Adam Martersteck1,2, Jaiashre Sridhar1, Christina Coventry1, Sandra Weintraub1,3, M-Marsel Mesulam1,4, Emily Rogalski1,3. 1. Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University (NU) Feinberg School of Medicine, Chicago, Illinois, USA. 2. NU Feinberg School of Medicine, Department of Radiology, Chicago, Illinois, USA. 3. NU Feinberg School of Medicine, Department of Psychiatry and Behavioral Sciences, Chicago, Illinois, USA. 4. NU Feinberg School of Medicine, Department of Neurology, Chicago, Illinois, USA.
Abstract
INTRODUCTION: Examination of pathologic, anatomic, and cognitive relationships has been limited in primary progressive aphasia (PPA) with underlying Alzheimer's disease (AD) neuropathology. METHODS: Spatial relationships between tau positron emission tomography (PET), cortical thickness, age, and naming on the Boston Naming Test (BNT) in PPA with biomarker evidence of AD (PPA-AD) were examined. RESULTS: Higher tau PET burden was associated with atrophy and younger age. There was a significant left-lateralized relationship between lower BNT and more atrophy, and between lower BNT and increased tau burden. Variance in naming was primarily shared between tau and atrophy (51%), but naming was uniquely explained more by atrophy (32%) than tau (16%). Higher left anterior temporal tau burden was associated with greater 1-year rate of decline in naming. DISCUSSION: PPA-AD has a similar relationship between abnormal biomarkers as first described in amnestic AD, with differing spatial extent, reflecting the left-lateralized nature of the language network.
INTRODUCTION: Examination of pathologic, anatomic, and cognitive relationships has been limited in primary progressive aphasia (PPA) with underlying Alzheimer's disease (AD) neuropathology. METHODS: Spatial relationships between tau positron emission tomography (PET), cortical thickness, age, and naming on the Boston Naming Test (BNT) in PPA with biomarker evidence of AD (PPA-AD) were examined. RESULTS: Higher tau PET burden was associated with atrophy and younger age. There was a significant left-lateralized relationship between lower BNT and more atrophy, and between lower BNT and increased tau burden. Variance in naming was primarily shared between tau and atrophy (51%), but naming was uniquely explained more by atrophy (32%) than tau (16%). Higher left anterior temporal tau burden was associated with greater 1-year rate of decline in naming. DISCUSSION: PPA-AD has a similar relationship between abnormal biomarkers as first described in amnestic AD, with differing spatial extent, reflecting the left-lateralized nature of the language network.
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