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Cited by 42Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

Increased EID1 nuclear translocation impairs synaptic plasticity and memory function associated with pathogenesis of Alzheimer’s disease

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Liu, Rugao, Lei, Joy X., Luo, Chun, Lan, Xun, Chi, Liying, Deng, Panyue, Lei, Saobo, Ghribi, Othman +1 more·2012·Neurobiology of Disease
DOI 10.1016/j.nbd.2011.12.007PMC PMC3276739
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Abstract

Though loss of function in CBP/p300, a family of CREB-binding proteins, has been causally associated with a variety of human neurological disorders, such as Rubinstein-Taybi syndrome, Huntington's disease and drug addiction, the role of EP300 interacting inhibitor of differentiation 1 (EID1), a CBP/p300 inhibitory protein, in modulating neurological functions remains completely unknown. Through the examination of EID1 expression and cellular distribution, we discovered that there is a significant increase of EID1 nuclear translocation in the cortical neurons of Alzheimer's disease (AD) patient brains compared to that of control brains. To study the potential effects of EID1 on neurological functions associated with learning and memory, we generated a transgenic mouse model with a neuron-specific expression of human EID1 gene in the brain. Overexpression of EID1 led to an increase in its nuclear localization in neurons mimicking that seen in human AD brains. The transgenic mice had a disrupted neurofilament organization and increase of astrogliosis in the cortex and hippocampus. Furthermore, we demonstrated that overexpression of EID1 reduced hippocampal long-term potentiation and impaired spatial learning and memory function in the transgenic mice. Our results indicated that the negative effects of extra nuclear EID1 in transgenic mouse brains are likely due to its inhibitory function on CBP/p300 mediated histone and p53 acetylation, thus affecting the expression of downstream genes involved in the maintenance of neuronal structure and function. Together, our data raise the possibility that alteration of EID1 expression, particularly the increase of EID1 nuclear localization that inhibits CBP/p300 activity in neuronal cells, may play an important role in AD pathogenesis.

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  • CBP/p300 transcriptional co-activators are a conserved mechanism for responding to mitochondrial stress.

    “The CBP/p300 transcriptional co-activators are a conserved mechanism for responding to mitochondrial stress”

    From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [121]

    The Introduction (page unavailable) identifies CBP and p300 as transcriptional co-activators involved in signal-responsive gene expression. It does not say they are a conserved mechanism for responding to mitochondrial stress; the paper instead discusses their roles in neuronal survival, memory and Alzheimer’s disease. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • Loss of function of CBP/p300 is associated with familial AD and neuronal apoptosis.

    “and the loss of function of CBP/p300 is associated with familial AD and neuronal apoptosis [117,118,119,120,121].”

    From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [121]

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Authors
Liu, R., Lei, J. X., Luo, C., Lan, X., Chi, L., Deng, P., Lei, S., Ghribi, O., & Liu, Q. Y.
Affiliations
  • University of North Dakota (US)
  • Institute for Biological Sciences (CA)
Corresponding author
  • Ghribi, Othman
  • Liu, Qing Yan
ORCID
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2012-03
Volume
45
Issue
3
Pages
902-912
ISSN
0969-9961 (ISSN-L)
DOI
10.1016/j.nbd.2011.12.007
PMC
PMC3276739
OpenAlex
W2038239227
Cited by
42
References
4
Citations by year
2026: 2 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 1 · 2019: 4 · 2018: 6 · 2017: 1 · 2016: 2 · 2015: 4 · 2014: 7 · 2013: 4 · 2012: 1
FWCI
2.48
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neurobiology of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • NPARC (acceptedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
NIH (NS45829, HL75034)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
EID1, Alzheimer's disease, CBP/p300, nuclear translocation, synaptic plasticity, long-term potentiation, spatial learning and memory, astrocyte activation, histone acetylation, p53 acetylation, CREB-binding protein, transgenic mouse model, hippocampus, cortical neurons
MeSH terms
Alzheimer Disease, Animals, Brain, Cell Nucleus, Electric Stimulation, Glial Fibrillary Acidic Protein, Histones, Humans, Membrane Potentials, Membrane Proteins, Memory Disorders, Mice, Transgenic, Microtubule-Associated Proteins, Neuronal Plasticity, Neurons, Nuclear Proteins, Phosphoproteins, Phosphopyruvate Hydratase, Repressor Proteins, Transfection, Tumor Suppressor Protein p53, Teratocarcinoma, Patch-Clamp Techniques, Maze Learning, Cell Cycle Proteins, Protein Transport, Cell Line, Tumor, p300-CBP Transcription Factors, Mice, In Vitro Techniques

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