ArticleCNS neuroscience & therapeutics2014
Valproic acid reduces neuritic plaque formation and improves learning deficits in APP(Swe) /PS1(A246E) transgenic mice via preventing the prenatal hypoxia-induced down-regulation of neprilysin.
Article in CNS neuroscience & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 51 citations in OpenAlex.
- Histone Deacetylase Inhibitors Improve Memory Function and Decrease Neuropathology in APP/PS1 Mice.Research square · 2026Article
- Beyond epilepsy: The expanding role of valproic acid in Alzheimer disease therapy - a review.The Journal of pharmacology and experimental therapeutics · 2025Review
- Molecular Pathways of Altered Brain Development in Fetuses Exposed to Hypoxia.International journal of molecular sciences · 2023Review
- Strategies for Treatment of Disease-Associated Dementia Beyond Alzheimer's Disease: An Update.Current neuropharmacology · 2023Review
- Article
- Developmental Profile of Brain Neprilysin Expression Correlates with Olfactory Behaviour of Rats.Journal of molecular neuroscience : MN · 2021Article
- Glucocorticoid-Dependent Mechanisms of Brain Tolerance to Hypoxia.International journal of molecular sciences · 2021Review
- 8a, a New Acridine Antiproliferative and Pro-Apoptotic Agent Targeting HDAC1/DNMT1.International journal of molecular sciences · 2021Article
- Targeting Neprilysin (NEP) pathways: A potential new hope to defeat COVID-19 ghost.Biochemical pharmacology · 2020Review
- Bidirectional relationship between sleep and Alzheimer's disease: role of amyloid, tau, and other factors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Review
- Targeting amyloid clearance in Alzheimer's disease as a therapeutic strategy.British journal of pharmacology · 2019Review
- Vascular Dysfunction in Alzheimer's Disease: A Prelude to the Pathological Process or a Consequence of It?Journal of clinical medicine · 2019Review
- Valproic Acid Stimulates Hippocampal NeurogenesisFrontiers in aging neuroscience · 2019Article
- What are the links between hypoxia and Alzheimer's disease?Neuropsychiatric disease and treatment · 2019Article
- 5-HIAA induces neprilysin to ameliorate pathophysiology and symptoms in a mouse model for Alzheimer's disease.Acta neuropathologica communications · 2018Article
- Age-related epigenetic changes in hippocampal subregions of four animal models of Alzheimer's disease.Molecular and cellular neurosciences · 2018Article
- Role of Prenatal Hypoxia in Brain Development, Cognitive Functions, and Neurodegeneration.Frontiers in neuroscience · 2018Review
- Age-related Disturbances in DNA (hydroxy)methylation in APP/PS1 Mice.Translational neuroscience · 2018Article
- Effect of pregabalin on contextual memory deficits and inflammatory state-related protein expression in streptozotocin-induced diabetic mice.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Neuroprotection as a Potential Therapeutic Perspective in Neurodegenerative Diseases: Focus on Antiepileptic Drugs.Neurochemical research · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsPreviously, we have documented that prenatal hypoxia can aggravate the cognitive impairment and Alzheimer's disease (AD) neuropathology in APP(Swe) /PS1(A246E) (APP/PS1) transgenic mice, and valproic acid (VPA) can prevent hypoxia-induced down-regulation of β-amyloid (Aβ) degradation enzyme neprilysin (NEP) in primary neurons. In this study, we have investigated the molecular mechanisms of VPA's anti-AD effects and found that VPA can reduce the prenatal hypoxia-induced neuritic plaque formation and improve the learning deficits in the AD mouse model.
methodsThe pregnant APP/PS1 transgenic mice were exposed in a hypobaric chamber. Neuritic plaque staining, Morris water maze, and enzyme-linked immunosorbent assay (ELISA) were used to detect the effects of VPA on Aβ neuropathology, learning, and memory. Chromatin immunoprecipitation (ChIP) assays and real-time PCR (RT-PCR) were used to determine the effect of VPA on the histone3 acetylation (H3-Ace).
resultsWe found that VPA can inhibit neuritic plaque formation and improve the learning and memory in the prenatal hypoxic APP/PS1 transgenic mice. In addition, VPA treatment can decrease the soluble and insoluble Aβ42 levels and increase the NEP expression via up-regulation of H3-Ace in the APP/PS1 transgenic mice.
conclusionValproic acid is able to attenuate the prenatal hypoxia-induced Aβ neuropathology and learning and memory deficits via inhibiting the activation of histone deacetylase 1 (HDAC1), preventing the decrease in H3-Ace in the NEP promoter regions and reducing the down-regulation of NEP.
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.