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Articles, Cellular/Molecular

PPARγ Recruitment to Active ERK during Memory Consolidation Is Required for Alzheimer's Disease-Related Cognitive Enhancement

Jordan B. Jahrling, Caterina M. Hernandez, Larry Denner and Kelly T. Dineley
Journal of Neuroscience 12 March 2014, 34 (11) 4054-4063; DOI: https://doi.org/10.1523/JNEUROSCI.4024-13.2014
Jordan B. Jahrling
1Mitchell Center for Neurodegenerative Diseases,
2Departments of Neurology and
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Caterina M. Hernandez
1Mitchell Center for Neurodegenerative Diseases,
2Departments of Neurology and
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Larry Denner
1Mitchell Center for Neurodegenerative Diseases,
3Internal Medicine, Division of Endocrinology,
4McCoy Stem Cells and Diabetes Mass Spectrometry Research Laboratory,
5Sealy Center for Molecular Medicine, and
6Institute for Translational Science, University of Texas Medical Branch, Galveston, Texas 77555
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Kelly T. Dineley
1Mitchell Center for Neurodegenerative Diseases,
2Departments of Neurology and
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Abstract

Cognitive impairment is a quintessential feature of Alzheimer's disease (AD) and AD mouse models. The peroxisome proliferator-activated receptor-γ (PPARγ) agonist rosiglitazone improves hippocampus-dependent cognitive deficits in some AD patients and ameliorates deficits in the Tg2576 mouse model for AD amyloidosis. Tg2576 cognitive enhancement occurs through the induction of a gene and protein expression profile reflecting convergence of the PPARγ signaling axis and the extracellular signal-regulated protein kinase (ERK) cascade, a critical mediator of memory consolidation. We therefore tested whether PPARγ and ERK associated in protein complexes that subserve cognitive enhancement through PPARγ agonism. Coimmunoprecipitation of hippocampal extracts revealed that PPARγ and activated, phosphorylated ERK (pERK) associated in Tg2576 in vivo, and that PPARγ agonism facilitated recruitment of PPARγ to pERK during memory consolidation. Furthermore, the amount of PPARγ recruited to pERK correlated with the cognitive reserve in humans with AD and in Tg2576. Our findings implicate a previously unidentified PPARγ–pERK complex that provides a molecular mechanism for the convergence of these pathways during cognitive enhancement, thereby offering new targets for therapeutic development in AD.

  • Alzheimer's
  • hippocampus
  • in vitro reconstitution
  • protein complex
  • transgenic
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The Journal of Neuroscience: 34 (11)
Journal of Neuroscience
Vol. 34, Issue 11
12 Mar 2014
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PPARγ Recruitment to Active ERK during Memory Consolidation Is Required for Alzheimer's Disease-Related Cognitive Enhancement
Jordan B. Jahrling, Caterina M. Hernandez, Larry Denner, Kelly T. Dineley
Journal of Neuroscience 12 March 2014, 34 (11) 4054-4063; DOI: 10.1523/JNEUROSCI.4024-13.2014

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PPARγ Recruitment to Active ERK during Memory Consolidation Is Required for Alzheimer's Disease-Related Cognitive Enhancement
Jordan B. Jahrling, Caterina M. Hernandez, Larry Denner, Kelly T. Dineley
Journal of Neuroscience 12 March 2014, 34 (11) 4054-4063; DOI: 10.1523/JNEUROSCI.4024-13.2014
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Keywords

  • Alzheimer's
  • hippocampus
  • in vitro reconstitution
  • protein complex
  • transgenic

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