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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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“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]
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“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]
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“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]
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“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]
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“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
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“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
Metadata
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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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