The DOI matches its Crossref record; 40 of the 41 references it cites were found in a registry or an index.
Larger temporal volume in elderly with high versus low beta-amyloid deposition
Abstract
β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amyloid burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [¹¹C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[¹¹C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippocampal) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[¹¹C]Pittsburgh compound B healthy controls. The same finding was obtained using different [¹¹C]Pittsburgh compound B thresholds, correcting [¹¹C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subsamples, and using manual hippocampal delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[¹¹C]Pittsburgh compound B cases compared to low-[¹¹C]Pittsburgh compound B cases, as well as in high-[¹¹C]Pittsburgh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[¹¹C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[¹¹C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[¹¹C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“A between-group analysis performed by Chetelat et al. indicated that, in participants with SCD, individuals with a higher level of amyloid deposition showed significant gray matter atrophy compared with individuals with a low level of amyloid deposition [180].”
From Neuroimaging advances regarding subjective cognitive decline in preclinical Alzheimer's disease (2020) · cites this paper as [180]
Citations
Cites
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Voxel-Based Morphometry—The Methods
Ashburner, J., & Friston, K. J. (2000) · NeuroImage · doi:10.1006/nimg.2000.0582 · Cited by 8,676
A Voxel-Based Morphometric Study of Ageing in 465 Normal Adult Human Brains
Good, C. D., Johnsrude, I. S., Ashburner, J., Henson, R. N. A., Friston, K. J., & Frackowiak, R. S. J. (2001) · NeuroImage · doi:10.1006/nimg.2001.0786 · Cited by 4,561
Katzman, R., Terry, R., DeTeresa, R., Brown, T., Davies, P., Fuld, P., Renbing, X., & Peck, A. (1988) · Annals of Neurology · doi:10.1002/ana.410230206 · Cited by 1,225
Dickerson, B. C., Bakkour, A., Salat, D. H., Feczko, E., Pacheco, J., Greve, D. N., Grodstein, F., Wright, C. I., Blacker, D., Rosas, H. D., et al. (2009) · Cerebral Cortex · doi:10.1093/cercor/bhn113 · Cited by 1,153
[ 11 C]PIB in a nondemented population: Potential antecedent marker of Alzheimer disease
Mintun, M. A., LaRossa, G. N., Sheline, Y. I., Dence, C. S., Lee, S. Y., Mach, R. H., Klunk, W. E., Mathis, C. A., DeKosky, S. T., & Morris, J. C. (2006) · Neurology · doi:10.1212/01.wnl.0000228230.26044.a4 · Cited by 1,036
Ellis, K. A., Bush, A. I., Darby, D., Fazio, D. D., Foster, J. K., Hudson, P. J., Lautenschlager, N. T., Lenzo, N. P., Martins, R. N., Maruff, P. T., et al. (2009) · International Psychogeriatrics · doi:10.1017/s1041610209009405 · Cited by 1,005
Self-citationRapid appearance and local toxicity of amyloid-β plaques in a mouse model of Alzheimer’s disease
Meyer-Luehmann, M., Spires-Jones, T. L., Prada, C., Garcia-Alloza, M., de Calignon, A., Rozkalne, A., Koenigsknecht-Talboo, J., Holtzman, D. M., Bacskai, B. J., & Hyman, B. T. (2008) · Nature · doi:10.1038/nature06616 · Cited by 987
Jack, C. R., Lowe, V. J., Senjem, M. L., Weigand, S. D., Kemp, B. J., Shiung, M. M., Knopman, D. S., Boeve, B. F., Klunk, W. E., Mathis, C. A., et al. (2008) · Brain · doi:10.1093/brain/awm336 · Cited by 958
Cited by
Sorted by citations
Jessen, F., Amariglio, R. E., van Boxtel, M., Breteler, M., Ceccaldi, M., Chételat, G., Dubois, B., Dufouil, C., Ellis, K. A., van der Flier, W. M., et al. (2014) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.01.001 · Cited by 3,014
Self-citationThe Alzheimer's Disease Neuroimaging Initiative: A review of papers published since its inception
Weiner, M. W., Veitch, D. P., Aisen, P. S. S., Beckett, L. A., Cairns, N. J., Green, R. C., Harvey, D. J., Jack, C. R., Jagust, W. J., Liu, E., et al. (2013) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2013.05.1769 · Cited by 1,033
Fjell, A. M., McEvoy, L., Holland, D., Dale, A. M., & Walhovd, K. B. (2014) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2014.02.004 · Cited by 799
“The main conclusions are that Ab levels are not related to ial temporal lobe (green box). though the results sometimes are complex (Bourgeat et al., 2010; Chetelat et al., 2010a,b).”
BackgroundThe Evolution of Preclinical Alzheimer’s Disease: Implications for Prevention Trials
Sperling, R., Mormino, E., & Johnson, K. (2014) · Neuron · doi:10.1016/j.neuron.2014.10.038 · Cited by 725
“However, other studies have not found a cross-sectional relationship between Ab and ND (Chételat et al., 2010; Wirth et al., 2013a).”
β-Amyloid burden in healthy aging: Regional distribution and cognitive consequences
Rodrigue, K. M., Kennedy, K. M., Devous, M. D., Rieck, J. R., Hebrank, A. C., Diaz-Arrastia, R., Mathews, D., & Park, D. C. (2012) · Neurology · doi:10.1212/wnl.0b013e318245d295 · Cited by 419
Metadata
- Authors
- Chételat, G., Villemagne, V. L., Pike, K. E., Baron, J.-C., Bourgeat, P., Jones, G., Faux, N. G., Ellis, K. A., Salvado, O., Szoeke, C., Martins, R. N., Ames, D., Masters, C. L., & Rowe, C. C.
- Affiliations
- Inserm (FR)
- Mental Health Research Institute (AU)
- University of Cambridge (GB)
- Commonwealth Scientific and Industrial Research Organisation (AU)
- Austin Health (AU)
- The University of Melbourne (AU)
- Edith Cowan University (AU)
- National Ageing Research Institute (AU)
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-08-25
- Volume
- 133
- Issue
- 11
- Pages
- 3349-3358
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2075668621
- Cited by
- 159
- References
- 41
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 8 · 2023: 6 · 2022: 5 · 2021: 10 · 2020: 10 · 2019: 11 · 2018: 13 · 2017: 13 · 2016: 8 · 2015: 8 · 2014: 15 · 2013: 17 · 2012: 8
- FWCI
- 8.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Commonwealth Scientific and Industrial Research Organisation
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Oncology › Cancer-related cognitive impairment studies
- Keywords
- amyloid-beta deposition, Alzheimer's disease, hippocampal volume, brain reserve, gray matter atrophy, mild cognitive impairment, subjective cognitive impairment, episodic memory, 11C-Pittsburgh compound B, amyloid PET
- MeSH terms
- Age Factors, Aged, Aged, 80 and over, Alzheimer Disease, Apolipoproteins E, Female, Heterozygote, Humans, Male, Organ Size, Temporal Lobe, Cohort Studies, Amyloid beta-Peptides
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review