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101. Sulfotransferase 1A3/4 copy number variation is associated with neurodegenerative disease

Author

Butcher, N J, Horne, M K, Mellick, G D, Fowler, C J, Masters, C L, and Minchin, R F

Abstract

The cytosolic aryl sulfotransferase genes SULT1A3 and SULT1A4 are located on chromosome 16p11.2 in a region of chromosomal instability. SULT1A3/4 are important enzymes in the metabolism of catecholamines linked to neurodegenerative diseases such as Parkinson’s and Alzheimer’s. In the present study, copy number variation of the SULT1A3/4 genes in healthy individuals, as well as a cohort of Parkinson’s disease and Alzheimer’s disease patients was examined. In all subjects, SULT1A3/4 copy number varied from 1 to 10. In Alzheimer’s disease patients, there was a significantly lower copy number compared to controls, and a positive correlation between copy number and age of disease onset. By contrast, there were no differences in Parkinson’s disease patients. However, when early-onset Parkinson’s disease was evaluated separately, there appeared to be an association with gene copy number and risk. The current study shows that these neurodegenerative diseases may be related to SULT1A3/4 copy number.

Published
2018
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102. Reduced TRPC6 mRNA levels in the blood cells of patients with Alzheimer’s disease and mild cognitive impairment

Author

Lu, R, Wang, J, Tao, R, Wang, J, Zhu, T, Guo, W, Sun, Y, Li, H, Gao, Y, Zhang, W, Fowler, C J, Li, Q, Chen, S, Wu, Z, Masters, C L, Zhong, C, Jing, N, Wang, Y, and Wang, Y

Abstract

Transient receptor potential canonical 6 (TRPC6) inhibits β-amyloid (Aβ) production. Hyperforin, the TRPC6 agonist, reduces Aβ levels and improves cognitive performance in Alzheimer’s disease (AD) models. However, it’s unknown whether TRPC6 expression is changed in AD patients. In this case–control study, we measured TRPC6 expression levels in the peripheral blood cells of four independent AD sets from five hospitals and one mild cognitive impairment (MCI) set from a local community (229 AD, 70 MCI, 40 Parkinson disease and 359 controls from China, total n=698) using quantitative real-time PCR assay. We found a specific reduction of TRPC6 mRNA levels in four AD sets and one MCI set. The median TRPC6 mRNA levels were lower in the following: (1) combined AD patients than in age-matched controls (0.78 vs 1.73, P<0.001); (2) mild-to-moderate AD patients than in age-matched controls (0.81 vs 1.73, P<0.001); and (3) MCI patients than in age-matched controls (0.76 vs 1.72, P<0.001). In the receiver-operating characteristic curve analysis, the area under curve was 0.85 for combined AD, 0.84 for mild-to-moderate AD and 0.79 for MCI. In a subgroup of AD patients with brain Aβ examination, TRPC6 was associated with standardized uptake value ratio of Pittsburgh Compound B (Spearman’s r=−0.49, P=0.04) and cerebrospinal fluid Aβ42 (Spearman’s r=0.43, P=0.04). The TRPC6 reduction in AD patients was further confirmed in blood RNA samples from The Australian Imaging, Biomarkers and Lifestyle Flagship Study of Aging, in post-mortem brain tissues from The Netherlands Brain Bank and in induced pluripotent stem cells-derived neurons from Chinese donors. We conclude that TRPC6 mRNA levels in the blood cells are specifically reduced in AD and MCI patients, and TRPC6 might be a biomarker for the early diagnosis of AD.

Published
2018
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103. Manifold drived MR-less PiB SUVR normalisation

Author

Bourgeat, P, Raniga, P, Dore, V, Zhou, L, Macaulay, S L, Martins, R, Masters, C L, Ames, D, Ellis, K, Villemagne, V L, Rowe, C C, Salvado, O, Fripp, J, Bourgeat, P, Raniga, P, Dore, V, Zhou, L, Macaulay, S L, Martins, R, Masters, C L, Ames, D, Ellis, K, Villemagne, V L, Rowe, C C, Salvado, O, and Fripp, J

Abstract

Pittsburgh Compound B (PiB) is a C11 PET tracer designed to bind to amyloid plaques, one of the hallmark of Alzheimer's disease. The potential of PiB as an early marker of Alzheimer's disease has lead to an increasing use of PiB and the development of several F18 equivalents. Quantitative analysis of PiB images requires an accurate normalisation, parcellation and estimation of retention in the brain's gray matter. Typically this relies on co-registered MRI to extract the cerebellum, compute the standardized uptake value ratio (SUVR) and provide parcellation and segmentation for quantification of neocortical SUVR. However, not all subjects undergo MRI. In this paper we propose a highly accurate MR-less parcellation, SUVR normalisation and quantification method for PiB images. This involves rigidly registering the raw PiB images to a PiB atlas, computing pair-wise normalised mutual information, and constructing a 2D manifold. Each new scan is mapped on the manifold and its k nearest neighbours are selected as atlases in a segmentation propagation scheme with their associated MRI segmentations and parcellation used as priors to estimate the SUVR normalisation and quantification. Comparison of our MRless approach to an MR-based approach showed a coefficient of correlation of neocortical PiB SUVR of R2=0.94 and an absolute mean error of 5.9%.

