Aline Mendes1, Vincent Noblet2,3, Mary Mondino2,3, Paulo Loureiro de Sousa2,3, Sumayya Manji2,3, Anne Archenault2,3, Michel Casanovas2,3, Olivier Bousiges4,5,6, Nathalie Philippi3,7,7, Seyyid Baloglu2,3,5, Lucie Rauch7, Benjamin Cretin3,7,7, Catherine Demuynck7, Catherine Milch7, Frédéric Blanc3,7,7
1Division of Geriatrics and Geneva Memory Center Geneva University Hospitals Geneva Switzerland
2Fédération de Médecine Translationnelle de Strasbourg (FMTS), University of Strasbourg, Strasbourg, France
3IMIS Team and IRIS Plateform ICube Laboratory UMR 7357 French National Centre for Scientific Research (CNRS) Strasbourg France
4Laboratoire de Biochimie et Biologie Moléculaire University Hospital of Strasbourg Strasbourg France
5Laboratoire de Neurosciences Cognitives et Adaptatives (LNCA) UMR 7364 CNRS Strasbourg France
6Neuroradiology Service University Hospital of Strasbourg Strasbourg France
7Memory Resources and Research Centre (CM2R) Geriatrics Day Hospital and Neuropsychology Unit Geriatrics Department and Neurology Service University Hospital of Strasbourg Strasbourg France
Tóm tắt
AbstractObjectivesTo determine the prevalence, localization and associations of cerebral microbleeds (CMB) in dementia with Lewy bodies (DLB) with its core clinical symptoms and cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD). We hypothesize DLB patients with CMB have increased amyloid burden compared to those without CMB, which could also translate into clinical differences.MethodsRetrospective cross‐sectional analysis from the AlphaLewyMA study (https://clinicaltrials.gov/ct2/show/NCT01876459). Patients underwent a standardized protocol of brain MRI including 3D T1, 3D FLAIR and T2* sequences, and CSF analysis of AD biomarkers. CMB and white matter hyperintensities (WMHs) were visually assessed in prodromal and mild demented (DLB, N = 91) and AD (AD, N = 67) patients.ResultsCMB prevalence did not differ among DLB and AD (24.2% vs. 37.3%; p = 0.081). CMB were mainly distributed in lobar topographies in both DLB (74%) and AD (89%). CMB in DLB was not associated with global cognitive performance, executive functioning, speed of information processing, or AD CSF biomarkers. Similarly, there was no difference regarding specific clinical symptoms: fluctuations, psychotic phenomena, sleep behavior disorder and Parkinsonism between DLB patients with and without CMB. AD patients with CMB had increased burden of WMH compared to those without (2.1 ± 0.86 vs. 1.4 ± 0.89; p = 0.005), according to Fazekas scale, whereas no significant difference was observed in DLB patients (1.68 ± 0.95 vs. 1.42 ± 0.91; p = 0.25).ConclusionCMB were equally prevalent with similar topographic distribution in both DLB and AD patients. CMB was not associated with CSF AD biomarkers or core clinical symptoms in DLB.
