Nicolaas I Bohnen1, Martijn L T M Müller2,3, Kirk A Frey2,4. 1. Departments of Radiology and Neurology, University of Michigan, and Neurology service and GRECC, VA Ann Arbor Healthcare System, Ann Arbor, MI, USA. nbohnen@umich.edu. 2. Departments of Radiology and Neurology, University of Michigan, and Neurology service and GRECC, VA Ann Arbor Healthcare System, Ann Arbor, MI, USA. 3. Functional Neuroimaging, Cognitive and Mobility Laboratory, Domino's Farms, University of Michigan, Lobby B, Suite 1000, Level I; 24 Frank Lloyd Wright Drive, Box 362, Ann Arbor, MI, 48105-9755, USA. 4. Department of Radiology, Division of Nuclear Medicine, 1500 East Medical Center Drive, Room B1-G505 UH, Ann Arbor, MI, 48109-5028, USA.
Abstract
PURPOSE OF REVIEW: The aims of the study were to review recent advances in molecular imaging in the Lewy body dementias (LBD) and determine if these may support the clinical but contested temporal profile distinction between Parkinson disease (PD) with dementia (PDD) versus dementia with Lewy bodies (DLB). RECENT FINDINGS: There do not appear to be major regional cerebral metabolic or neurotransmitter distinctions between PDD and DLB. However, recent studies highlight the relative discriminating roles of Alzheimer proteinopathies. PDD patients have lower cortical β-amyloid deposition than DLB. Preliminary tau PET studies suggest a gradient of increasing tau binding from cognitively normal PD (absent to lowest) to cognitively impaired PD (low) to DLB (intermediate) to Alzheimer disease (AD; highest). However, tau binding in DLB, including the medial temporal lobe, is substantially lower than in AD. Alzheimer-type proteinopathies appear to be more common in DLB compared to PDD with relative but no absolute differences. Given the spectrum of overlapping pathologies, future α-synuclein ligands are expected to have the best potential to distinguish the LBD from pure AD.
PURPOSE OF REVIEW: The aims of the study were to review recent advances in molecular imaging in the Lewy body dementias (LBD) and determine if these may support the clinical but contested temporal profile distinction between Parkinson disease (PD) with dementia (PDD) versus dementia with Lewy bodies (DLB). RECENT FINDINGS: There do not appear to be major regional cerebral metabolic or neurotransmitter distinctions between PDD and DLB. However, recent studies highlight the relative discriminating roles of Alzheimer proteinopathies. PDDpatients have lower cortical β-amyloid deposition than DLB. Preliminary tau PET studies suggest a gradient of increasing tau binding from cognitively normal PD (absent to lowest) to cognitively impaired PD (low) to DLB (intermediate) to Alzheimer disease (AD; highest). However, tau binding in DLB, including the medial temporal lobe, is substantially lower than in AD. Alzheimer-type proteinopathies appear to be more common in DLB compared to PDD with relative but no absolute differences. Given the spectrum of overlapping pathologies, future α-synuclein ligands are expected to have the best potential to distinguish the LBD from pure AD.
Entities:
Keywords:
Acetylcholine; Dementia with Lewy bodies; Diagnostic criteria; Dopamine; Parkinson disease with dementia; β-Amyloid
Authors: Roger L Albin; Amanda Fisher-Hubbard; Krithika Shanmugasundaram; Robert A Koeppe; James F Burke; Sandra Camelo-Piragua; Andrew P Lieberman; Bruno Giordani; Kirk A Frey Journal: Ann Neurol Date: 2015-08-25 Impact factor: 10.422
Authors: Igor F Tsigelny; Leslie Crews; Paula Desplats; Gideon M Shaked; Yuriy Sharikov; Hideya Mizuno; Brian Spencer; Edward Rockenstein; Margarita Trejo; Oleksandr Platoshyn; Jason X-J Yuan; Eliezer Masliah Journal: PLoS One Date: 2008-09-04 Impact factor: 3.240
Authors: Sean J Colloby; Rosie Watson; Andrew M Blamire; John T O'Brien; John-Paul Taylor Journal: Aust N Z J Psychiatry Date: 2019-11-07 Impact factor: 5.744