The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Amyloid deposition, hypometabolism, and longitudinal cognitive decline
Open accessAbstract
Objective: Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) population, we examined (1) cross‐sectional relationships between amyloid deposition, hypometabolism, and cognition, and (2) associations between amyloid and hypometabolism measurements and longitudinal cognitive measurements. Methods: We examined associations between mean cortical florbetapir uptake, mean 18 F‐fluorodeoxyglucose–positron emission tomography (FDG‐PET) within a set of predefined regions, and Alzhiemer's Disease Assessment Scale (ADAS‐cog) performance in 426 ADNI participants (126 normal, 162 early mild cognitive impairment [EMCI], 85 late MCI [LMCI], 53 Alzheimer disease [AD] patients). For a subset of these (76 normal, 81 LMCI) we determined whether florbetapir and FDG‐PET were associated with retrospective decline in longitudinal ADAS‐cog measurements. Results: Twenty‐nine percent of normal subjects, 43% of EMCI patients, 62% of LMCI patients, and 77% of AD patients were categorized as florbetapir positive. Florbetapir was negatively associated with concurrent FDG and ADAS‐cog in both MCI groups. In longitudinal analyses, florbetapir‐positive subjects in both normal and LMCI groups had greater ongoing ADAS‐cog decline than those who were florbetapir negative. However, in normal subjects, florbetapir positivity was associated with greater ADAS‐cog decline than FDG, whereas in LMCI, FDG positivity was associated with greater decline than florbetapir. Interpretation: Although both hypometabolism and β‐amyloid (Aβ) deposition are detectable in normal subjects and all diagnostic groups, Aβ showed greater associations with cognitive decline in normal participants. In view of the minimal cognitive deterioration overall in this group, this suggests that amyloid deposition has an early and subclinical impact on cognition that precedes metabolic changes. At moderate and later stages of disease (LMCI/AD), hypometabolism becomes more pronounced and more closely linked to ongoing cognitive decline. ANN NEUROL 2012;72:578–586
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Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70299-6 · Cited by 4,806
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Self-citation[ 11 C]PIB in a nondemented population: Potential antecedent marker of Alzheimer disease
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Self-citationAmyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging
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Comparing predictors of conversion and decline in mild cognitive impairment
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Self-citationAmyloid, hypometabolism, and cognition in Alzheimer disease: An [11C]PIB and [18F]FDG PET study
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Self-citationPET Imaging of Tau Deposition in the Aging Human Brain
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Self-citationAssociation of plasma neurofilament light with neurodegeneration in patients with Alzheimer disease
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Metadata
- Authors
- Landau, S. M., Mintun, M. A., Joshi, A. D., Koeppe, R. A., Petersen, R. C., Aisen, P. S., Weiner, M. W., Jagust, W. J., & Initiative, F. T. A. D. N.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2012-10
- Volume
- 72
- Issue
- 4
- Pages
- 578-586
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2160597466
- Cited by
- 727
- References
- 13
- FWCI
- 25.21
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Landau, S. M., Mintun, M. A., Joshi, A. D., Koeppe, R. A., Petersen, R. C., Aisen, P. S., Weiner, M. W., Jagust, W. J., & Initiative, F. T. A. D. N. (2012). Amyloid deposition, hypometabolism, and longitudinal cognitive decline. Annals of Neurology. https://doi.org/10.1002/ana.23650
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