Cortical PIB binding in Lewy body disease is associated with Alzheimer-like characteristics

Maetzler, Walter; Liepelt, Inga; Reimold, Matthias; Reischl, Gerald; Solbach, Christoph; Becker, Clemens; Schulte, Claudia; Leyhe, Thomas; Keller, Stefanie; Melms, Arthur; Gasser, Thomas; Berg, Daniela

doi:10.1016/j.nbd.2008.12.008

Cited by 158 publications

(113 citation statements)

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“…PiB retention is on average higher in patients with DLB than Parkinson's disease and Parkinson's disease dementia (Gomperts et al, 2008(Gomperts et al, , 2012, but lower than patients with Alzheimer's disease (Kantarci et al, 2012b;Catafau and Bullich, 2015). Furthermore, PiB retention has been shown to be associated with older age, higher prevalence of APOE "4 carriers (Maetzler et al, 2009), impaired cognitive performance (Gomperts et al, 2008(Gomperts et al, , 2012Maetzler et al, 2009) and lower PET glucose metabolism (Claassen et al, 2011) in patients with DLB. Villemagne et al (2011) suggested that greater amyloid-b deposition on PET is associated with a faster development of diagnostic clinical features after the onset of cognitive impairment in patients with DLB.…”

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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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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“…However, extracellular Aβ-amyloid plaques and intracellular tau neurofibrillary tangle are also observed at autopsy in PD, PDD, and DLB patients (Horvath, Herrmann, Burkhard, Bouras, & K€ ovari, 2013;Jellinger & Attems, 2008;Jellinger, Seppi, Wenning, & Poewe, 2002 of amyloid deposition in PD, PDD, and DLB. Overall these studies found that amyloid deposition tends to be modest in PD with normal cognition occurring in about 0%-13% of PD patients (Edison et al, 2013(Edison et al, , 2008Foster et al, 2010;Gomperts et al, 2012Gomperts et al, , 2008Johansson et al, 2008;Jokinen et al, 2010;Maetzler et al, 2009;Siderowf et al, 2014;Villemagne et al, 2011). Amyloid burden is generally low in PD subjects with mild cognitive impairment (MCI), and does not distinguish cognitively normal PD patients from PD-MCI (Foster et al, 2010;Gomperts et al, 2012Gomperts et al, , 2013Petrou et al, 2012).…”

Section: Misfolded Proteinsmentioning

confidence: 99%

“…Amyloid burden is generally low in PD subjects with mild cognitive impairment (MCI), and does not distinguish cognitively normal PD patients from PD-MCI (Foster et al, 2010;Gomperts et al, 2012Gomperts et al, , 2013Petrou et al, 2012). PDD patients have higher incidence of cortical Aβ-amyloid deposition compared to healthy subjects, PD and PD-MCI, ranging from 0% to 80% (Edison et al, 2013(Edison et al, , 2008Foster et al, 2010;Gomperts et al, 2012Gomperts et al, , 2008Jokinen et al, 2010;Maetzler et al, 2009Maetzler et al, , 2008. Amyloid burden in PDD patients is heterogeneous with cases of PDD, where amyloid deposition overlaps with the levels observed in healthy subjects and in PD patients (Edison et al, 2013(Edison et al, , 2008Foster et al, 2010;Gomperts et al, 2012Gomperts et al, , 2008Jokinen et al, 2010;Maetzler et al, 2009Maetzler et al, , 2008 and other cases of PDD showing elevated cortical amyloid deposition in the Alzheimer's disease (AD) range (Edison et al, 2013(Edison et al, , 2008Foster et al, 2010;Gomperts et al, 2012;Jokinen et al, 2010;Maetzler et al, 2009Maetzler et al, , 2008Shimada et al, 2013).…”

