Evidence map›Paper›PMID 38421101›Full record

ArticleCNS neuroscience & therapeutics2024

HDAC9-mediated calmodulin deacetylation induces memory impairment in Alzheimer's disease.

Hai-Long Zhang, Shufen Hu, Pin Yang, Han-Chun Long, Quan-Hong Ma, Dong-Min Yin, Guang-Yin Xu

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. 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.

Hai-Long ZhangJiangsu Key Laboratory of Neuropsychiatric Diseases, Institute of Neuroscience, Suzhou Medical College of Soochow University, Medical Center of Soochow University, Suzhou, China.ORCID 0000-0002-8720-2734
Shufen HuJiangsu Key Laboratory of Neuropsychiatric Diseases, Institute of Neuroscience, Suzhou Medical College of Soochow University, Medical Center of Soochow University, Suzhou, China.
Pin YangKey Laboratory of Brain Functional Genomics, Ministry of Education and Shanghai, School of Life Science, East China Normal University, Shanghai, China.
Han-Chun LongDepartment of Neurology, The Affiliated Xingyi City Hospital of Guizhou Medical University, Xingyi, China.
Quan-Hong MaJiangsu Key Laboratory of Neuropsychiatric Diseases, Institute of Neuroscience, Suzhou Medical College of Soochow University, Medical Center of Soochow University, Suzhou, China.
Dong-Min YinKey Laboratory of Brain Functional Genomics, Ministry of Education and Shanghai, School of Life Science, East China Normal University, Shanghai, China.
Guang-Yin XuJiangsu Key Laboratory of Neuropsychiatric Diseases, Institute of Neuroscience, Suzhou Medical College of Soochow University, Medical Center of Soochow University, Suzhou, China.ORCID 0000-0002-5465-5892
Soochow University · CNEast China Normal University · CNGuiyang Medical University · CN

Funding

China Postdoctoral Science Foundation 2022M712314National Natural Science Foundation of China 31970900National Natural Science Foundation of China 32230041National Natural Science Foundation of China 82201575
6 · The paper itself

Abstract

aimsAlzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive dysfunction and memory impairment. AD pathology involves protein acetylation. Previous studies have mainly focused on histone acetylation in AD, however, the roles of nonhistone acetylation in AD are less explored.

methodsThe protein acetylation and expression levels were detected by western blotting and co-immunoprecipitation. The stoichiometry of acetylation was measured by home-made and site-specific antibodies against acetylated-CaM (Ac-CaM) at K22, K95, and K116. Hippocampus-dependent learning and memory were evaluated by using the Morris water maze, novel object recognition, and contextual fear conditioning tests.

resultsWe showed that calmodulin (CaM) acetylation is reduced in plasma of AD patients and mice. CaM acetylation and its target Ca

conclusionsHDAC9-mediated CaM deacetylation induces memory impairment in AD, HDAC9, or CaM acetylation may become potential therapeutic targets for AD.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAnimalsCalmodulinDisease Models, AnimalHippocampusHistone DeacetylasesHumansMemory DisordersMiceMice, TransgenicRepressor ProteinsCalmodulinHDAC9 protein, humanHistone DeacetylasesRepressor ProteinsacetylationAlzheimer's diseaseCaMHDAC9memory impairment

Identifiers

PMID38421101
PMCPMC10850929
OpenAlexW4391650871

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.