Fibrillar amyloid-β burden in cognitively normal people at 3 levels of genetic risk for Alzheimer's disease
Open accessAbstract
Fibrillar amyloid-beta (Aβ) is found in the brains of many cognitively normal older people. Whether or not this reflects a predisposition to Alzheimer's disease (AD) is unknown. We used Pittsburgh Compound B (PiB) PET to characterize the relationship between fibrillar Aβ burden and this predisposition in cognitively normal older people at 3 mean levels of genetic risk for AD. Dynamic PiB PET scans, the Logan method, statistical parametric mapping, and automatically labeled regions of interest (ROIs) were used to characterize and compare cerebral-to-cerebellar PIB distribution volume ratios, reflecting fibrillar Aβ burden, in 28 cognitively normal persons (mean age, 64 years) with a reported family history of AD and 2 copies, 1 copy, and no copies of the apolipoprotein E (APOE) ε4 allele. The 8 ε4 homozygotes, 8 heterozygotes, and 12 noncarriers did not differ significantly in terms of age, sex, or cognitive scores. Fibrillar Aβ was significantly associated with APOE ε4 carrier status and ε4 gene dose in AD-affected mean cortical, frontal, temporal, posterior cingulate-precuneus, parietal, and basal ganglia ROIs, and was highest in an additional homozygote who had recently developed mild cognitive impairment. These findings suggest that fibrillar Aβ burden in cognitively normal older people is associated with APOE ε4 gene dose, the major genetic risk factor for AD. Additional studies are needed to track fibrillar Aβ accumulation in persons with different kinds and levels of AD risk; to determine the extent to which fibrillar Aβ, alone or in combination with other biomarkers and risk factors, predicts rates of cognitive decline and conversion to clinical AD; and to establish the role of fibrillar Aβ imaging in primary prevention trials.
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Crossing a transgenic mouse model of Alzheimer's disease that has high levels of human Aβ in the brain with human APOE targeted replacement mice demonstrated age-dependent and APOE isoform-dependent (E4>>E3>E2) Aβ deposition and amyloid burden in the brain in a manner that recapitulates the human condition observed in pre-symptomatic elderly APOE4 carriers as well as Alzheimer's disease patients.
“Crossing a transgenic mouse model of AD that has high levels of human Aβ in the brain with human APOE targeted replacement mice demonstrated age-dependent and APOE isoform-dependent (E4>>E3>E2) Aβ deposition and amyloid burden in the brain in a manner that recapitulates the human condition observed in pre-symptomatic elderly APOE4 carriers as well as AD patients.18–21”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [20]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredIn AD, amyloid deposition spreads and the disease pathogenesis progressively involves a broad region of the brain.
“the amyloid deposition spreads, and the disease pathogenesis progressively involves a broad region of the brain”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [20]
The Discussion (page unavailable) reports fibrillar amyloid-β burden across several brain regions associated with AD, supporting the claim that deposition involves a broad region of the brain. But the paper does not establish that deposition spreads over time or that disease pathogenesis progressively involves more regions; the Discussion notes the absence of longitudinal amyloid data. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe association of the APOE4 isoform with amyloid deposition has been well established in human studies, where APOE4 carriers exhibit higher Aβ plaque burden and earlier onset of amyloid positivity compared with non-carriers.
“The association of the APOE4 isoform with amyloid deposition has been well established in human studies, where APOE4 carriers exhibit higher A β plaque burden and earlier onset of amyloid positivity compared with non-carriers 35 -37 .”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [37]
The Results and Discussion (page numbers unavailable) report greater fibrillar Aβ burden in cognitively normal APOE ε4 carriers than in noncarriers, and more carriers met the study’s PiB-positivity criterion. The study does not establish an earlier age of onset of amyloid positivity: its positivity comparison is cross-sectional, while the younger onset described in the Abstract concerns dementia, not amyloid positivity. (LLM, conf=0.89)
Experimental — accuracy not yet measuredAPOE status modulates the onset of extracellular amyloid plaque deposition.