Published
2012

104. Alzheimer's disease

Author

Masters, C. L. and Beyreuther, K.

Subjects
Alzheimer Disease, Risk Factors, Humans, Research Article, Forecasting
Published
1998

105. Three-Month Stability of the CogState Brief Battery in Healthy Older Adults, Mild Cognitive Impairment, and Alzheimer's Disease: Results from the Australian Imaging, Biomarkers, and Lifestyle-Rate of Change Substudy (AIBL-ROCS)

Author

Lim, Y. Y., primary, Jaeger, J., additional, Harrington, K., additional, Ashwood, T., additional, Ellis, K. A., additional, Stoffler, A., additional, Szoeke, C., additional, Lachovitzki, R., additional, Martins, R. N., additional, Villemagne, V. L., additional, Bush, A., additional, Masters, C. L., additional, Rowe, C. C., additional, Ames, D., additional, Darby, D., additional, and Maruff, P., additional

Published
2013
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107. 18F-THK523: a novel in vivo tau imaging ligand for Alzheimer's disease

Author

Fodero-Tavoletti, M. T., primary, Okamura, N., additional, Furumoto, S., additional, Mulligan, R. S., additional, Connor, A. R., additional, McLean, C. A., additional, Cao, D., additional, Rigopoulos, A., additional, Cartwright, G. A., additional, O'Keefe, G., additional, Gong, S., additional, Adlard, P. A., additional, Barnham, K. J., additional, Rowe, C. C., additional, Masters, C. L., additional, Kudo, Y., additional, Cappai, R., additional, Yanai, K., additional, and Villemagne, V. L., additional

Published
2011
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112. β-Amyloid burden in the temporal neocortex is related to hippocampal atrophy in elderly subjects without dementia

Author

Bourgeat, P., primary, Chételat, G., additional, Villemagne, V. L., additional, Fripp, J., additional, Raniga, P., additional, Pike, K., additional, Acosta, O., additional, Szoeke, C., additional, Ourselin, S., additional, Ames, D., additional, Ellis, K. A., additional, Martins, R. N., additional, Masters, C. L., additional, Rowe, C. C., additional, and Salvado, O., additional

Published
2010
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117. In Vitro Characterization of Pittsburgh Compound-B Binding to Lewy Bodies

Author

Fodero-Tavoletti, M. T., primary, Smith, D. P., additional, McLean, C. A., additional, Adlard, P. A., additional, Barnham, K. J., additional, Foster, L. E., additional, Leone, L., additional, Perez, K., additional, Cortes, M., additional, Culvenor, J. G., additional, Li, Q.-X., additional, Laughton, K. M., additional, Rowe, C. C., additional, Masters, C. L., additional, Cappai, R., additional, and Villemagne, V. L., additional

Published
2007
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118. Imaging -amyloid burden in aging and dementia

Author

Rowe, C. C., primary, Ng, S., additional, Ackermann, U., additional, Gong, S. J., additional, Pike, K., additional, Savage, G., additional, Cowie, T. F., additional, Dickinson, K. L., additional, Maruff, P., additional, Darby, D., additional, Smith, C., additional, Woodward, M., additional, Merory, J., additional, Tochon-Danguy, H., additional, O'Keefe, G., additional, Klunk, W. E., additional, Mathis, C. A., additional, Price, J. C., additional, Masters, C. L., additional, and Villemagne, V. L., additional

Published
2007
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120. Visual Assessment Versus Quantitative Assessment of 11C-PIB PET and 18F-FDG PET for Detection of Alzheimer's Disease

Author

Ng, S., primary, Villemagne, V. L., additional, Berlangieri, S., additional, Lee, S.-T., additional, Cherk, M., additional, Gong, S. J., additional, Ackermann, U., additional, Saunder, T., additional, Tochon-Danguy, H., additional, Jones, G., additional, Smith, C., additional, O'Keefe, G., additional, Masters, C. L., additional, and Rowe, C. C., additional

Published
2007
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129. Creutzfeldt–Jakob disease in Australia 1970–1999

Author

Collins, S., primary, Boyd, A., additional, Lee, J. S., additional, Lewis, V., additional, Fletcher, A., additional, McLean, C. A., additional, Law, M., additional, Kaldor, J., additional, Smith, M. J., additional, and Masters, C. L., additional

