The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Lack of Pathology in a Triple Transgenic Mouse Model of Alzheimer’s Disease after Overexpression of the Anti-Apoptotic Protein Bcl-2
Open accessAbstract
Alzheimer's disease (AD) is characterized by the accumulation of plaques containing beta-amyloid (Abeta) and neurofibrillary tangles (NFTs) consisting of modified tau. Although Abeta deposition is thought to precede the formation of NFTs in AD, the molecular steps connecting these two pathologies is not known. Previous studies have suggested that caspase activation plays an important role in promoting the pathology associated with AD. To further understand the contribution of caspases in disease progression, a triple transgenic Alzheimer's mouse model overexpressing the anti-apoptotic protein Bcl-2 was generated. Here we show that overexpression of Bcl-2 limited caspase-9 activation and reduced the caspase cleavage of tau. Moreover, overexpression of Bcl-2 attenuated the processing of APP (amyloid precursor protein) and tau and reduced the number of NFTs and extracellular deposits of Abeta associated with these animals. In addition, overexpression of Bcl-2 in 3xTg-AD mice improved place recognition memory. These findings suggest that the activation of apoptotic pathways may be an early event in AD and contributes to the pathological processes that promote the disease mechanisms underlying AD.
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 source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Recent evidence suggests that executioner caspases 3 and 7 may contribute to tau, the protein responsible for forming NFTs, pathology by cleaving tau after Asp421 to yield a cytotoxic Δtau fragment (Rissman et al., 2004; Rohn et al., 2008; de Calignon et al., 2010).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Rohn et al., 2008
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Interestingly, staining with Fluoro Jade C, a marker for degenerating neurons, did not reveal evidence for neurodegeneration [109] and a quantitative analysis of CA1 neuron numbers revealed a lack of neuron loss in this brain region in 3xTg mice during aging [110].”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [109]
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
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
Mirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961
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
Cell death during development of the nervous system
Oppenheim, R. W. (1991) · Annual Review of Neuroscience · doi:10.1146/annurev.ne.14.030191.002321 · Cited by 3,084
Consortium to Establish a Registry for Alzheimer's Disease (CERAD)
Fillenbaum, G., & Heyman, A. (2002) · doi:10.1002/0470846410.ch42(iii · Cited by 2,859
Molecular mechanisms of caspase regulation during apoptosis
Riedl, S. J., & Shi, Y. (2004) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1496 · Cited by 1,933
Vaux, D. L., & Korsmeyer, S. J. (1999) · Cell · doi:10.1016/s0092-8674(00)80564-4 · Cited by 1,564
Martinou, J., Dubois‐Dauphin, M., Staple, J. K., Rodríguez, I., Frankowski, H., Missotten, M., Albertini, P., Talabot, D., Catsicas, S., & Pietra, C. (1994) · Neuron · doi:10.1016/0896-6273(94)90266-6 · Cited by 1,087
Caspase cleavage of tau: Linking amyloid and neurofibrillary tangles in Alzheimer's disease
Gamblin, T. C., Chen, F., Zambrano, A., Abraha, A., Lagalwar, S., Guillozet, A. L., Lu, M., Fu, Y., Garcia-Sierra, F., LaPointe, N., et al. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1630428100 · Cited by 831
Hippocampal damage and exploratory preferences in rats: memory for objects, places, and contexts
Mumby, D. G., Gaskin, S., Glenn, M. J., Schramek, T. E., & Lehmann, H. (2002) · Learning & Memory · doi:10.1101/lm.41302 · Cited by 714
Cited by
Sorted by citations
Amyloid Precursor Protein Processing and Alzheimer's Disease
O'Brien, R. J., & Wong, P. C. (2011) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-061010-113613 · Cited by 2,061
Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins
Singh, R., Letai, A., & Sarosiek, K. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0089-8 · Cited by 2,111
The Inositol Trisphosphate/Calcium Signaling Pathway in Health and Disease
Berridge, M. J. (2016) · Physiological Reviews · doi:10.1152/physrev.00006.2016 · Cited by 779
Favaloro, B., Allocati, N., Graziano, V., Ilio, C. D., & Laurenzi, V. D. (2012) · Aging · doi:10.18632/aging.100459 · Cited by 608
Autophagy and Alzheimer’s Disease: From Molecular Mechanisms to Therapeutic Implications
Uddin, M. S., Stachowiak, A., Mamun, A. A., Tzvetkov, N. T., Takeda, S., Atanasov, A. G., Bergantin, L. B., Abdel-Daim, M. M., & Stankiewicz, A. M. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00004 · Cited by 395
Metadata
- Authors
- Rohn, T. T., Vyas, V., Hernandez-Estrada, T., Nichol, K. E., Christie, L.-A., & Head, E.
- Affiliations
- Boise State University (US)
- University of California, Irvine (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-03-19
- Volume
- 28
- Issue
- 12
- Pages
- 3051-3059
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6670712
- OpenAlex
- W2086662417
- Cited by
- 146
- References
- 43
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 8 · 2023: 9 · 2022: 8 · 2021: 6 · 2020: 7 · 2019: 9 · 2018: 9 · 2017: 2 · 2016: 10 · 2015: 6 · 2014: 9 · 2013: 7 · 2012: 8
- FWCI
- 9.28
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- ScholarWorks (Boise State University) (submittedVersion)
- Funders
- American Health Assistance Foundation
- National Institutes of Health (AG16573)
- Directorate for Biological Sciences
- University of California, Irvine (P20RR016454, P50 AG16573)
- National Research Council Canada
- National Institute on Aging (P50 AG 16573, P50AG016573)
- National Center for Research Resources (P50 AG16573, P20RR016454)
- 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, Bcl-2, caspase-9, apoptosis, neurofibrillary tangles, amyloid plaques, tau cleavage, APP processing, 3xTg-AD mice, triple transgenic mouse model
- MeSH terms
- Alzheimer Disease, Amyloid, Animals, Behavior, Animal, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Fluoresceins, Gene Expression Regulation, Humans, Memory, Mice, Transgenic, Organic Chemicals, Amyloid beta-Protein Precursor, tau Proteins, Proto-Oncogene Proteins c-bcl-2, Caspases, Infarction, Middle Cerebral Artery, Mice, Presenilin-1
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
