Temporal Profile of Amyloid-β (Aβ) Oligomerization in an in Vivo Model of Alzheimer Disease
Open accessAbstract
Accumulation of amyloid-beta (Abeta) is one of the earliest molecular events in Alzheimer disease (AD), whereas tau pathology is thought to be a later downstream event. It is now well established that Abeta exists as monomers, oligomers, and fibrils. To study the temporal profile of Abeta oligomer formation in vivo and to determine their interaction with tau pathology, we used the 3xTg-AD mice, which develop a progressive accumulation of plaques and tangles and cognitive impairments. We show that SDS-resistant Abeta oligomers accumulate in an age-dependent fashion, and we present evidence to show that oligomerization of Abeta appears to first occur intraneuronally. Finally, we show that a single intrahippocampal injection of a specific oligomeric antibody is sufficient to clear Abeta pathology, and more importantly, tau pathology. Therefore, Abeta oligomers may play a role in the induction of tau pathology, making the interference of Abeta oligomerization a valid therapeutic target.
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In 3xTg-AD mice, both Aβ and tau exhibit age- and region-dependent formation, with Aβ plaques appearing prior to tangles, which are extensive in older transgenic mice.
“Both Aβ and tau exhibit age- and region-dependent formation in these mice, with Aβ plaques appearing prior to tangles, which are extensive in older transgenic mice.”
From Brain microstructure abnormalities in the 3xTg-AD mouse – A diffusion MRI and morphology correlation study (2022) · cites this paper as [4]
The Results section (page unavailable) describes age-dependent Aβ accumulation in the hippocampus and reports early tau pathology at 6 months and advanced tangles at 20 months. It does not establish that plaques appear before tangles or that both Aβ and tau formation are region-dependent; its explicit timing comparison is between Aβ oligomers and plaques. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAβ plaque and tau pathology are evident in 15-month-old TG mice, and significantly increased with age.
“In our morphological analysis (Fig. 2 and 3), as previously described [3–6, 28], Aβ plaque and tau pathology are evident in 15-month-old TG mice, and significantly increased with age (online supplementary Fig.1 and 2).”
From Brain microstructure abnormalities in the 3xTg-AD mouse – A diffusion MRI and morphology correlation study (2022) · cites this paper as [4]
The Results section (page unavailable) describes age-related Aβ accumulation in 3xTg-AD mice and tau pathology that is apparent by 6 months and advanced by 20 months. It does not specifically assess 15-month-old mice or establish a statistically significant age-related increase in both plaques and tau pathology; the citing sentence points to its own figures for that finding. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe 3xTg-AD mouse develops both amyloid-β and neurofibrillary tangles in a temporal and spatial pattern similar to human AD pathology.
“It develops both amyloid-β (Aβ) and neurofibrillary tangles in a temporal and spatial pattern similar to human AD pathology [3–6].”
From Brain microstructure abnormalities in the 3xTg-AD mouse – A diffusion MRI and morphology correlation study (2022) · cites this paper as [4]
Due to the variability of the degree of AD pathology described in this model, large ROIs, as used for the HD and HV, may have attenuated some effects.
“Additionally, due to the variability of the degree of AD pathology described in this model [4, 6, 26], large ROIs, as used for the HD and HV, may have attenuated some effects.”
From Brain microstructure abnormalities in the 3xTg-AD mouse – A diffusion MRI and morphology correlation study (2022) · cites this paper as [4]
The section on age-dependent oligomer accumulation describes changes in pathology with age and within the CA1/subiculum, but does not report variability in the degree of AD pathology among mice in this model. Searches for variability, differences among animals, and regional heterogeneity found no passage establishing the premise attributed to this source. The suggestion that large ROIs attenuated effects is the citing authors’ own inference. (LLM, conf=0.70)
Experimental — accuracy not yet measuredAntibodies can reverse intracellular tau and synapse pathology and provide cognitive benefits.
“the ability of antibodies to reverse intracellular tau and synapse pathology (Chauhan et al., 2008; Oddo et al., 2006) and to provide cognitive benefits (Hillen et al., 2010; Takamura et al., 2011).”
From The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer’s disease (2011) · cites this paper as Oddo et al., 2006
Synapse deterioration in transgenic mice is prevented by ICV injections of oligomer-specific antibodies.
“Synapse deterioration in tg-mice is prevented by ICV injections of oligomer-specific antibodies (Chauhan, 2007; Oddo et al., 2006).”
From The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer’s disease (2011) · cites this paper as Oddo et al., 2006
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Self-citation
- Authors
- Oddo, S., Caccamo, A., Tran, L., Lambert, M. P., Glabe, C. G., Klein, W. L., & LaFerla, F. M.
- Affiliations
- University of California, Irvine (US)
- Northwestern University (US)
- Corresponding author
- LaFerla, Frank M.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2006-01
- Volume
- 281
- Issue
- 3
- Pages
- 1599-1604
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2020497815
- Cited by
- 379
- References
- 41
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 8 · 2023: 5 · 2022: 9 · 2021: 8 · 2020: 12 · 2019: 13 · 2018: 14 · 2017: 16 · 2016: 17 · 2015: 15 · 2014: 21 · 2013: 21 · 2012: 22
- FWCI
- 18.98
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Larry L. Hillblom Foundation
- National Institutes of Health (AG00538)
- National Institute on Aging (AG-11385, AG18877, AG0212982, AG 00538, AG 22547, R01AG022547, R01AG018877)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta oligomers, Alzheimer's disease, 3xTg-AD mice, tau pathology, age-dependent accumulation, intrahippocampal injection, amyloid plaques, cognitive impairment, therapeutic target
- MeSH terms
- Aging, Alzheimer Disease, Animals, Disease Models, Animal, Hippocampus, Humans, Functional Laterality, Mice, Transgenic, Neurons, Recombinant Proteins, Amyloid beta-Peptides, tau Proteins, Macromolecular Substances, Mice
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