Amyloid burden and neural function in people at risk for Alzheimer's Disease
Open accessAbstract
To determine the relationship between amyloid burden and neural function in healthy adults at risk for Alzheimer's Disease (AD), we used multimodal imaging with [C-11]Pittsburgh compound B positron emission tomography, [F-18]fluorodeoxyglucose, positron emission tomography , and magnetic resonance imaging, together with cognitive measurement in 201 subjects (mean age, 60.1 years; range, 46-73 years) from the Wisconsin Registry for Alzheimer's Prevention. Using a qualitative rating, 18% of the samples were strongly positive Beta-amyloid (Aβ+), 41% indeterminate (Aβi), and 41% negative (Aβ-). Aβ+ was associated with older age, female sex, and showed trends for maternal family history of AD and APOE4. Relative to the Aβ- group, Aβ+ and Aβi participants had increased glucose metabolism in the bilateral thalamus; Aβ+ participants also had increased metabolism in the bilateral superior temporal gyrus. Aβ+ participants exhibited increased gray matter in the lateral parietal lobe bilaterally relative to the Aβ- group, and no areas of significant atrophy. Cognitive performance and self report cognitive and affective symptoms did not differ between groups. Amyloid burden can be identified in adults at a mean age of 60 years and is accompanied by glucometabolic increases in specific areas, but not atrophy or cognitive loss. This asymptomatic stage may be an opportune window for intervention to prevent progression to symptomatic AD.
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Increased thalamic volume and hypermetabolism with amyloid pathology have been reported among APOE4 carriers.
“The role of thalamic structure and function in AD appears complex and perhaps nonlinear, as thalamic atrophy in MCI [48] and hypometabolism in APOE4 carriers [49] have been observed, whereas others have reported increased thalamic volume [50] and hypermetabolism with amyloid pathology [51] among APOE4 carriers.”
From Effects of APOE2 and APOE4 on brain microstructure in older adults: modification by age, sex, and cognitive status (2024) · cites this paper as [51]
Results §3.3 reports greater medial-thalamic glucose metabolism in participants with indeterminate or positive amyloid burden than in amyloid-negative participants. The cohort was enriched for APOE4 carriers, but the analysis grouped participants by amyloid burden, not carrier status; the Discussion also reports no significant APOE-genotype association. The separate increased-volume finding is attributed to citation [50], not this paper. (LLM, conf=0.88)
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Reas, E. T., Triebswetter, C., Banks, S. J., & McEvoy, L. K. (2024) · Alzheimer's Research & Therapy · doi:10.1186/s13195-023-01380-w · Cited by 20 · see citing works
“…structure and function in AD appears complex and perhaps nonlinear, as thalamic atrophy in MCI [48] and hypometabolism in APOE4 carriers [49] have been observed, whereas others have reported increased thalamic volume [50] and hypermetabolism with amyloid pathology [51] among APOE4 carriers.”
BackgroundAPOE-ε4-related differences in left thalamic microstructure in cognitively healthy adults
Mole, J. P., Fasano, F., Evans, J., Sims, R., Kidd, E., Aggleton, J. P., & Metzler-Baddeley, C. (2020) · Scientific Reports · doi:10.1038/s41598-020-75992-9 · Cited by 15 · see citing works
Greater tau pathology is associated with altered predictive coding
Gjini, K., Casey, C., Tanabe, S., Bo, A., Parker, M., White, M., Kunkel, D., Lennertz, R., Pearce, R. A., Betthauser, T., et al. (2022) · Brain Communications · doi:10.1093/braincomms/fcac209 · Cited by 9 · see citing works
Self-citation
- Authors
- Johnson, S. C., Christian, B. T., Okonkwo, O. C., Oh, J. M., Harding, S., Xu, G., Hillmer, A. T., Wooten, D. W., Murali, D., Barnhart, T. E., Hall, L. T., Racine, A. M., Klunk, W. E., Mathis, C. A., Bendlin, B. B., Gallagher, C. L., Carlsson, C. M., Rowley, H. A., Hermann, B. P., Dowling, N. M., Asthana, S., & Sager, M. A.
- Affiliations
- University of Wisconsin–Madison (US)
- University of Pittsburgh (US)
- Corresponding author
- Johnson, Sterling C.
- ORCID
- Johnson, Sterling C.
- Christian, Bradley T.
- Okonkwo, Ozioma C.
- Oh, Jennifer M.
- Xu, Guofan
- Hillmer, Ansel T.
- Barnhart, Todd E.
- Hall, Lance T.
- Racine, Annie M.
- Klunk, William E.
- Mathis, Chester A.
- Bendlin, Barbara B.
- Gallagher, Catherine L.
- Carlsson, Cynthia M.
- Rowley, Howard A.
- Hermann, Bruce P.
- Dowling, N. Maritza
- Asthana, Sanjay
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2014-03
- Volume
- 35
- Issue
- 3
- Pages
- 576-584
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC4018215
- OpenAlex
- W2054509396
- Cited by
- 218
- References
- 64
- Citations by year
- 2026: 11 · 2025: 28 · 2024: 23 · 2023: 16 · 2022: 20 · 2021: 23 · 2020: 14 · 2019: 16 · 2018: 11 · 2017: 12 · 2016: 13 · 2015: 13 · 2014: 18
- FWCI
- 10.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIA (AG021155, AG027161, P50 AG033514)
- Veterans Administration Merit Review (I01CX000165, P50 HD03352)
- Helen Bader Foundation
- Northwestern Mutual Foundation
- Extendicare Foundation
- Geriatric Research Education
- Clinical Center of the William S. Middleton Memorial Veterans Hospital
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cancer-related cognitive impairment studies
- Keywords
- amyloid burden, amyloid-beta, Alzheimer's disease risk, superior temporal gyrus, gray matter volume, APOE ε4, family history of Alzheimer's disease, cognitive performance, Wisconsin Registry for Alzheimer's Prevention, amyloid imaging
- MeSH terms
- Aged, Alzheimer Disease, Brain, Cognition, Female, Glucose, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Registries, Risk Factors, Cohort Studies, Amyloid beta-Peptides, Disease Progression, Positron-Emission Tomography
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