Silvia Morbelli1,2, Andrea Chincarini3, Matthias Brendel4, Axel Rominger4,5, Rose Bruffaerts6,7, Rik Vandenberghe6,7, Milica G Kramberger8, Maja Trost8,9, Valentina Garibotto10, Nicolas Nicastro11,12, Giovanni B Frisoni13, Afina W Lemstra14, Jessica van der Zande14, Andrea Pilotto15,16, Alessandro Padovani15, Sara Garcia-Ptacek17,18, Irina Savitcheva19, Miguel A Ochoa-Figueroa20,21,22, Annette Davidsson20, Valle Camacho23, Enrico Peira3,24, Dario Arnaldi1,24, Matteo Bauckneht1,2, Matteo Pardini1,24, Gianmario Sambuceti1,2, Dag Aarsland25,26, Flavio Nobili1,24. 1. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. 2. Nuclear Medicine Unit, Department of Health Sciences, University of Genoa. 3. National Institute of Nuclear Physics (INFN), Genoa section, Genoa, Italy. 4. Department of Nuclear Medicine, University Hospital, LMU Munich, Munich, Germany. 5. Department of Nuclear Medicine, Inselspital, University Hospital Bern, Bern, Switzerland. 6. Laboratory for Cognitive Neurology, Department of Neurosciences, KU Leuven, Belgium. 7. Neurology Department, University Hospitals Leuven, Leuven, Belgium. 8. Department of Neurology, University Medical Centre, Ljubljana, Slovenia. 9. Faculty of Medicine, University of Ljubljana, Slovenia. 10. Division of Nuclear Medicine and Molecular Imaging, Geneva University Hospitals and NIMTLab, Geneva University. 11. Department of Clinical Neurosciences, Geneva University Hospitals, Switzerland. 12. Department of Psychiatry, University of Cambridge, United Kingdom. 13. LANVIE (Laboratoire de Neuroimagerie du Vieillissement), Department of Psychiatry, Geneva University Hospitals, Geneva, Switzerland. 14. VU Medical Center Alzheimer Center, Amsterdam, The Netherlands. 15. Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy. 16. Parkinson's Disease Rehabilitation Centre, FERB ONLUS - S. Isidoro Hospital, Trescore Balneario (BG), Italy. 17. Department of Clinical Geriatrics, division of Neurobiology, Care Sciences and Society, Karolinska Institutet. 18. Internal Medicine, section for Neurology, Sädersjukhuset, Stockholm, Sweden. 19. Department of Radiology, Karolinska Institutet, Stockholm, Sweden. 20. Department of Clinical Physiology, Institution of Medicine and Health Sciences, Linköping, Sweden. 21. Department of Diagnostic Radiology, Linköping University Hospital, Linköping, Sweden. 22. Center for Medical Image Science and Visualization (CMIV), Linköping University, Linköping, Sweden. 23. Servicio de Medicina Nuclear, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, España. 24. Clinical Neurology, Department of Neuroscience (DINOGMI), University of Genoa, Italy. 25. Centre for Age-Related Medicine (SESAM), Stavanger University Hospital, Stavanger, Norway. 26. Department of Old Age Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King's College London.
Abstract
OBJECTIVE: To identify brain regions whose metabolic impairment contributes to dementia with Lewy bodies (DLB) clinical core features expression and to assess the influence of severity of global cognitive impairment on the DLB hypometabolic pattern. METHODS: Brain fluorodeoxyglucose positron emission tomography and information on core features were available in 171 patients belonging to the imaging repository of the European DLB Consortium. Principal component analysis was applied to identify brain regions relevant to the local data variance. A linear regression model was applied to generate core-feature-specific patterns controlling for the main confounding variables (Mini-Mental State Examination [MMSE], age, education, gender, and center). Regression analysis to the locally normalized intensities was performed to generate an MMSE-sensitive map. RESULTS: Parkinsonism negatively covaried with bilateral parietal, precuneus, and anterior cingulate metabolism; visual hallucinations (VH) with bilateral dorsolateral-frontal cortex, posterior cingulate, and parietal metabolism; and rapid eye movement sleep behavior disorder (RBD) with bilateral parieto-occipital cortex, precuneus, and ventrolateral-frontal metabolism. VH and RBD shared a positive covariance with metabolism in the medial temporal lobe, cerebellum, brainstem, basal ganglia, thalami, and orbitofrontal and sensorimotor cortex. Cognitive fluctuations negatively covaried with occipital metabolism and positively with parietal lobe metabolism. MMSE positively covaried with metabolism in the left superior frontal gyrus, bilateral-parietal cortex, and left precuneus, and negatively with metabolism in the insula, medial frontal gyrus, hippocampus in the left hemisphere, and right cerebellum. INTERPRETATION: Regions of more preserved metabolism are relatively consistent across the variegate DLB spectrum. By contrast, core features were associated with more prominent hypometabolism in specific regions, thus suggesting a close clinical-imaging correlation, reflecting the interplay between topography of neurodegeneration and clinical presentation in DLB patients. Ann Neurol 2019;85:715-725.
OBJECTIVE: To identify brain regions whose metabolic impairment contributes to dementia with Lewy bodies (DLB) clinical core features expression and to assess the influence of severity of global cognitive impairment on the DLB hypometabolic pattern. METHODS: Brain fluorodeoxyglucose positron emission tomography and information on core features were available in 171 patients belonging to the imaging repository of the European DLB Consortium. Principal component analysis was applied to identify brain regions relevant to the local data variance. A linear regression model was applied to generate core-feature-specific patterns controlling for the main confounding variables (Mini-Mental State Examination [MMSE], age, education, gender, and center). Regression analysis to the locally normalized intensities was performed to generate an MMSE-sensitive map. RESULTS:Parkinsonism negatively covaried with bilateral parietal, precuneus, and anterior cingulate metabolism; visual hallucinations (VH) with bilateral dorsolateral-frontal cortex, posterior cingulate, and parietal metabolism; and rapid eye movement sleep behavior disorder (RBD) with bilateral parieto-occipital cortex, precuneus, and ventrolateral-frontal metabolism. VH and RBD shared a positive covariance with metabolism in the medial temporal lobe, cerebellum, brainstem, basal ganglia, thalami, and orbitofrontal and sensorimotor cortex. Cognitive fluctuations negatively covaried with occipital metabolism and positively with parietal lobe metabolism. MMSE positively covaried with metabolism in the left superior frontal gyrus, bilateral-parietal cortex, and left precuneus, and negatively with metabolism in the insula, medial frontal gyrus, hippocampus in the left hemisphere, and right cerebellum. INTERPRETATION: Regions of more preserved metabolism are relatively consistent across the variegate DLB spectrum. By contrast, core features were associated with more prominent hypometabolism in specific regions, thus suggesting a close clinical-imaging correlation, reflecting the interplay between topography of neurodegeneration and clinical presentation in DLB patients. Ann Neurol 2019;85:715-725.
Authors: E E Wolters; M van de Beek; R Ossenkoppele; S S V Golla; S C J Verfaillie; E M Coomans; T Timmers; D Visser; H Tuncel; F Barkhof; R Boellaard; A D Windhorst; W M van der Flier; Ph Scheltens; A W Lemstra; B N M van Berckel Journal: Neuroimage Clin Date: 2020-11-19 Impact factor: 4.881
Authors: Nicolas Nicastro; Elijah Mak; Ajenthan Surendranathan; Timothy Rittman; James B Rowe; John T O'Brien Journal: Brain Imaging Behav Date: 2021-01-29 Impact factor: 3.978