Published
2002
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131. Alzheimer’s Disease

Author

Christie, G., primary, Markwell, R. E., additional, Gray, C. W., additional, Smith, L., additional, Godfrey, F., additional, Mansfield, F., additional, Wadsworth, H., additional, King, R., additional, McLaughlin, M., additional, Cooper, D. G., additional, Ward, R. V., additional, Howlett, D. R., additional, Hartmann, T., additional, Lichtenthaler, S. F., additional, Beyreuther, K., additional, Underwood, J., additional, Gribble, S. K., additional, Cappai, R., additional, Masters, C. L., additional, Tamaoka, A., additional, Gardner, R. L., additional, Rivett, A. J., additional, Karran, E. H., additional, and Allsop, D., additional

Published
2002
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144. Factors affecting subjective memory complaints in the AIBL aging study: biomarkers, memory, affect, and age.

Author

Buckley, R., Saling, M. M., Ames, D., Rowe, C. C., Lautenschlager, N. T., Macaulay, S. L., Martins, R. N., Masters, C. L., O'Meara, T., Savage, G., Szoeke, C., Villemagne, V. L., and Ellis, K. A.

Abstract

Background:The prognostic value of subjective memory complaints (SMCs) in the diagnosis of dementia of the Alzheimer's type is unclear. While some studies have found an association between SMCs and cognitive decline, many have found a stronger association with depression, which raises questions about their diagnostic utility.Methods:We examined the cross-sectional association between SMC severity (as measured using the MAC-Q, a brief SMC questionnaire) and affect, memory, and Alzheimer's disease (AD) biomarkers (β-amyloid deposition and the apolipoprotein E ε4 (APOEε4) allele) in healthy elderly controls (HC; M = 78.74 years, SD = 6.7) and individuals with mild cognitive impairment (MCI; M = 72.74 years, SD = 8.8). We analyzed a subset of individuals drawn from the Australian Imaging Biomarkers and Lifestyle (AIBL) Study of Aging.Results:SMCs were more severe in MCI patients than in HCs. SMC severity was related to affective variables and the interaction between age and group membership (HC/MCI). Within the HC group, SMC severity was related to affective variables only, while severity correlated only with age in the MCI group. SMCs were not related to cognitive variables or AD biomarkers.Conclusion:SMCs were related to solely by poorer mood (greater depressive and anxious symptomatology) in the cognitively healthy elderly however mean levels were subclinical. This finding argues for the assessment of affective symptomatology in conjunction with cognitive assessment in elderly memory complainers. Future AIBL research will focus on assessing other AD biomarkers, such as brain atrophy and Aβ plasma markers, in relation to complaint severity. Once our 36-month follow-up data are collected, we propose to assess whether SMCs can predict future cognitive decline. [ABSTRACT FROM AUTHOR]

Published
2013
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150. 11C-PiB PET studies in typical sporadic Creutzfeldt—Jakob disease.

Author

Villemagne, L., McLean, C. A., Reardon, K., Boyd, A., Lewis, V., Klug, G., Jones, G., Baxendale, D., Masters, C. L., Rowe, C. C., and Collins, S. J.

Subjects
CREUTZFELDT-Jakob disease, POSITRON emission tomography, DEMENTIA, ALZHEIMER'S disease, CEREBELLUM
Abstract

OBJECTIVE: Brain amyloid imaging using positron emission tomography (PET) is of increasing importance in the premortem evaluation of dementias, particularly in relation to Alzheimer disease (AD). The purpose of this study was to explore the premortem diagnostic utility of 11C-PiB PET in sporadic Creutzfeldt–Jakob disease (CJD). METHODS: Two patients, 72 and 59 years old, underwent evaluation for rapidly progressive cognitive decline, dying after illness durations of 5 and 7 months, respectively. As part of their comprehensive assessment, 18F-FDG PET and 11C-PiB PET studies were performed approximately 2–4 weeks prior to death, and the brain regional distributions compared with those from cohorts of healthy controls (HC) and AD patients. RESULTS: Routine investigations, including brain MRI scans, revealed changes typical of sporadic CJD, with the diagnosis confirmed at autopsy in both patients. The 18F-FDG PET showed global hypometabolism in one patient and thalamic and frontal hypometabolism with unexpected hypermetabolism in the dentate nuclei of the cerebellum in the other. Neither patient displayed cerebral cortical 11C-PiB PET retention above the levels observed in HC. CONCLUSIONS: No grey-matter 11C-PiB retention was observed in two pathologically confirmed cases of typical sporadic CJD. We speculate that low PrP plaque density and small plaque size, as well as a relatively low affinity of the radioligand, explain the absence of 11C-PiB retention. More studies to validate this hypothesis are warranted. [ABSTRACT FROM AUTHOR]

Published
2009
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