title: Inverse relationship between cerebrovascular lesions and severity of lewy body pathology in patients with lewy body diseases.
abstract: Cerebrovascular pathology is a major cause of stroke and mortality. Studies on prevalence of cerebrovascular pathologies in dementia with Lewy bodies (DLBs) and Parkinson disease (PD) patients are scarce and contradictory. We aimed to determine the prevalence and severity of cerebrovascular pathologies in DLB and PD and to analyze their relationship to LB pathology. The prevalence and severity of atherosclerosis in the circle of Willis, cerebral amyloid angiopathy, cerebral infarcts, hemorrhages, small-vessel disease, white matter lesions, including the Consortium to Establish a Registry for Alzheimer Disease (CERAD) protocol as well as Braak neurofibrillary tangle stages for AD pathology were analyzed in autopsy-verified DLB (n = 13), PD (n = 102), and control subjects (n = 53). In all patient groups, the extent of LB pathology was inversely correlated to the severity of most vascular pathologies (atherosclerosis, infarcts, and small-vessel disease; all p < 0.05). By contrast, cerebral amyloid angiopathy, CERAD, and Braak neurofibrillary tangle stages were positively correlated with LB pathology (p < 0.05). Whereas the overall prevalence and severity of small-vessel disease, infarcts, hemorrhages, and white matter lesions were comparable among both disease groups, the extents of atherosclerosis, cerebral amyloid angiopathy, CERAD, and Braak neurofibrillary tangle stages were significantly higher in DLB than in those of PD patients (p < 0.05). Microinfarcts were statistically more prevalent in each patient group than in controls, whereas gross infarcts predominated in controls (p < 0.05 each). In conclusion, DLB and PD patients with advanced LB pathology were less likely to show severe cerebrovascular disease or history of stroke.
authors.affiliation: Institute for Clinical Neuroanatomy, J.W. Goethe-University, Frankfurt/Main, Germany. e.ghebremedhin@uq.edu.au
authors.forename: Estifanos
authors.initials: E
authors.lastname: Ghebremedhin
authors.forename: Albert
authors.initials: A
authors.lastname: Rosenberger
authors.forename: Udo
authors.initials: U
authors.lastname: Rüb
authors.forename: Mario
authors.initials: M
authors.lastname: Vuksic
authors.forename: Tzeggai
authors.initials: T
authors.lastname: Berhe
authors.forename: Heike
authors.initials: H
authors.lastname: Bickeböller
authors.forename: Rob A I
authors.initials: RA
authors.lastname: de Vos
authors.forename: Dietmar R
authors.initials: DR
authors.lastname: Thal
authors.forename: Thomas
authors.initials: T
authors.lastname: Deller
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016229:Amyloid beta-Peptides / Q000378:metabolism; D020520:Brain Infarction / Q000209:etiology / Q000473:pathology; D016022:Case-Control Studies; D002533:Cerebral Angiography / Q000379:methods; D002561:Cerebrovascular Disorders / Q000209:etiology*; D016009:Chi-Square Distribution; D002941:Circle of Willis / Q000473:pathology; D005260:Female; D006470:Hemorrhage / Q000209:etiology; D006801:Humans; D016631:Lewy Bodies / Q000473:pathology*; D020961:Lewy Body Disease / Q000150:complications* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D016874:Neurofibrillary Tangles / Q000473:pathology; D009460:Neurologic Examination / Q000379:methods; D010300:Parkinson Disease / Q000150:complications / Q000473:pathology; D025341:Principal Component Analysis / Q000379:methods; D012189:Retrospective Studies
chemical_list: D016229:Amyloid beta-Peptides