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American Academy of Neurology (AAN), Neurology, 17(92), p. e2015-e2026, 2019

DOI: 10.1212/wnl.0000000000007373

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Effects of Lewy body disease and Alzheimer disease on brain atrophy and cognitive dysfunction

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

ObjectivesTo investigate the independent and interaction effects of Alzheimer disease (AD) and Lewy body disease (LBD) on cognition and brain atrophy.MethodsWe consecutively recruited 38 controls and 108 patients with AD-related cognitive impairment (ADCI) and/or LBD-related cognitive impairment (LBCI) from university-based dementia and movement clinics. Diagnoses of ADCI and LBCI were supported by 18F-florbetaben PET and 18F-N-(3-fluoropropyl)-2β-carbon ethoxy-3β-(4-iodophenyl) nortropane–PET, respectively. There were 38 controls, 26 patients with pure ADCI (18 mild cognitive impairment [MCI] and 8 dementia), 28 patients with pure LBCI (13 MCI and 15 dementia), and 54 patients with mixed ADCI and LBCI (17 MCI and 37 dementia). We performed group-wise comparisons for neuropsychological z scores and regional cortical thickness. We also evaluated the effects of ADCI and LBCI using general linear models.ResultsCompared to the controls, patients in the pure ADCI group and pure LBCI group had focused cortical thinning in the bilateral entorhinal/right anterior temporal cortices and bilateral anteromedial temporal/basal frontal cortices, respectively, while the mixed disease group had additional cortical thinning in the widespread association cortices. The independent effects of ADCI and LBCI on regional cortical thinning overlapped in the widespread association cortices, especially at the bilateral temporoparietal junction and parietal cortices. ADCI and LBCI had independent detrimental effects on the copying item of the Rey-Osterrieth Complex Figure Test.ConclusionsConcomitant ADCI and LBCI are associated with the accentuation of neurodegeneration to widespread association cortices, and both diseases contribute to visuospatial dysfunction.