Cited by 149Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Acute inhibition of calcineurin restores associative learning and memory in Tg2576 APP transgenic mice

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Dineley, Kelly T., Hogan, Dale, Zhang, Wen-Ru, Taglialatela, Giulio·2007·Neurobiology of Learning and Memory

DOI 10.1016/j.nlm.2007.03.010PMC PMC2031869

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Abstract

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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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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Cleary, 2005, Natural oligomers of the amyloid-beta protein specifically disrupt cognitive function, Nature Neuroscience, 8, 79, 10.1038/nn1372 · DOI

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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
ORCID: Dineley, Kelly T.
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)
DOI: 10.1016/j.nlm.2007.03.010
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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Acute inhibition of calcineurin restores associative learning and memory in Tg2576 APP transgenic mice

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