isotropic resolution). Two trained raters independently assessed all scans for abnormalities, with confirmation and adjudication where needed by neuroradiologists. Participants were referred for diagnostic work-up depending on the potential benefit. Results: Of 3589 participants (mean age 55 ± 14 years, 2072 women), 867 had at least one possible incidental finding (24.2%). Most common were pituitary abnormalities (12.3%), arachnoid cysts (4.1%), developmental venous anomalies (2.5%), non-acute infarcts (1.8%), cavernomas (1.0%), and meningiomas (0.7%). Forty-six participants were informed about their findings, which was hitherto unknown in 40 of them (1.1%). Of these, in 19 participants (48%), a wait-and-see policy was applied and nine (23%) received treatment, while lesions in the remainder were benign, could not be confirmed, or the participant refused to inform us about their clinical diagnosis. Conclusion: Nearly one-quarter of participants had an incidental finding, but only 5% of those required referral, that mostly remained without direct clinical consequences.
- 29 November 2021
- Published by Springer Nature in Neuroradiology
- Vol. 64 (3) , 503-512
Open AccessIncidental findings on 3 T neuroimaging: cross-sectional observations from the population-based Rhineland Study
Purpose: Development of best practices for dealing with incidental findings on neuroimaging requires insight in their frequency and clinical relevance. Methods: Here, we delineate prevalence estimates with 95% confidence intervals and clinical management of incidental findings, based on the first 3589 participants of the population-based Rhineland Study (age range 30–95 years) who underwent 3 Tesla structural neuroimaging (3D, 0.8 mm3 isotropic resolution). Two trained raters independently assessed all scans for abnormalities, with confirmation and adjudication where needed by neuroradiologists. Participants were referred for diagnostic work-up depending on the potential benefit. Results: Of 3589 participants (mean age 55 ± 14 years, 2072 women), 867 had at least one possible incidental finding (24.2%). Most common were pituitary abnormalities (12.3%), arachnoid cysts (4.1%), developmental venous anomalies (2.5%), non-acute infarcts (1.8%), cavernomas (1.0%), and meningiomas (0.7%). Forty-six participants were informed about their findings, which was hitherto unknown in 40 of them (1.1%). Of these, in 19 participants (48%), a wait-and-see policy was applied and nine (23%) received treatment, while lesions in the remainder were benign, could not be confirmed, or the participant refused to inform us about their clinical diagnosis. Conclusion: Nearly one-quarter of participants had an incidental finding, but only 5% of those required referral, that mostly remained without direct clinical consequences.
- Open Access
- 26 March 2021
- Published by Wiley in Human Brain Mapping
- Vol. 42 (8) , 2434-2444
Insulin resistance accounts for metabolic syndrome‐related alterations in brain structure
Metabolic syndrome (MetS) is a major public health burden worldwide and associated with brain abnormalities. Although insulin resistance is considered a pivotal feature of MetS, its role in the pathogenesis of MetS‐related brain alterations in the general population is unclear. Therefore, in 973 participants (mean age 52.5 years) of the population‐based Rhineland Study, we assessed brain morphology in relation to MetS and insulin resistance, and evaluated to what extent the pattern of structural brain changes seen in MetS overlap with those associated with insulin resistance. Cortical reconstruction and volumetric segmentation were obtained from high‐resolution brain images at 3 Tesla using FreeSurfer. The relations between metabolic measures and brain structure were assessed through (generalized) linear models. Both MetS and insulin resistance were associated with smaller cortical gray matter volume and thickness, but not with white matter or subcortical gray matter volume. Age‐ and sex‐adjusted vertex‐based brain morphometry demonstrated that MetS and insulin resistance were related to cortical thinning in a similar spatial pattern. Importantly, no independent effect of MetS on cortical gray matter was observed beyond the effect of insulin resistance. Our findings suggest that addressing insulin resistance is critical in the prevention of MetS‐related brain changes in later life.