“APOE status has been found to modulate the onset of extracellular amyloid plaque deposition, one of the key pathognomonic features of the disease (6, 7).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [6]
The Discussion (page unavailable) reports greater fibrillar amyloid-β burden in cognitively normal APOE ε4 carriers than in noncarriers, supporting an association between APOE status and deposition. It does not establish when plaque deposition begins or show that APOE status modulates its onset; the younger onset discussed in the paper concerns dementia, not deposition. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe APOE ε4 allele increases brain amyloid burden assessed by PIB-PET imaging in a gene dose-dependent manner.
“Additionally, the APOE ε4 allele increases brain amyloid burden assessed by PIB-PET imaging in a gene dose-dependent manner (6).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [6]
The Results report that PiB-PET measures of fibrillar amyloid-β burden increased progressively with each additional APOE ε4 allele in the cognitively normal participants. The Discussion describes this as an association; the study does not establish that the allele causes amyloid burden to increase. (LLM, conf=0.84)
Experimental — accuracy not yet measured
APOE isoform-dependent amyloid deposition has been consistently observed in humans and Aβ depositing mouse models.
“APOE isoform-dependent amyloid deposition has been consistently observed in humans and Aβ depositing mouse models (Holtzman et al., 2000; Bales et al., 2009; Reiman et al., 2009; Morris et al., 2010).”
From Haploinsufficiency of Human APOE Reduces Amyloid Deposition in a Mouse Model of Amyloid-β Amyloidosis (2011) · cites this paper as Reiman et al., 2009
The Abstract reports an association between fibrillar Aβ burden and APOE ε4 gene dose in cognitively normal older humans; the Discussion likewise reports greater burden in ε4 carriers than noncarriers. The cited paper does not report amyloid deposition in Aβ-depositing mouse models, so it supports only the human portion of the sentence. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe ε4 allele increased brain amyloid burden in a dose-dependent manner in normal elderly individuals and in mild cognitive impairment patients.
“The ε4 allele increased brain amyloid burden in a dose-dependent manner in normal elderly individuals and in mild cognitive impairment patients [93,94].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [93]
The Results report that fibrillar amyloid-β burden increased with APOE ε4 gene dose among 28 cognitively normal participants. The paper includes only one participant with mild cognitive impairment, whose burden was high; it does not establish a dose-dependent relationship in MCI patients. (LLM, conf=0.90)
Experimental — accuracy not yet measuredCognitively normal subjects had an ε4 dose-dependent increase in fibrillar Aβ burden in brain as detected with an amyloid imaging agent.
“This finding has now been confirmed more directly in a study that showed cognitively normal subjects had an ε4 dose-dependent increase in fibrillar Aβ burden in brain as detected with an amyloid imaging agent (Reiman et al., 2009).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Reiman et al., 2009
Case-control studies without neuropathological or biomarker assessments of AD may have underestimated the impact of APOE genotypes on Alzheimer's dementia odds ratios due to the confounding effects of APOE genotypes on the percentages of neuropathologically misclassified cases and controls.
“This possibility has remained unaddressed, because case–control studies without neuropathological or biomarker assessments of AD may have underestimated the impact of APOE genotypes on Alzheimer’s dementia ORs due to the confounding effects of APOE genotypes on the percentages of neuropathologically misclassified cases and controls8–10.”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [9]
The Abstract reports an association between APOE ε4 gene dose and Alzheimer’s disease risk, and the Discussion reports an association with fibrillar amyloid-β burden. Neither addresses whether case–control studies lacking neuropathological or biomarker assessments underestimated dementia odds ratios because of genotype-related misclassification. Searches for misclassified cases and controls and for underestimated case–control odds ratios found no passage addressing that claim. (LLM, conf=0.73)
Experimental — accuracy not yet measuredDue to prioritized ascertainment, the number of misclassified cases and controls available through the AD Genetics Consortium is much smaller than the estimated number of neuropathologically misclassified cases and controls, limiting the ability to clarify the impact of brain donation on APOE ORs in post hoc analyses.
