The DOI matches its Crossref record; 44 of the 45 references it cites were found in a registry or an index.
A Dynamic Relationship between Intracellular and Extracellular Pools of Aβ
Open accessAbstract
The accumulation of the amyloid-beta peptide (Abeta) in the brain is considered to have a primary role in Alzheimer's disease (AD). In addition to the extracellular accumulation of Abeta in the parenchyma and cerebrovasculature, emerging evidence indicates that intraneuronal Abeta also plays a pathophysiological role in AD. It is unclear, however, if the intracellular and extracellular pools of Abeta are unrelated or connected. In these studies, we sought to establish a relationship between these two pools of Abeta. We identified an inverse relationship between intracellular and extracellular Abeta in the 3xTg-AD transgenic model of AD. Using an immunotherapy approach, we further found that extracellular Abeta was cleared before intracellular Abeta. After the antibody dissipated, however, the reappearance of extracellular plaques was preceded by the accumulation of intraneuronal Abeta. Taken together, these results provide strong experimental evidence that intraneuronal Abeta may serve as a source for some of the extracellular amyloid deposits.
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“Interestingly, a recent study has indicated an inverse dynamic relationship between intracellular and extracellular pools of A 𝛃 that appears to influence deposit formation in 3XTg-AD mouse brain (Oddo et al., 2006).”
From Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006) · cites this paper as Oddo et al., 2006
In the citing paper
“Indeed, intracellular Aβ accumulation in neurons that are particularly vulnerable in AD precedes plaque formation but decreases later on with the progression of Aβ deposition in both mice [89, 117] and humans [41, 81].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [89]
In the citing paper
“Indeed, there is a dynamic correlation between extra- and intracellular pools of Aβ, the latter being the source for some of the extracellular Aβ plaques [89].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [89]
In the citing paper
“this and subsequent studies noted an apparent decline in intraneuronal Aβ42 labeling with advancing plaque pathology [95, 139].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [139]
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Citations
Cites
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Alzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126
Self-citationJarrett, J. T., & Lansbury, P. T. (1993) · Cell · doi:10.1016/0092-8674(93)90635-4 · Cited by 2,178
DeMattos, R. B., Bales, K. R., Cummins, D. J., Dodart, J.-C., Paul, S. M., & Holtzman, D. M. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.151261398 · Cited by 1,298
Billings, L. M., Oddo, S., Green, K. N., McGaugh, J. L., & LaFerla, F. M. (2005) · Neuron · doi:10.1016/j.neuron.2005.01.040 · Cited by 1,294
Self-citationIntraneuronal Aβ42 Accumulation in Human Brain
Gouras, G. K., Tsai, J., Naslund, J., Vincent, B., Edgar, M., Checler, F., Greenfield, J. P., Haroutunian, V., Buxbaum, J. D., Xu, H., et al. (2000) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)64700-1 · Cited by 991
Metabolic Regulation of Brain Aβ by Neprilysin
Iwata, N., Tsubuki, S., Takaki, Y., Shirotani, K., Lu, B., Gerard, N. P., Gerard, C. J., Hama, E., Lee, H.-J., & Saido, T. C. (2001) · Science · doi:10.1126/science.1059946 · Cited by 982
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1 of the 45 references couldn’t be matched to a known paper.
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Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Oakley, H., Cole, S. L., Logan, S., Maus, E., Shao, P., Craft, J., Guillozet-Bongaarts, A., Ohno, M., Disterhoft, J., Van Eldik, L., et al. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.1202-06.2006 · Cited by 3,530
Intracellular amyloid-β in Alzheimer's disease
LaFerla, F. M., Green, K. N., & Oddo, S. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2168 · Cited by 1,942
Self-citationLacor, P. N., Buniel, M. C., Furlow, P. W., Sanz Clemente, A., Velasco, P. T., Wood, M., Viola, K. L., & Klein, W. L. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.3501-06.2007 · Cited by 1,188
Classification and basic pathology of Alzheimer disease
Duyckaerts, C., Delatour, B., & Potier, M.-C. (2009) · Acta Neuropathologica · doi:10.1007/s00401-009-0532-1 · Cited by 1,031
Metadata
- Authors
- Oddo, S., Caccamo, A., Smith, I. F., Green, K. N., & LaFerla, F. M.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- LaFerla, Frank M.
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2006-01
- Volume
- 168
- Issue
- 1
- Pages
- 184-194
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1592652
- OpenAlex
- W2110998913
- Cited by
- 261
- References
- 45
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 21 · 2023: 12 · 2022: 8 · 2021: 5 · 2020: 9 · 2019: 14 · 2018: 15 · 2017: 8 · 2016: 3 · 2015: 10 · 2014: 8 · 2013: 11 · 2012: 11
- FWCI
- 16.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Institute on Aging (AG0212982)
- 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, intraneuronal amyloid-beta, Alzheimer's disease, immunotherapy, amyloid plaques, amyloid clearance
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Brain Chemistry, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Immunohistochemistry, Intracellular Fluid, Mice, Transgenic, Neurons, Blotting, Western, Amyloid beta-Peptides, Extracellular Fluid, Mice
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