The DOI matches its Crossref record; 185 of the 186 references it cites were found in a registry or an index.
Amyloid Oligomers Exacerbate Tau Pathology in a Mouse Model of Tauopathy
Open accessAbstract
BACKGROUND: We aimed to investigate the influence of oligomeric forms of β-amyloid (Aβ) and the influence of the duration of exposure on the development of tau phosphorylation. METHODS: Aβ oligomers were injected intracranially either acutely into 5-month-old rTg4510 mice and tissue was collected 3 days later, or chronically into 3-month-old mice and tissue was collected 2 months later. Several forms of phosphorylated tau (p-tau), GSK3 (glycogen synthase kinase-3) and microglial and astrocyte activation were measured. RESULTS: Acute injections of Aβ oligomers had no effect on p-tau epitopes but did result in elevation of phosphorylated/activated GSK3 (pGSK3). Chronic infusion of Aβ oligomers into the right hippocampus resulted in 3- to 4-fold elevations in several p-tau isoforms with no changes in total tau levels. A significant elevation in pGSK3 accompanied these changes. Microglial staining with CD68 paralleled the increase in tau phosphorylation, however, CD45 staining was unaffected by Aβ. Control experiments revealed that the infusion of Aβ from the minipumps was largely complete by 10 days after implantation. Thus, the elevation in p-tau 2 months after implantation implies that the changes are quite persistent. CONCLUSION: Soluble Aβ(1-42) oligomers have long-lasting effects on tau phosphorylation in the rTg4510 model, possibly due to elevations in GSK3. These data suggest that even brief elevations in Aβ production, may have enduring impact on the risk for tauopathy.
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“The relationship between DTI-detected WM changes and histologically detected axonal loss has been observed in several animal and human studies 25, 51–54”
From Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model (2019) · cites this paper as [52]
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“Similar to our findings, reductions in FA and increases in RAD were found to correlate with axon loss in abnormal WM in both MCI and AD patients 25,51–54”
From Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model (2019) · cites this paper as [52]
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1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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RetractedThe Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
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Alzheimer's Disease Is a Synaptic Failure
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Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
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Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17
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A protein factor essential for microtubule assembly
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NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., Holtzman, D. M., Jagust, W., Jessen, F., Karlawish, J., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.02.018 · Cited by 10,537
Polazzi, E., Mengoni, I., Caprini, M., Peña‐Altamira, E., Kurtys, E., & Monti, B. (2012) · Neurosignals · doi:10.1159/000337115 · Cited by 9,023
The amyloid hypothesis of Alzheimer's disease at 25 years
Selkoe, D. J., & Hardy, J. (2016) · EMBO Molecular Medicine · doi:10.15252/emmm.201606210 · Cited by 6,164
Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia
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Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70299-6 · Cited by 4,806
Metadata
- Authors
- Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D.
- Affiliations
- University of South Florida (US)
- Venue
- Neurodegenerative Diseases
- Publisher
- S. Karger AG
- Published
- 2012-07-10
- Volume
- 11
- Issue
- 4
- Pages
- 165-181
- ISSN
- 1660-2854 (ISSN-L)
- 1660-2862
- PMC
- PMC3739054
- OpenAlex
- W2082429191
- Cited by
- 10,359
- References
- 186
- Citations by year
- 2026: 7 · 2025: 280 · 2024: 673 · 2023: 878 · 2022: 924 · 2021: 753 · 2020: 704 · 2019: 697 · 2018: 812 · 2017: 836 · 2016: 793 · 2015: 823 · 2014: 330 · 2013: 215 · 2012: 191
- FWCI
- 334.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurodegenerative Diseases (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG 15490, R01AG015490, R29AG010282)
- National Institute of Neurological Disorders and Stroke (R01NS030352, NS76308, R01NS076308, R01NS073899)
- National Center for Research Resources (S10RR025633)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- amyloid-beta oligomers, tau phosphorylation, tauopathy, glycogen synthase kinase-3, rTg4510 mice, microglial activation, astrocyte activation, hippocampus, Alzheimer's disease
- MeSH terms
- CD68 Molecule, Animals, Disease Models, Animal, Hippocampus, Mice, Transgenic, Neurons, Peptide Fragments, Phosphorylation, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Amyloid beta-Peptides, tau Proteins, Leukocyte Common Antigens, Microglia, Tauopathies, Glycogen Synthase Kinase 3, Mice
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