The DOI matches its Crossref record; 38 of the 39 references it cites were found in a registry or an index.
Soluble fibrillar oligomer levels are elevated in Alzheimer's disease brain and correlate with cognitive dysfunction
Open accessAbstract
Recent evidence has suggested a role for soluble oligomeric Abeta species in the pathology of Alzheimer's disease (AD). Fibrillar plaque deposits are present in non-demented individuals and levels of soluble Abeta correlate better with cognitive dysfunction in AD and transgenic mouse models. We have previously reported that there are at least two conformationally distinct types of Abeta oligomers: prefibrillar oligomers that are kinetic intermediates in fibril assembly reactions and are specifically recognized by A11 antibody and fibrillar oligomers that may represent fibril seeds or small pieces of fibrils and are recognized by a fibril specific antibody, OC. We have examined the levels of these two types of oligomers in the PBS soluble fraction of brain tissue from control cases, cases with senile degenerative changes (SDC) and AD patients. We found that the levels of soluble fibrillar oligomers detected by OC antibody are significantly elevated in multiple brain regions of AD patients. The elevated fibrillar oligomer levels were found not to be an artifact of tissue homogenization, nor a result of increased Abeta or APP levels. The concentration of fibrillar oligomers in adjacent brain regions of the same patient can vary widely and were not detected in post-mortem cerebrospinal fluid. In contrast, the level of prefibrillar oligomers are variable in both AD and age matched controls, indicating that they are not correlated with cognitive dysfunction and suggesting that they precede dementia in AD. Significant correlations were found between the levels of fibrillar oligomers and cognitive decline (MMSE scores) as well as the neuropathological hallmarks of AD. These results indicate that fibrillar oligomers may play a key role in the pathology of AD and may be a new target for diagnostic and therapeutic development.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“soluble oligomers correlate with cognitive decline (Mini Mental State Examination (MMSE) scores) and tangle stage (20).”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [20]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
Lesné, S., Koh, M. T., Kotilinek, L., Kayed, R., Glabe, C. G., Yang, A., Gallagher, M., & Ashe, K. H. (2006) · Nature · doi:10.1038/nature04533 · Cited by 2,769 · cited 1×
“…distinguished on the basis of size and elevated levels of approximately 56 kDa Aβ oligomers (ADDLs) have been identified in human brain (Gong et al., 2003) and a 56 kDa oligomer (Aβ⁎56) has been reported that is correlated with cognitive dysfunction in transgenic mouse models (Lesne et al., 2006).”
Self-citationRetractedFolstein, M. F., Folstein, S. E., & McHugh, P. R. (1975) · Journal of Psychiatric Research · doi:10.1016/0022-3956(75)90026-6 · Cited by 88,282
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
Terry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397
Blessed, G., Tomlinson, B. E., & Roth, M. (1968) · British Journal of Psychiatry · doi:10.1192/bjp.114.512.797 · Cited by 4,117
Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis
Kayed, R., Head, E., Thompson, J. L., McIntire, T. M., Milton, S. C., Cotman, C. W., & Glabe, C. G. (2003) · Science · doi:10.1126/science.1079469 · Cited by 4,064
Self-citationShankar, G. M., Li, S., Mehta, T. H., Garcia-Munoz, A., Shepardson, N. E., Smith, I., Brett, F. M., Farrell, M. A., Rowan, M. J., Lemere, C. A., et al. (2008) · Nature Medicine · doi:10.1038/nm1782 · Cited by 3,685
Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
Lambert, M. P., Barlow, A. K., Chromy, B. A., Edwards, C., Freed, R., Liosatos, M., Morgan, T. E., Rozovsky, I., Trommer, B., Viola, K. L., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.11.6448 · Cited by 3,506
Phases of Aβ-deposition in the human brain and its relevance for the development of AD
Thal, D. R., Rüb, U., Orantes, M., & Braak, H. (2002) · Neurology · doi:10.1212/wnl.58.12.1791 · Cited by 3,490
Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective
Tanzi, R. E., & Bertram, L. (2005) · Cell · doi:10.1016/j.cell.2005.02.008 · Cited by 1,849
Flagged first, then by citations
1 of the 39 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Items 301–337 of 337
Is AD a homogeneous nosologic entity? Yes
Martínez‐Martín, P. (2013) · Journal of Neural Transmission · doi:10.1007/s00702-013-1059-0
Jayalal, L. P. M. (2012) · Journal of the Chosun Natural Science · doi:10.13160/ricns.2012.5.2.107
Multipotent neural stem/progenitor cells as a model of genetic neuronal diseases
Kärkkäinen, V. (2012) · UEF eRepo (University of Eastern Finland)
IMMUNOTHERAPY IN COMBINATION WITH BEHAVIORAL ENRICHMENT IN A CANINE MODEL OF AGING
Davis, P. R. (2014) · UKnowledge (University of Kentucky)
Mass Spectrometry-Based Investigation of APP-Dependent Mechanisms in Neurodegeneration
Chaput, D. (2015) · Digital Commons - University of South Florida (University of South Florida)
Merlin, J. L. P. (2013) · Journal of the Chosun Natural Science · doi:10.13160/ricns.2013.6.4.220
Tuyet, P. T. D. (2014) · Journal of the Chosun Natural Science · doi:10.13160/ricns.2014.7.1.11
Is AD a homogeneous nosologic entity? Yes
Wien, S.-V. (2013)
Kaye, E. D. (2011) · TSpace (University of Toronto)
Neuro-pathological Implications of β-Amyloid Protein: An Update
Maurya, N., & Agarwal, N. R. (2018) · Proceedings of the Nature Research Society · doi:10.11605/j.pnrs.2018020061 · Cited by 2
Pinheiro, N. R. (2018) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/d.17.2018.tde-25042018-112913
Romanucci, M., & Salda, L. D. (2019) · Heat shock proteins · doi:10.1007/978-3-030-24285-5_8
Isolamento de oligômeros tóxicos do peptídeo B-amiloide usando o anticorpo de cadeia única NUsc1
Bitencourt, A. L. B. (2020) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.17.2020.tde-12022020-170537
McKeever, P. M. (2018) · TSpace (University of Toronto)
Marchi, P. M., Marrone, L., Brasseur, L., Bousset, L., Webster, C. P., Destro, M., Smith, E. F., Walther, C. G., Alfred, V., Marroccella, R., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.10.11.463891
Customer Loyalty in E-Business.
