Evidence map›Paper›PMID 36429082›Full record

ArticleCells2022

Higher Circulating Trimethylamine N-Oxide Aggravates Cognitive Impairment Probably via Downregulating Hippocampal SIRT1 in Vascular Dementia Rats.

Yang Deng, Junqing Zou, Ye Hong, Qiang Peng, Xinxin Fu, Rui Duan, Jie Chen, Xiangliang Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  6. Is Ergothioneine an Important Source of Plasma TrimethylamineAntioxidants (Basel, Switzerland) · 2026
    Article
  7. Trimethylamine-N-oxide: the microbial cue in immune-mediated disorders.Trends in endocrinology and metabolism: TEM · 2026
    Review
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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

8 authors at 2 institutions in 1 country.

Yang DengDepartment of Neurology, Nanjing First Hospital, China Pharmaceutical University, Nanjing 210006, China.
Junqing ZouDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Ye HongDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Qiang PengDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Xinxin FuDepartment of Neurology, Nanjing First Hospital, China Pharmaceutical University, Nanjing 210006, China.
Rui DuanDepartment of Neurology, Nanjing First Hospital, China Pharmaceutical University, Nanjing 210006, China.
Jie ChenDepartment of Personnel, Nanjing First Hospital, Nanjing 210006, China.
Xiangliang ChenDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.ORCID 0000-0002-3658-2941
Nanjing Medical University · CNChina Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and inflammation damage play pivotal roles in vascular dementia (VaD). Trimethylamine N-oxide (TMAO), an intestinal microbiota-stemming metabolite, was reported to promote inflammation and oxidative stress, involved in the etiology of several diseases. Still, these effects have not been investigated in VaD. Here, we tested whether pre-existing, circulating, high levels of TMAO could affect VaD-induced cognitive decline. TMAO (120 mg/kg) was given to rats for a total of 8 weeks, and these rats underwent a sham operation or bilateral common carotid artery (2VO) surgery after 4 weeks of treatment. Four weeks after surgery, the 2VO rats exhibited hippocampal-dependent cognitive function declines and synaptic plasticity dysfunction, accompanied by an increase in oxidative stress, neuroinflammation, and apoptosis. TMAO administration, which increased plasma and hippocampal TMAO at 4 weeks postoperatively, further aggravated these effects, resulting in exaggerated cognitive and synaptic plasticity impairment, though not within the Sham group. Moreover, TMAO treatment activated the NLRP3 inflammasome and decreased SIRT1 protein expression within the hippocampus. However, these effects of TMAO were significantly attenuated by the overexpression of SIRT1. Our findings suggest that TMAO increases oxidative stress-induced neuroinflammation and apoptosis by inhibiting the SIRT1 pathway, thereby exacerbating cognitive dysfunction and neuropathological changes in VaD rats.

Indexed as

Cognitive DysfunctionDementia, VascularVascular DiseasesAnimalsHippocampusInflammationMethylaminesRatsSirtuin 1MethylaminesSirt1 protein, ratSirtuin 1trimethyloxamineinflammationoxidative stressSIRT1synaptic plasticitytrimethylamine N-oxidevascular dementia

Identifiers

PMID36429082
PMCPMC9688447
OpenAlexW4309455544

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.