Amyloid load and cerebral atrophy in Alzheimer's disease: An <sup>11</sup>C‐PIB positron emission tomography study

Archer, Hilary; Edison, Paul; Brooks, David J.; Barnes, Jo; Frost, Chris; Yeatman, Tom; Fox, Nick C.; Rossor, Martin N.

doi:10.1002/ana.20889

Cited by 175 publications

(103 citation statements)

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“…Some studies have reported higher atrophy rates for AD subjects although subjects were often more severely affected at the time of imaging. For example, O'Brien et al reported a brain atrophy rate of 2.0%/year (0.9%/year) in patients with a mean age of 75 and mean MMSE of 16 [9]; Fox et al reported a brain atrophy rate of 2.4%/year (1.1%/year) for a mean age of 65 and mean MMSE of 20 [30]; Archer et al reported a brain atrophy rate of 1.8%/year (1.4%/year) for a mean age of 66 and mean MMSE 21 [31]; Wang et al reported a brain atrophy rate of 2.4%/year (1.2%/year) for a mean age of 67 and mean MMSE 20 [32]; Sluimer et al reported a rate of 1.9%/year (0.9%/year) for a mean age of 67 years and mean MMSE 22 [12]. The mean MMSE in ADNI is higher than the studies reported above, as ADNI enrolled at an early disease stage.…”

Section: Discussionmentioning

confidence: 99%

Volume changes in Alzheimer’s disease and mild cognitive impairment: cognitive associations

et al. 2009

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Objective: To assess the relationship between MRI-derived changes in whole-brain and ventricular volume with change in cognitive scores in Alzheimer's disease (AD), mild cognitive impairment (MCI) and control subjects. Material and methods: In total 131 control, 231 MCI and 99 AD subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort with T1-weighted volumetric MRIs from baseline and 12-month follow-up were used to derive volume changes. Mini mental state examination (MMSE), Alzheimer's disease assessment scale (ADAS)-cog and trails test changes were calculated over the same period. Results: Brain atrophy rates and ventricular enlargement differed between subject groups (p<0.0005) and in MCI and AD were associated with MMSE changes. Both measures were additionally associated with ADAS-cog and trails-B in MCI patients, and ventricular expansion was associated with ADAS-cog in AD patients. Brain atrophy (p<0.0005) and ventricular expansion rates (p=0.001) were higher in MCI subjects who progressed to AD within 12 months of follow-up compared with MCI subjects who remained stable. MCI subjects who progressed to AD within 12 months had similar atrophy rates to AD subjects. Conclusion: Whole-brain atrophy rates and ventricular enlargement differed between patient groups and healthy controls, and tracked disease progression and psychological decline, demonstrating their relevance as biomarkers.

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Section: Discussionmentioning

confidence: 99%

Volume changes in Alzheimer’s disease and mild cognitive impairment: cognitive associations

et al. 2009

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“…Amyloid imaging with PiB retention and its relation to atrophy on MRI has been widely studied in Alzheimer's disease dementia (Archer et al, 2006;Jack et al, 2009;Chetelat et al, 2010), amnestic mild cognitive impairment and preclinical Alzheimer's disease (Andrews et al, 2013;Knopman et al, 2013;Petersen et al, 2013Petersen et al, , 2016Whitwell et al, 2013;Jack et al, 2014;Araque Caballero et al, 2015). Patients with probable DLB and Parkinson's disease dementia with high PiB retention have an Alzheimer's disease-like pattern of atrophy (Shimada et al, 2013) but longitudinal imaging studies investigating whether amyloid-b deposition influences rate of atrophy in patients with probable DLB are lacking.…”

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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“…PIB also demonstrated the ability to discriminate between healthy young controls and older patients, with no significant retention seen in controls [6]. Subsequent studies were able to demonstrate congruence of findings, with retention of PIB and diagnosis consistent with AD [7][8][9][10] . Equivocal findings in patients with PIB retention and clinical diagnoses of MCI are variable likely owing to cofounders, including amnesia, depression, and alternative dementias playing a role.…”

Section: Compounds Of Interestmentioning

confidence: 83%

Amyloid Imaging: Poised for Integration into Medical Practice

Anand

Sabbagh

2017

Neurotherapeutics

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Amyloid imaging represents a significant advance as an adjunct in the diagnosis of Alzheimer's disease (AD) because it is the first imaging modality that identifies in vivo changes known to be associated with the pathogenesis. Initially, 11 C-PIB was developed, which was the prototype for many 18 F compounds, including florbetapir, florbetaben, and flutemetamol, among others. Despite the high sensitivity and specificity of amyloid imaging, it is not commonly used in clinical practice, mainly because it is not reimbursed under current Center for Medicare and Medicaid Services guidelines in the USA. To guide the field in who would be most appropriate for the utility of amyloid positron emission tomography, current studies are underway [Imaging Dementia Evidence for Amyloid Scanning (IDEAS) Study] that will inform the field on the utilization of amyloid positron emission tomography in clinical practice. With the advent of monoclonal antibodies that specifically target amyloid antibody, there is an interest, possibly a mandate, to screen potential treatment recipients to ensure that they are suitable for treatment. In this review, we summarize progress in the field to date.

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Amyloid load and cerebral atrophy in Alzheimer's disease: An ¹¹C‐PIB positron emission tomography study

Cited by 175 publications

References 18 publications

Volume changes in Alzheimer’s disease and mild cognitive impairment: cognitive associations

Volume changes in Alzheimer’s disease and mild cognitive impairment: cognitive associations

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

Amyloid Imaging: Poised for Integration into Medical Practice

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Amyloid load and cerebral atrophy in Alzheimer's disease: An 11C‐PIB positron emission tomography study

Cited by 175 publications

References 18 publications

Volume changes in Alzheimer’s disease and mild cognitive impairment: cognitive associations

Volume changes in Alzheimer’s disease and mild cognitive impairment: cognitive associations

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

Amyloid Imaging: Poised for Integration into Medical Practice

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Amyloid load and cerebral atrophy in Alzheimer's disease: An ¹¹C‐PIB positron emission tomography study