- 26 March 2021
- Published by Wiley in Human Brain Mapping
- Vol. 42 (8) , 2434-2444
Open AccessInsulin resistance accounts for metabolic syndrome‐related alterations in brain structure
Metabolic syndrome (MetS) is a major public health burden worldwide and associated with brain abnormalities. Although insulin resistance is considered a pivotal feature of MetS, its role in the pathogenesis of MetS‐related brain alterations in the general population is unclear. Therefore, in 973 participants (mean age 52.5 years) of the population‐based Rhineland Study, we assessed brain morphology in relation to MetS and insulin resistance, and evaluated to what extent the pattern of structural brain changes seen in MetS overlap with those associated with insulin resistance. Cortical reconstruction and volumetric segmentation were obtained from high‐resolution brain images at 3 Tesla using FreeSurfer. The relations between metabolic measures and brain structure were assessed through (generalized) linear models. Both MetS and insulin resistance were associated with smaller cortical gray matter volume and thickness, but not with white matter or subcortical gray matter volume. Age‐ and sex‐adjusted vertex‐based brain morphometry demonstrated that MetS and insulin resistance were related to cortical thinning in a similar spatial pattern. Importantly, no independent effect of MetS on cortical gray matter was observed beyond the effect of insulin resistance. Our findings suggest that addressing insulin resistance is critical in the prevention of MetS‐related brain changes in later life.
- Open Access
- 7 December 2020
- Published by Wiley in Alzheimer's & Dementia
- Vol. 16 (S10)
Insulin resistance accounts for metabolic syndrome‐related alterations in brain structure
Background: Metabolic syndrome (MetS) is a major public health burden worldwide and associated with brain abnormalities. Although insulin resistance is considered a pivotal feature of MetS, its role in the pathogenesis of MetS‐related brain alterations in the general population is unclear. Therefore, we aimed to 1) assess the relation of metabolic syndrome (MetS) and insulin resistance with brain structure, and 2) determine to what extent the effects of MetS on brain structure are due to insulin resistance.Methods: We used cross‐sectional data from 973 participants (43.4% male, mean age 52.5 years) of the Rhineland Study, an ongoing population‐based cohort study. MetS was defined in accordance with the revised criteria of the National Cholesterol Education Program Adult Treatment Panel III. Insulin resistance was assessed through fasting serum insulin and the homeostatic model assessment of insulin resistance. Cortical reconstruction and volumetric segmentation were obtained from high‐resolution brain images at 3 Tesla. The relation between metabolic measures and brain structural features was assessed through (generalized) linear models.Results: MetS and insulin resistance were both associated with smaller cortical gray matter volume and mean cortical thickness, but not with white matter or subcortical gray matter volume. Vertex‐based brain morphometry showed that MetS and insulin resistance were related to brain structure in a similar spatial pattern, with the largest effect sizes observed in the precentral cortex, transverse and superior temporal cortex, and the cuneus and its neighboring regions. There was no independent effect of MetS on cortical gray matter when additionally adjusted for insulin resistance.Conclusion: MetS and insulin resistance are associated with cortical gray matter thinning, especially in regions involved in motor regulation and auditory and visual processing, with insulin resistance largely accounting for MetS‐related changes in brain structure.
- 7 December 2020
- Published by Wiley in Alzheimer's & Dementia
- Vol. 16 (S10)
Open AccessInsulin resistance accounts for metabolic syndrome‐related alterations in brain structure
Background: Metabolic syndrome (MetS) is a major public health burden worldwide and associated with brain abnormalities. Although insulin resistance is considered a pivotal feature of MetS, its role in the pathogenesis of MetS‐related brain alterations in the general population is unclear. Therefore, we aimed to 1) assess the relation of metabolic syndrome (MetS) and insulin resistance with brain structure, and 2) determine to what extent the effects of MetS on brain structure are due to insulin resistance.Methods: We used cross‐sectional data from 973 participants (43.4% male, mean age 52.5 years) of the Rhineland Study, an ongoing population‐based cohort study. MetS was defined in accordance with the revised criteria of the National Cholesterol Education Program Adult Treatment Panel III. Insulin resistance was assessed through fasting serum insulin and the homeostatic model assessment of insulin resistance. Cortical reconstruction and volumetric segmentation were obtained from high‐resolution brain images at 3 Tesla. The relation between metabolic measures and brain structural features was assessed through (generalized) linear models.Results: MetS and insulin resistance were both associated with smaller cortical gray matter volume and mean cortical thickness, but not with white matter or subcortical gray matter volume. Vertex‐based brain morphometry showed that MetS and insulin resistance were related to brain structure in a similar spatial pattern, with the largest effect sizes observed in the precentral cortex, transverse and superior temporal cortex, and the cuneus and its neighboring regions. There was no independent effect of MetS on cortical gray matter when additionally adjusted for insulin resistance.Conclusion: MetS and insulin resistance are associated with cortical gray matter thinning, especially in regions involved in motor regulation and auditory and visual processing, with insulin resistance largely accounting for MetS‐related changes in brain structure.