Evidence map›Paper›PMID 37222223›Full record

ArticleCNS neuroscience & therapeutics2023

Increasing brain N-acetylneuraminic acid alleviates hydrocephalus-induced neurological deficits.

Zhangyang Wang, Xiaoqun Nie, Fang Gao, Yanmin Tang, Yuanyuan Ma, Yiying Zhang, Yanqin Gao, Chen Yang, Jing Ding, Xin Wang

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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

10 authors at 3 institutions in 1 country.

Zhangyang WangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaoqun NieCAS Key Laboratory of Synthetic Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences (CAS), Shanghai, China.
Fang GaoCAS Key Laboratory of Synthetic Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences (CAS), Shanghai, China.
Yanmin TangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yuanyuan MaDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yiying ZhangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yanqin GaoDepartment of the State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.ORCID 0000-0002-4915-9819
Chen YangCAS Key Laboratory of Synthetic Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences (CAS), Shanghai, China.
Jing DingDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0001-5135-4210
Xin WangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Sun Yat-sen University · CNChinese Academy of Sciences · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThis metabolomic study aimed to evaluate the role of N-acetylneuraminic acid (Neu5Ac) in the neurological deficits of normal pressure hydrocephalus (NPH) and its potential therapeutic effect.

methodsWe analyzed the metabolic profiles of NPH using cerebrospinal fluid with multivariate and univariate statistical analyses in a set of 42 NPH patients and 38 controls. We further correlated the levels of differential metabolites with severity-related clinical parameters, including the normal pressure hydrocephalus grading scale (NPHGS). We then established kaolin-induced hydrocephalus in mice and treated them using N-acetylmannosamine (ManNAc), a precursor of Neu5Ac. We examined brain Neu5Ac, astrocyte polarization, demyelination, and neurobehavioral outcomes to explore its therapeutic effect.

resultsThree metabolites were significantly altered in NPH patients. Only decreased Neu5Ac levels were correlated with NPHGS scores. Decreased brain Neu5Ac levels have been observed in hydrocephalic mice. Increasing brain Neu5Ac by ManNAc suppressed the activation of astrocytes and promoted their transition from A1 to A2 polarization. ManNAc also attenuated the periventricular white matter demyelination and improved neurobehavioral outcomes in hydrocephalic mice.

conclusionIncreasing brain Neu5Ac improved the neurological outcomes associated with the regulation of astrocyte polarization and the suppression of demyelination in hydrocephalic mice, which may be a potential therapeutic strategy for NPH.

Indexed as

Demyelinating DiseasesHydrocephalus, Normal PressureAnimalsBrainHumansMetabolomicsMiceN-Acetylneuraminic AcidN-Acetylneuraminic AcidhydrocephalusmetabolomicsN-acetylmannosamineN-acetylneuraminic acid

Identifiers

PMID37222223
PMCPMC10580356
OpenAlexW4377940516

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.