Section: Misfolded Proteinsmentioning

confidence: 99%

“…PDD patients have higher incidence of cortical Aβ-amyloid deposition compared to healthy subjects, PD and PD-MCI, ranging from 0% to 80% (Edison et al, 2013(Edison et al, , 2008Foster et al, 2010;Gomperts et al, 2012Gomperts et al, , 2008Jokinen et al, 2010;Maetzler et al, 2009Maetzler et al, , 2008. Amyloid burden in PDD patients is heterogeneous with cases of PDD, where amyloid deposition overlaps with the levels observed in healthy subjects and in PD patients (Edison et al, 2013(Edison et al, , 2008Foster et al, 2010;Gomperts et al, 2012Gomperts et al, , 2008Jokinen et al, 2010;Maetzler et al, 2009Maetzler et al, , 2008 and other cases of PDD showing elevated cortical amyloid deposition in the Alzheimer's disease (AD) range (Edison et al, 2013(Edison et al, , 2008Foster et al, 2010;Gomperts et al, 2012;Jokinen et al, 2010;Maetzler et al, 2009Maetzler et al, , 2008Shimada et al, 2013). In contrast, amyloid burden is usually elevated in DLB patients compared to healthy subjects and PD patients and the incidence ranges between 33% and 100% (Burke et al, 2011;Claassen, Lowe, Peller, Petersen, & Josephs, 2011;Edison et al, 2008;Foster et al, 2010;Gomperts et al, 2012Gomperts et al, , 2008Graff-Radford et al, 2012;Kantarci et al, 2012;Maetzler et al, 2009Maetzler et al, , 2008Rowe et al, 2007;<...>…”

Section: Misfolded Proteinsmentioning

confidence: 99%

“…Similarly to healthy subjects, apolipoprotein ε4 allele and older age are risk factors for increased cortical amyloid burden in DLB and PDD patients (Gomperts et al, 2012;Maetzler et al, 2009;Rowe et al, 2007). Global amyloid deposition has been associated to worse cognitive performance (Foster et al, 2010;Gomperts et al, 2013;Petrou et al, 2012;Villemagne et al, 2011), and the absence of cortical amyloid deposition was associated with a better response to ACh inhibitors (Burke et al, 2011).…”

Section: Misfolded Proteinsmentioning

confidence: 99%

See 2 more Smart Citations

Imaging in Parkinson's Disease

Politis

Pagano

Niccolini

2017

International Review of Neurobiology

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In Vivo Assessment of Vesicular Monoamine Transporter Type 2 in Dementia With Lewy Bodies and Alzheimer Disease

Villemagne

Okamura²,

Pejoska

et al. 2011

Arch Neurol

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To assess the diagnostic potential of imaging striatal monoaminergic terminal integrity with the vesicular monoamine transporter type 2 (VMAT2) radioligand 18 F 9-fluropropyl-(ϩ)-dihydrotetrabenazine ([ 18 F]AV-133) and positron emission tomography to distinguish dementia with Lewy bodies (DLB) from Alzheimer disease (AD). Design, Setting, and Participants: Nine patients with DLB, 10 patients with AD, 20 patients with Parkinson disease (PD), and 10 healthy age-matched control subjects underwent [ 18 F]AV-133 positron emission tomography studies. VMAT2 density was calculated through normalized tissue uptake value ratios at 120 to 140 minutes postinjection using the primary visual cortex as the reference region. Main Outcome Measure: Comparison of the tissue ratio for [ 18 F]AV-133 between the different clinical diagnostic groups. Results: Lower VMAT2 densities were observed in patients with DLB when compared with patients with AD especially in the posterior putamen (caudate: mean [SD], 1.24 [0.6] vs 2.83 [0.9]; PϽ.001; effect size=2.1; anterior putamen: mean [SD], 0.90 [0.5] vs 3.01 [0.9]; PϽ.001; effect size=2.9; posterior putamen: mean [SD], 0.62 [0.5] vs 2.87 [0.8]; PϽ.001; effect size=3.4). Compared with healthy controls, [ 18 F]AV-133 tissue ratios were significantly lower by 88% and 74% in the posterior putamen, 74% and 65% in the anterior putamen, and 53% and 51% in the caudate nucleus of patients with PD and DLB, respectively. In contrast to patients with PD and DLB, no reductions were observed in patients with AD. Conclusions: [ 18 F]AV-133 allows assessment of nigrostriatal degeneration in Lewy body diseases. [ 18 F]AV-133 can robustly detect reductions of dopaminergic nigrostriatal afferents in patients with DLB and assist in the differential diagnosis from AD.

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Cortical PIB binding in Lewy body disease is associated with Alzheimer-like characteristics

Cited by 158 publications

References 41 publications

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

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

Imaging in Parkinson's Disease

In Vivo Assessment of Vesicular Monoamine Transporter Type 2 in Dementia With Lewy Bodies and Alzheimer Disease

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