Evidence map›Paper›PMID 28771976›Full record

ArticleAging cell2017

HDAC3 negatively regulates spatial memory in a mouse model of Alzheimer's disease.

Xiaolei Zhu, Sulei Wang, Linjie Yu, Jiali Jin, Xing Ye, Yi Liu, Yun Xu

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.1field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 107 citations in OpenAlex.

  1. Simvastatin rescues cognitive impairment in an AβNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Xiaolei ZhuThe State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Medical School, Drum Tower Hospital, Nanjing University, Nanjing, China.
Sulei WangDepartment of Neurology, Nanjing Hospital of Traditional Chinese Medicine, Nanjing, China.
Linjie YuThe State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Medical School, Drum Tower Hospital, Nanjing University, Nanjing, China.
Jiali JinThe State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Medical School, Drum Tower Hospital, Nanjing University, Nanjing, China.
Xing YeThe State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Medical School, Drum Tower Hospital, Nanjing University, Nanjing, China.
Yi LiuThe State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Medical School, Drum Tower Hospital, Nanjing University, Nanjing, China.
Yun XuThe State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Medical School, Drum Tower Hospital, Nanjing University, Nanjing, China.
Nanjing Drum Tower Hospital · CNNanjing Traditional Chinese Medicine Hospital · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accumulation and deposition of beta-amyloid (Aβ) is a key neuropathological hallmark of Alzheimer's disease (AD). Histone deacetylases (HDACs) are promising therapeutic targets for the treatment of AD, while the specific HDAC isoforms associated with cognitive improvement are poorly understood. In this study, we investigate the role of HDAC3 in the pathogenesis of AD. Nuclear HDAC3 is significantly increased in the hippocampus of 6- and 9-month-old APPswe/PS1dE9 (APP/PS1) mice compared with that in age-matched wild-type C57BL/6 (B6) mice. Lentivirus -mediated inhibition or overexpression of HDAC3 was used in the hippocampus of APP/PS1 mice to investigate the role of HDAC3 in spatial memory, amyloid burden, dendritic spine density, glial activation and tau phosphorylation. Inhibition of HDAC3 in the hippocampus attenuates spatial memory deficits, as indicated in the Morris water maze test, and decreases amyloid plaque load and Aβ levels in the brains of APP/PS1 mice. Dendritic spine density is increased, while microglial activation is alleviated after HDAC3 inhibition in the hippocampus of 9-month-old APP/PS1 mice. Furthermore, HDAC3 overexpression in the hippocampus increases Aβ levels, activates microglia, and decreases dendritic spine density in 6-month-old APP/PS1 mice. In conclusion, our results indicate that HDAC3 negatively regulates spatial memory in APP/PS1 mice and HDAC3 inhibition might represent a potential therapy for the treatment of AD.

Indexed as

AcrylamidesAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCell NucleusDendritic SpinesDisease Models, AnimalGene Expression RegulationGenetic VectorsHippocampusHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHumansLentivirusMaze LearningAcrylamidesAmyloid beta-PeptidesHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesMapt protein, mousePhenylenediaminesRGFP966tau ProteinsAlzheimer's diseasebeta-amyloidhistone deacetylase3spatial memory

Identifiers

PMID28771976
PMCPMC5595690
OpenAlexW2744186560

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.