ArticleMolecular neurobiology2018
Early Preclinical Changes in Hippocampal CREB-Binding Protein Expression in a Mouse Model of Familial Alzheimer's Disease.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Integration of phytochemical profiling and computational approaches to evaluate the neuroprotective potential ofBiotechnology reports (Amsterdam, Netherlands) · 2025Article
- Impact of semaphorin, Sema3F, on the gene transcription and protein expression of CREB and its binding protein CREBBP in primary hippocampal neurons of rats.Open life sciences · 2025Article
- Assessing cognitive flexibility in mice using a custom-built touchscreen chamber.Frontiers in behavioral neuroscience · 2025Article
- Neuroprotective Potential of Aminonaphthoquinone Derivatives Against Amyloid Beta-Induced Neuronal Cell Death Through Modulation of SIRT1 and BACE1.Neurochemical research · 2024Article
- An enriched environment improves maternal sleep deprivation-induced cognitive deficits and synaptic plasticity via hippocampal histone acetylation.Brain and behavior · 2023Article
- The effect of Aβ seeding is dependent on the presence of knock-in genes in theFrontiers in dementia · 2022Article
- The CBP KIX domain regulates long-term memory and circadian activity.BMC biology · 2020Article
- More than anti-malarial agents: therapeutic potential of artemisinins in neurodegeneration.Neural regeneration research · 2019Review
- The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia.Frontiers in aging neuroscience · 2019Article
- TMP21 in Alzheimer's Disease: Molecular Mechanisms and a Potential Target.Frontiers in cellular neuroscience · 2019Review
- Adenosine Augmentation Evoked by an ENT1 Inhibitor Improves Memory Impairment and Neuronal Plasticity in the APP/PS1 Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2018Article
- Chronic Hippocampal Expression of Notch Intracellular Domain Induces Vascular Thickening, Reduces Glucose Availability, and Exacerbates Spatial Memory Deficits in a Rat Model of Early Alzheimer.Molecular neurobiology · 2018Article
- The Contribution and Therapeutic Potential of Epigenetic Modifications in Alzheimer's Disease.Frontiers in neuroscience · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
Abstract
The molecular basis of memory loss in Alzheimer's disease (AD), the main cause of senile dementia, is under investigation. In the present study, we have focused on the early hippocampal memory-related changes in APPswe/PS1dE9 (APP/PS1) mice, a well-established mouse model of familial AD. It is well known that molecules like cAMP response element binding (CREB) and binding protein (CBP) play a crucial role in memory consolidation. We analyzed CBP on its transcriptional activity and protein levels, finding a significant downregulation of both of them at 3-month-old mice. In addition, the downregulation of this molecule was associated with a decrease on acetylation levels of histone H3 in the hippocampus of APP/PS1 mice. Moreover, the p-CREB levels, which are important for memory acquisition at 3 months in APP/PS1 mice, were downregulated. Furthermore, we suggest that early neuroinflammation, especially due to the Tnfα gene increased expression, could also be responsible to this process of memory loss. Given all the previously mentioned results, we propose that an early suitable treatment to prevent the evolution of the disease should include a combination of drugs, including anti-inflammatories, which may decrease glial activation and Tnfα levels, and phosphodiesterase inhibitors that increase cAMP levels.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.