Evidence map›Paper›PMID 28473768›Full record

ArticleFrontiers in aging neuroscience2017

Knockdown of pp32 Increases Histone Acetylation and Ameliorates Cognitive Deficits.

Qiong Feng, Gao-Shang Chai, Zhi-Hao Wang, Yu Hu, Dong-Sheng Sun, Xiao-Guang Li, Rong-Hong Ma, Yi-Rong Li, Dan Ke, Jian-Zhi Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

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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

11 authors at 3 institutions in 1 country.

Qiong FengKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Gao-Shang ChaiKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Zhi-Hao WangKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Yu HuKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Dong-Sheng SunKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Xiao-Guang LiKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Rong-Hong MaDepartment of Laboratory Medicine, Tongji Medical College, Union Hospital, Huazhong University of Science and TechnologyWuhan, China.
Yi-Rong LiDepartment of Laboratory Medicine, Zhongnan Hospital, Wuhan UniversityWuhan, China.
Dan KeKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Jian-Zhi WangKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Gong-Ping LiuKey Laboratory of Ministry of Education of China for Neurological Disorders, Department of Pathophysiology, Collaborative Innovation Center for Brain Science, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and TechnologyWuhan, China.
Huazhong University of Science and Technology · CNUnion Hospital · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a cause of cognitive decline in the elderly and the major risk factor for Alzheimer's disease, however, aging people are not all destined to develop into cognitive deficits, the molecular mechanisms underlying this difference in cognition of aging people are obscure. Epigenetic modifications, particularly histone acetylation in the nervous system, play a critical role in regulation of gene expression for learning and memory. An inhibitor of acetyltransferases (INHAT) is reported to suppress histone acetylation via a histone-masking mechanism, and pp32 is a key component of INHAT complex. In the present study, we divided ~18 m-old aged mice into the cognitive-normal and the cognitive-impaired group by Morris water maze, and found that pp32 level was significantly increased in the hippocampus of cognitive-impaired aged mice. The mRNA and protein levels of synaptic-associated proteins decreased with reduced dendrite complexity and histone acetylation. Knockdown of pp32 rescued cognitive decline in cognitive-impaired aged mice with restoration of synaptic-associated proteins, the increase of spine density and elevation of histone acetylation. Our study reveals a novel mechanism underlying the aging-associated cognitive disturbance, indicating that suppression of pp32 might represent a promising therapeutic approach for learning and memory impairments.

Indexed as

agingcognitiondendritic complexityhistone acetylationpp32

Identifiers

PMID28473768
PMCPMC5397422
OpenAlexW2608661777

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.