“Due to the prioritized ascertainment of those cases who met the clinical and neuropathological criteria for Alzheimer’s dementia and those unimpaired controls without AD, the number of misclassified cases and controls available through the AD Genetics Consortium12 is much smaller than our estimated number of neuropathologically misclassified cases and controls8–11, limiting our ability to clarify”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [9]
Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredIn a previous autopsy study, 25% of persons with the clinical diagnosis of mild-to-moderate Alzheimer's dementia lacked at least moderately frequent neuritic plaques, including 37% of APOE4 non-carriers and 13% of carriers.
“In a previous autopsy study, we found that 25% of persons with the clinical diagnosis of mild-to-moderate Alzheimer’s dementia lacked at least moderately frequent neuritic plaques, one of the cardinal features of AD, including 37% of APOE4 non-carriers and 13% of carriers, findings that are consistent with those in living patients9,10.”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [9]
The Results and Discussion describe PiB PET measurements of fibrillar amyloid-β in cognitively normal people and a comparison group with probable AD. Searches for the autopsy finding, neuritic plaques, and the 25%, 37%, and 13% figures found no passage reporting the claimed finding in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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Hardy, J., Bogdanović, N., Winblad, B. G., Portelius, E., Andreasen, N. C., Cedazo-Mı́nguez, Á., & Zetterberg, H. (2014) · Journal of Internal Medicine · doi:10.1111/joim.12192 · Cited by 177 · see citing works
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PET amyloid-beta imaging in preclinical Alzheimer's disease
Vlassenko, A. G., Benzinger, T. L. S., & Morris, J. C. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.11.005 · Cited by 173 · see citing works
- Authors
- Reiman, E. M., Chen, K., Liu, X., Bandy, D., Yu, M., Lee, W., Ayutyanont, N., Keppler, J., Reeder, S. A., Langbaum, J. B. S., Alexander, G. E., Klunk, W. E., Mathis, C. A., Price, J. C., Aizenstein, H. J., DeKosky, S. T., & Caselli, R. J.
- Affiliations
- Translational Genomics Research Institute (US)
- Banner - University Medical Center Phoenix (US)
- University of Arizona (US)
- Departments of iPsychiatry,
- University of Pittsburgh (US)
- Mayo Clinic in Arizona (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2009-04-21
- Volume
- 106
- Issue
- 16
- Pages
- 6820-6825
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2665196
- OpenAlex
- W2171346860
- Semantic Scholar
- 50d5adab23ba1a800626a6f613f94a2c667b07e4
- Cited by
- 785
- References
- 44
- Citations by year
- 2026: 15 · 2025: 26 · 2024: 34 · 2023: 36 · 2022: 36 · 2021: 45 · 2020: 44 · 2019: 39 · 2018: 34 · 2017: 34 · 2016: 40 · 2015: 50 · 2014: 66 · 2013: 61 · 2012: 65
- FWCI
- 45.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- McKnight Foundation
- National Institute on Aging (R01AG025526, R01AG018402, P01AG025204, RF1AG025516, P50AG005133, R01AG031581, P30AG019610, R37AG025516)
- National Institute of Mental Health (R01MH070729, R01MH057899)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- fibrillar amyloid-beta, Alzheimer's disease, APOE ε4, genetic risk, cognitively normal older adults, Pittsburgh compound B PET, family history of Alzheimer's disease, mild cognitive impairment, primary prevention
- MeSH terms
- Aged, Alzheimer Disease, Brain Mapping, Cognition, Heterozygote, Homozygote, Humans, Magnetic Resonance Imaging, Middle Aged, Neuropsychological Tests, Amyloid beta-Peptides, Gene Dosage, Genetic Predisposition to Disease, Apolipoprotein E4
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