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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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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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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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