Cognitive differences in dementia patients with autopsy-verified AD, Lewy body pathology, or both

Kraybill, Matthew; Larson, Eric B.; Tsuang, Debby W.; Teri, Linda; McCormick, Wayne C.; Bowen, James D.; Kukull, Walter A.; Leverenz, James B.; Cherrier, Monique M.

doi:10.1212/01.wnl.0000165987.89198.65

Cited by 245 publications

(204 citation statements)

References 29 publications

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“…This pathological association seems to make part for cognitive alteration severity with a synergic effect (Clinton, Blurton-Jones et al 2010). Mixed dementia may be more aggressive than pure AD (Kraybill, Larson et al 2005). Since a low CSF -Syn level was detected in CSF of patients with DLB and Parkinson disease comparing to other neurodegenerative diseases, an association of this measurement with typical CSF biomarkers of AD seems interesting (Tokuda, Salem et al 2006;Kasuga, Tokutake et al 2010).…”

Section: Which Techniques Could Be Applied?mentioning

confidence: 97%

Alzheimer’s Diseases: Towards Biomarkers for an Early Diagnosis

Elmoualij¹,

Dupiereux-Fettweis²,

Seguin³

et al. 2011

The Clinical Spectrum of Alzheimer's Disease -the Charge Toward Comprehensive Diagnostic and Therapeutic Strategies

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Section: Which Techniques Could Be Applied?mentioning

confidence: 97%

Alzheimer’s Diseases: Towards Biomarkers for an Early Diagnosis

Elmoualij¹,

Dupiereux-Fettweis²,

Seguin³

et al. 2011

The Clinical Spectrum of Alzheimer's Disease -the Charge Toward Comprehensive Diagnostic and Therapeutic Strategies

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“…In the Lewy bodies disease spectrum of disorders, autopsy studies highlighted that co-occurrence of amyloid-b plaques and phosphorylated tau together with -synuclein deposition are associated with greater cognitive decline (Kraybill et al, 2005;Nelson et al, 2009;Ferman et al, 2015;Howlett et al, 2015), and shorter survival (Kotzbauer et al, 2012;Graff-Radford et al, 2015) .…”

Section: Introductionmentioning

confidence: 99%

Amyloid-β deposition and regional grey matter atrophy rates in dementia with Lewy bodies

Sarro¹,

Senjem

Lundt

et al. 2016

Brain

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Alzheimer's disease pathology frequently coexists with Lewy body disease at autopsy in patients with probable dementia with Lewy bodies. More than half of patients with probable dementia with Lewy bodies have high amyloid-b deposition as measured with 11 C-Pittsburgh compound B binding on positron emission tomography. Biomarkers of amyloid-b deposition precede neurodegeneration on magnetic resonance imaging during the progression of Alzheimer's disease, but little is known about how amyloid-b deposition relates to longitudinal progression of atrophy in patients with probable dementia with Lewy bodies. We investigated the associations between baseline 11 C-Pittsburgh compound B binding on positron emission tomography and the longitudinal rates of grey matter atrophy in a cohort of clinically diagnosed patients with dementia with Lewy bodies (n = 20), who were consecutively recruited to the Mayo Clinic Alzheimer's Disease Research Centre. All patients underwent 11 C-Pittsburgh compound B positron emission tomography and magnetic resonance imaging examinations at baseline. Follow-up magnetic resonance imaging was performed after a mean (standard deviation) interval of 2.5 (1.1) years. Regional grey matter loss was determined on threedimensional T 1 -weighted magnetic resonance imaging with the tensor-based morphometry-symmetric normalization technique. Linear regression was performed between baseline 11 C-Pittsburgh compound B standard unit value ratio and longitudinal change in regional grey matter volumes from an in-house modified atlas. We identified significant associations between greater baseline 11 C-Pittsburgh compound B standard unit value ratio and greater grey matter loss over time in the posterior cingulate gyrus, lateral and medial temporal lobe, and occipital lobe as well as caudate and putamen nuclei, after adjusting for age (P 5 0.05). Greater baseline 11 C-Pittsburgh compound B standard unit value ratio was also associated with greater ventricular expansion rates (P 5 0.01) and greater worsening over time in Clinical Dementia Rating Scale, sum of boxes (P = 0.02). In conclusion, in patients with probable dementia with Lewy bodies, higher amyloid-b deposition at baseline is predictive of faster neurodegeneration in the cortex and also in the striatum. This distribution is suggestive of possible interactions among amyloid-b, tau and a-synuclein aggregates, which needs further investigation. Furthermore, higher amyloid-b deposition at baseline predicts a faster clinical decline over time in patients with probable dementia with Lewy bodies. Keywords: DLB; structural MRI; beta-amyloid; amyloid imaging; brain atrophy Abbreviations: AChEI = acetylcholinesterase inhibitor; CDR-SOB = Clinical Dementia Rating scale, Sum of Boxes; DLB = dementia with Lewy bodies; MMSE = Mini-Mental State Examination; PiB = 11 C-Pittsburgh compound B; SUVR = standardized uptake value ratio; TBM-SyN = tensor-based morphometry using symmetric diffeomorphic image normalization; UPDRS-III =

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“…Research on the diagnosis and management of dementia with Lewy bodies (DLB) has increased greatly in the past decade [1][2][3][4][5][6][7][8][9][10][11]. Currently it is thought that DLB represents about 10-15% of all dementia cases [12].…”

Section: Introductionmentioning

confidence: 99%

Paired Studies Comparing Clinical Profiles of Lewy Body Dementia with Alzheimer’s and Parkinson’s Diseases

Scharre

Chang

Nagaraja

et al. 2016

JAD

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Abstract. Limited data compares clinical profiles of Lewy Body Dementia (LBD) with Alzheimer's disease (AD) andParkinson's disease (PD). Twenty-one mildly demented ambulatory LBD subjects were individually matched by MMSE score with 21 AD subjects and by UPDRS motor score with 21 PD subjects. Matched by age, gender, education, and race, pairs were compared using cognitive, functional, behavioral, and motor measures. LBD group performed worse than PD on axial motor, gait, and balance measures. AD had more amnesia and orientation impairments, but less executive and visuospatial deficits than LBD subjects. LBD group had more sleepiness, cognitive/behavioral fluctuations, hallucinations, and sleep apnea than AD or PD. Axial motor, gait, and balance disturbances correlated with executive, visuospatial, and global cognition deficits. LBD is differentiated from AD and PD by retrieval memory, visuospatial, and executive deficits; axial motor, gait and balance impairments; sleepiness, cognitive/behavioral fluctuations, hallucinations, and sleep apnea.

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Cognitive differences in dementia patients with autopsy-verified AD, Lewy body pathology, or both

Cited by 245 publications

References 29 publications

Alzheimer’s Diseases: Towards Biomarkers for an Early Diagnosis

Alzheimer’s Diseases: Towards Biomarkers for an Early Diagnosis

Amyloid-β deposition and regional grey matter atrophy rates in dementia with Lewy bodies

Paired Studies Comparing Clinical Profiles of Lewy Body Dementia with Alzheimer’s and Parkinson’s Diseases

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