Raggad, B. G., & Lawler, J. E. (2003) · International Conference on Enterprise Information Systems
Current awareness in geriatric psychiatry
(2010) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.2391
The role of N-truncated Aβ peptides in Alzheimer’s Disease
López‐Noguerola, J. S. (2018) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-6949
Friedman, D. J., & Lal, S. (2013) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.717972974.793469783
Purro, S. A., Farmer, M., Noble, E., Sarell, C. J., Powell, M., Yip, D. C.-M., Giggins, L., Zakka, L., Thomas, D. X., Farrow, M. A., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.09.25.508690
The Mechanistic Approach Involved in the Progression of Neurodegenerative Disorders
Rather, M. A., Khan, A., Alsharani, S., Jahan, S., Siddiqui, A. J., Mehan, S., & Alexiou, A. T. (2023) · Springer eBooks · doi:10.1007/978-981-99-3848-3_2
Yang, Y., Huh, K., & Kwak, Y. T. (2024) · Geriatrics and gerontology international/Geriatrics & gerontology international · doi:10.1111/ggi.14958
Lapcinski, I. P., Petersen, A. J., Ashe, K. H., & Liu, P. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.11.648457
Rôle des ADAM dans le processus physiopathologique de la maladie d'Alzheimer
Laumet, G. O. (2010) · theses.fr (ABES) · doi:10.70675/94126786zf990z488ezb471z5f1d5686766c
Rôle du peptide amyloïde dans les maladies neurodégénératives
Combes, M. (2018) · theses.fr (ABES) · doi:10.70675/a219ef4dzbca0z4272z8bf2z74080a1976e5 · Cited by 1
Montecinos-Oliva, C. (2018) · theses.fr (ABES) · doi:10.70675/1cb0a505zb904z4045z83b4z7ec8f3bc62b9
Lam, S. (2021) · theses.fr (ABES) · doi:10.70675/60b353ffz56fcz41a2z9e53zf0d9ac078167 · Cited by 1
柳沢, 大., 遠山, 育., Ibrahim, N. F., HAMEZAH, H. S. B., Yanagisawa, D., TSUJI, M., KIUCHI, Y., Ono, K., & Tooyama, I. (n.d.) · Institutional Repositories DataBase (IRDB)
Ex vivo comparison of ACU193 and lecanemab reveals binding differences in mouse brain
Grenon, M. B., Cline, E. N., Jerecı̀ć, J., Johnson, E. A., Siemers, E., & Lemere, C. A. (2026) · Alzheimer s & Dementia · doi:10.1002/alz.71509
In vivo evidence for soluble Aβ oligomer-driven neuronal metabolic dysfunction in 5xFAD mice
Dashora, C., & Patel, A. B. (2026) · Alzheimer s Research & Therapy · doi:10.1186/s13195-026-02130-4
Shrinking of Extracellular Space During Metabolic Stress Accelerates Amyloid-β Aggregation
Oliveira, L. F. D., Karunarathne, K., Zona, D., Muschol, M., & Ullah, G. (2026) · Biomolecules · doi:10.3390/biom16071053
Structural insights into pathological protein aggregates: from amyloid fibrils to inclusion bodies
Bej, A., Mandal, N., Das, A., & Nandi, A. (2026) · Elsevier eBooks · doi:10.1016/b978-0-443-36636-9.00002-2
Zhang, Z., Wu, J., Pulgar, I. M. R., Chang, E. H. T., Chai, K., Wang, P., Jiang, S., Li, X., Oishi, K., Smith, G. S., et al. (2026) · Neurology International · doi:10.3390/neurolint18090177
BindingDB (2020) · UC San Diego · doi:10.7270/q2vx0kjw
Metadata
- Authors
- Tomic, J. L., Pensalfini, A., Head, E., & Glabe, C. G.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- Glabe, Charles G.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2009-09
- Volume
- 35
- Issue
- 3
- Pages
- 352-358
- ISSN
- 0969-9961 (ISSN-L)
- PMC
- PMC2725199
- OpenAlex
- W1970016175
- Cited by
- 336
- References
- 39
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 9 · 2023: 12 · 2022: 16 · 2021: 16 · 2020: 13 · 2019: 13 · 2018: 27 · 2017: 18 · 2016: 20 · 2015: 27 · 2014: 29 · 2013: 35 · 2012: 35
- FWCI
- 19.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (P01AG000538, AG 00538)
- 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
- Alzheimer's disease, amyloid-beta oligomers, prefibrillar oligomers, soluble oligomers, cognitive impairment, brain tissue, neuropathology, diagnostic biomarkers
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Cognition Disorders, Female, Humans, Male, Psychiatric Status Rating Scales, Receptors, Cell Surface, Immunoblotting, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Fibrillar Collagens, Protease Nexins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review