The DOI matches its Crossref record; 38 of the 40 references it cites were found in a registry or an index.
Acute inhibition of calcineurin restores associative learning and memory in Tg2576 APP transgenic mice
Open accessAbstract
Misfolded amyloid beta peptide (Abeta) is a pathological hallmark of Alzheimer's disease (AD), a neurodegenerative illness characterized by cognitive deficits and neuronal loss. Transgenic mouse models of Abeta over-production indicate that Abeta-induced cognitive deficits occur in the absence of overt neuronal death, suggesting that while extensive neuronal death may be associated with later stages of the human disease, subtle physiological changes may underlie initial cognitive deficits. Therefore, identifying signaling elements involved in those Abeta-induced cognitive impairments that occur prior to loss of neurons may reveal new potential pharmacological targets. Here, we report that the enzymatic activity of calcineurin, a key protein phosphatase involved in phosphorylation-dependent kinase activity crucial for synaptic plasticity and memory function, is upregulated in the CNS of the Tg2576 animal model for Abeta over-production. Furthermore, acute treatment of Tg2576 mice with the calcineurin inhibitor FK506 (10mg/kg i.p.) improves memory function. These results indicate that calcineurin may mediate some of the cognitive effects of excess Abeta such that inhibition of calcineurin shall be further explored as a potential treatment to reverse cognitive impairments in AD.
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“These results are apparently in contrast with the evaluations of APP transgenic mice in fear conditioning test, which demonstrated clear memory impairments in Tg2576 model at ages preceding Aβ deposition [32].”
From Normal cognition in transgenic BRI2-Aβ mice (2013) · cites this paper as [32]
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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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory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×
“…the most fundamental neurotoxic event in AD (Van Gassen and Annaert, 2003), several lines of evidence indicate that oligomeric, soluble forms of Ab, rather than amyloid plaques, initiate the cognitive deficits characteristic of the disease (Cleary et al., 2005a; Glabe, 2006; Lesne et al., 2006).”
BackgroundRetractedAmyloid 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
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
Natural oligomers of the amyloid-β protein specifically disrupt cognitive function
Cleary, J. P., Walsh, D. M., Hofmeister, J. J., Shankar, G. M., Kuskowski, M. A., Selkoe, D. J., & Ashe, K. H. (2004) · Nature Neuroscience · doi:10.1038/nn1372 · Cited by 1,722
Regulation of NMDA receptor trafficking by amyloid-β
Snyder, E. M., Nong, Y., Almeida, C. G., Paul, S., Moran, T., Choi, E. Y., Nairn, A. C., Salter, M. W., Lombroso, P. J., Gouras, G. K., et al. (2005) · Nature Neuroscience · doi:10.1038/nn1503 · Cited by 1,561
Ca 2+ -Induced Apoptosis Through Calcineurin Dephosphorylation of BAD
Wang, H., Pathan, N., Ethell, I. M., Krajewski, S., Yamaguchi, Y., Shibasaki, F., McKeon, F., Bobo, T., Franke, T. F., & Reed, J. C. (1999) · Science · doi:10.1126/science.284.5412.339 · Cited by 1,132
Kawarabayashi, T., Younkin, L. H., Saido, T. C., Shoji, M., Ashe, K. H., & Younkin, S. G. (2001) · The Journal of Neuroscience · doi:10.1523/jneurosci.21-02-00372.2001 · Cited by 1,053
Clinical Pharmacokinetics and Pharmacodynamics of Tacrolimus in Solid Organ Transplantation
Staatz, C. E., & Tett, S. E. (2004) · Clinical Pharmacokinetics · doi:10.2165/00003088-200443100-00001 · Cited by 920
Alzheimer's Disease: Molecular Understanding Predicts Amyloid-Based Therapeutics
Selkoe, D. J., & Schenk, D. (2003) · The Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.43.100901.140248 · Cited by 829
The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's Disease
Westerman, M. A., Cooper-Blacketer, D., Mariash, A., Kotilinek, L., Kawarabayashi, T., Younkin, L. H., Carlson, G. A., Younkin, S. G., & Ashe, K. H. (2002) · Journal of Neuroscience · doi:10.1523/jneurosci.22-05-01858.2002 · Cited by 731
Research works printed but not linked: 1
- Cleary, 2005, Natural oligomers of the amyloid-beta protein specifically disrupt cognitive function, Nature Neuroscience, 8, 79, 10.1038/nn1372 · DOI
Cited by
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Animal models of Alzheimer's disease and frontotemporal dementia
Götz, J., & Ittner, L. M. (2008) · Nature Reviews Neuroscience · doi:10.1038/nrn2420 · Cited by 676
Kuchibhotla, K. V., Goldman, S. T., Lattarulo, C. R., Wu, H.-Y., Hyman, B. T., & Bacskai, B. J. (2008) · Neuron · doi:10.1016/j.neuron.2008.06.008 · Cited by 614
Synapses and Alzheimer's Disease
Sheng, M., Sabatini, B. L., & Sudhof, T. C. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a005777 · Cited by 436
Calcium hypothesis of Alzheimer’s disease
Berridge, M. J. (2009) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/s00424-009-0736-1 · Cited by 394
Wu, H.-Y., Hudry, E., Hashimoto, T., Kuchibhotla, K., Rozkalne, A., Fan, Z., Spires-Jones, T., Xie, H., Arbel-Ornath, M., Grosskreutz, C. L., et al. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.4456-09.2010 · Cited by 367
Metadata
- Authors
- Dineley, K. T., Hogan, D., Zhang, W.-R., & Taglialatela, G.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Taglialatela, Giulio
- Venue
- Neurobiology of Learning and Memory
- Publisher
- Elsevier BV
- Published
- 2007-09
- Volume
- 88
- Issue
- 2
- Pages
- 217-224
- ISSN
- 1074-7427 (ISSN-L)
- PMC
- PMC2031869
- OpenAlex
- W2067155622
- Cited by
- 149
- References
- 40
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 9 · 2023: 11 · 2022: 4 · 2021: 8 · 2020: 2 · 2019: 4 · 2018: 3 · 2017: 9 · 2016: 9 · 2015: 8 · 2014: 12 · 2013: 10 · 2012: 6
- FWCI
- 8.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Learning and Memory (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R21NS053986)
- 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
- calcineurin, amyloid-beta, Alzheimer's disease, Tg2576 mice, FK506, calcineurin inhibition, associative learning, memory impairment, protein phosphatase, synaptic plasticity, cognitive impairment
- MeSH terms
- Animals, Association Learning, Cognition, Conditioning, Psychological, Immunosuppressive Agents, Memory, Mice, Transgenic, Neurons, Amyloid beta-Peptides, Tacrolimus, Cell Death, Mice, Calcineurin Inhibitors
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