The role of CREB signaling in Alzheimer’s disease and other cognitive disorders
Open accessAbstract
Gene expression changes in the brain affect cognition during normal and pathological aging. Progress in understanding the cellular processes regulating gene expression networks in cognition is relevant to develop therapeutic interventions for age-related cognitive disorders. Synaptic efficacy mediating memory storage requires the activation of specific gene expression programs regulated, among others, by the transcription factor cAMP-response element binding protein (CREB). CREB signaling is essential for long-lasting changes in synaptic plasticity that mediates the conversion of short-term memory to long-term memory. CREB signaling has been recently involved in several brain pathological conditions including cognitive and neurodegenerative disorders. The β-amyloid (Aβ) peptide, which plays a crucial role in the pathogenesis of Alzheimer's disease, alters hippocampal-dependent synaptic plasticity and memory and mediates synapse loss through the CREB signaling pathway. The fact that altered CREB signaling has been implicated in other cognitive disorders including Huntington's disease and Rubinstein-Taybi and Coffin-Lowry syndromes suggests a crucial role of CREB signaling in cognitive dysfunction. In this review paper, we summarize recent findings indicating a role of CREB and its coactivators CREB binding protein and CREB-regulated transcription coactivator in cognition during normal and pathological aging. We also discuss the development of novel therapeutic strategies based…
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In addition to its crucial role in maintaining synaptic plasticity and facilitation of short-term memory to long-term memory, the CREB signaling pathway also mediates synapse loss induced by Aβ in AD.
“In addition to its crucial role in maintaining synaptic plasticity and facilitation of short-term memory to long-term memory, the CREB signaling pathway also mediates synapse loss induced by Aβ in AD [75].”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [75]
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- Authors
- Saura, C. A., & Valero, J.
- Affiliations
- Universitat Autònoma de Barcelona (ES)
- Corresponding author
- Saura, Carlos A.
- Venue
- revneuro
- Publisher
- Walter de Gruyter GmbH
- Published
- 2011-04-01
- Volume
- 22
- Issue
- 2
- Pages
- 153-169
- ISSN
- 0334-1763 (ISSN-L)
- 2191-0200
- OpenAlex
- W2014530155
- Cited by
- 312
- References
- 185
- Citations by year
- 2026: 8 · 2025: 22 · 2024: 35 · 2023: 23 · 2022: 20 · 2021: 29 · 2020: 22 · 2019: 14 · 2018: 27 · 2017: 18 · 2016: 20 · 2015: 13 · 2014: 13 · 2013: 20 · 2012: 23
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- green
- zenodo.org
- Licence
- other-oa
- Locations
- Reviews in the Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- CREB signaling, Alzheimer's disease, cognitive decline, synaptic plasticity, memory consolidation, amyloid-beta, hippocampus, CREB-binding protein, Huntington's disease, Rubinstein-Taybi syndrome, Coffin-Lowry syndrome, gene expression regulation
- MeSH terms
- Alzheimer Disease, Animals, Cognition Disorders, Humans, Signal Transduction, CREB-Binding Protein
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