The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.
Topography of Cross-sectional and Longitudinal Glucose Metabolic Deficits in Alzheimer's Disease: Pathophysiologic Implications
Abstract
Positron emission tomographic studies of cerebral glucose metabolism have shown high diagnostic specificity in distinguishing among the degenerative dementias and differentiating between Alzheimer's disease (AD) and normal aging. The current investigation was undertaken to characterize the regional glucose metabolic deficits in AD, using cross-sectional and longitudinal study designs. All subjects met the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria for AD (n = 45) or were normal (n = 20), and the AD subjects were subdivided into incipient and mild AD and moderate plus moderately severe subgroups based on the Global Deterioration Scale. The subjects underwent a non-contrast computed tomographic scan and a positron emission tomographic (PETT VI) scan. The AD subjects (n = 14) and normal control subjects (n = 15) received evaluations 2 to 3 years after baseline study. The brain regions that show glucose metabolic deficits cross-sectionally (temporal and parietal association areas, with lesser degrees of deficit in subcortical gray matter structures), over the stages of AD, also show further deficits longitudinally within the same AD subjects. The reduction in glucose metabolism is greater than would be expected from the degree of brain atrophy. The glucose metabolic deficits are discussed in the context of neuropathologic findings and neurotransmitter deficits in AD.
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
“abnormally low prefrontal and whole-brain levels in more severely affected patients”
From Preclinical Evidence of Alzheimer's Disease in Persons Homozygous for the ε4 Allele for Apolipoprotein E (1996) · cites this paper as [10]
In the citing paper
“When used to measure cerebral glucose metabolism, PET reveals characteristic abnormalities in patients with probable and definite Alzheimer's disease, including abnormally low parietal, temporal, and posterior cingulate levels”
From Preclinical Evidence of Alzheimer's Disease in Persons Homozygous for the ε4 Allele for Apolipoprotein E (1996) · cites this paper as [10]
In the citing paper
“and a progressive decline in these levels over time.”
From Preclinical Evidence of Alzheimer's Disease in Persons Homozygous for the ε4 Allele for Apolipoprotein E (1996) · cites this paper as [10]
In the citing paper
“This observation is consistent with reports that reductions in regional glucose metabolism increase as Alzheimer's disease progresses from a presymptomatic stage to one characterized by mild symptoms, and ultimately to increasingly severe stages.[9][10][11][12][13]”
From Preclinical Evidence of Alzheimer's Disease in Persons Homozygous for the ε4 Allele for Apolipoprotein E (1996) · cites this paper as [10]
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 cholinergic hypothesis of geriatric memory dysfunction
Bartus, R. T., Dean, R. L., Beer, B., & Lippa, A. S. (1982) · Science · doi:10.1126/science.7046051 · Cited by 5,545
The Global Deterioration Scale for assessment of primary degenerative dementia
Reisberg, ., Ferris, S. H., de Leon, M. J., & Crook, T. H. (1982) · American Journal of Psychiatry · doi:10.1176/ajp.139.9.1136 · Cited by 5,122
Alzheimer's disease: cell-specific pathology isolates the hippocampal formation.
Hyman, B. T., Van Hoesen, G. W., Damasio, A. R., & Barnes, C. L. (1984) · Science · doi:10.1126/science.6474172 · Cited by 2,268
Alzheimer disease: Evidence for selective loss of cholinergic neurons in the nucleus basalis
Whitehouse, P. J., Price, D. L., Clark, A. W., Coyle, J. T., & DeLong, M. R. (1981) · Annals of Neurology · doi:10.1002/ana.410100203 · Cited by 1,736
Siesjö, B. K. (1978) · Medical Entomology and Zoology · Cited by 1,426
Hamacher, K., Coenen, H. H., & Stöcklin, G. (1986) · PubMed · Cited by 1,368
Novelli, A., Reilly, J. A., Lysko, P. G., & Henneberry, R. C. (1988) · Brain Research · doi:10.1016/0006-8993(88)90765-2 · Cited by 961
Amino acid neurotransmitters and their pathways in the mammalian central nervous system
Fagg, G. E., & Foster, A. C. (1983) · Neuroscience · doi:10.1016/0306-4522(83)90263-4 · Cited by 651
Frahm, J., Bruhn, H., Gyngell, M. L., Merboldt, K. D., Hänicke, W., & Sauter, R. (1989) · Magnetic Resonance in Medicine · doi:10.1002/mrm.1910110105 · Cited by 522
Cited by
Sorted by citations
Reiman, E. M., Caselli, R. J., Yun, L. S., Chen, K., Bandy, D., Minoshima, S., Thibodeau, S. N., & Osborne, D. (1996) · New England Journal of Medicine · doi:10.1056/nejm199603213341202 · Cited by 1,366
Oxidative damage to mitochondrial DNA is increased in Alzheimer’s disease
Mecocci, P., MacGarvey, U., & Beal, M. F. (1994) · Annals of Neurology · doi:10.1002/ana.410360510 · Cited by 1,037
Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia
Reiman, E. M., Chen, K., Alexander, G. E., Caselli, R. J., Bandy, D., Osborne, D., Saunders, A. M., & Hardy, J. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2635903100 · Cited by 977
Positron Emission Tomography in Evaluation of Dementia
Silverman, D. H. S., Small, G. W., Chang, C. Y., Lu, C. S., de Aburto, M. A. K., Chen, W., Czernin, J. G., Rapoport, S. I., Pietrini, P., Alexander, G. E., et al. (2001) · JAMA · doi:10.1001/jama.286.17.2120 · Cited by 960
A phase I trial of deep brain stimulation of memory circuits in Alzheimer's disease
Laxton, A. W., Tang‐Wai, D. F., McAndrews, M. P., Zumsteg, D., Wennberg, R. A., Keren, R., Wherrett, J. R., Naglie, G., Hamani, C., Smith, G. S., et al. (2010) · Annals of Neurology · doi:10.1002/ana.22089 · Cited by 827
Self-citation
Metadata
- Authors
- Smith, G. S.
- Corresponding author
- Smith, Gwenn S.
- ORCID
- Smith, Gwenn S.
- Venue
- Archives of Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 1992-11-01
- Volume
- 49
- Issue
- 11
- Pages
- 1142
- ISSN
- 0003-9942 (ISSN-L)
- OpenAlex
- W2113406852
- Cited by
- 178
- References
- 67
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 7 · 2020: 4 · 2019: 2 · 2018: 6 · 2017: 4 · 2016: 7 · 2015: 7 · 2014: 6 · 2013: 2 · 2012: 8
- FWCI
- 4.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Archives of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (1P30-AG08051, P30AG008051)
- National Institute of Mental Health (1 ROI MH 43965-04)
- 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 › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
- Keywords
- Alzheimer's disease, brain glucose metabolism, longitudinal metabolic changes, temporal lobe, parietal association areas, subcortical gray matter, brain atrophy, disease stage, neuropathology, neurotransmitter deficits, dementia diagnosis
- MeSH terms
- Aged, Alzheimer Disease, Analysis of Variance, Cerebral Cortex, Cross-Sectional Studies, Female, Glucose, Humans, Longitudinal Studies, Male, Middle Aged, Tomography, Emission-Computed, Tomography, X-Ray Computed
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
