Evidence map›Paper›PMID 35479414›Full record

ArticleiScience2022

Selective activation of ABCA1/ApoA1 signaling in the V1 by magnetoelectric stimulation ameliorates depression via regulation of synaptic plasticity.

Qingbo Lu, Fangfang Wu, Jiao Jiao, Le Xue, Ruize Song, Yachen Shi, Yan Kong, Jianfei Sun, Ning Gu, Ming-Hu Han and 1 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 27 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 6 institutions in 2 countries.

Qingbo LuDepartment of Neurology, Affiliated Zhongda Hospital, School of Medicine, Institution of Neuropsychiatry, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, Jiangsu 210096, China.
Fangfang WuDepartment of Pharmacology, Nanjing University of Chinese Medicine, Nanjing, 210046, China.
Jiao JiaoDepartment of Neurology, Affiliated Zhongda Hospital, School of Medicine, Institution of Neuropsychiatry, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, Jiangsu 210096, China.
Le XueState Key Laboratory of Bioelectronics, Jiangsu Key Laboratory of Biomaterials and Devices, School of Biological Science and Medical Engineering, Southeast University, Nanjing, 210009, China.
Ruize SongDepartment of Neurology, Affiliated Zhongda Hospital, School of Medicine, Institution of Neuropsychiatry, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, Jiangsu 210096, China.
Yachen ShiDepartment of Neurology, Affiliated Zhongda Hospital, School of Medicine, Institution of Neuropsychiatry, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, Jiangsu 210096, China.
Yan KongDepartment of Biochemistry and Molecular Biology, School of Medicine, Southeast University, Nanjing, 210009, China.
Jianfei SunState Key Laboratory of Bioelectronics, Jiangsu Key Laboratory of Biomaterials and Devices, School of Biological Science and Medical Engineering, Southeast University, Nanjing, 210009, China.
Ning GuState Key Laboratory of Bioelectronics, Jiangsu Key Laboratory of Biomaterials and Devices, School of Biological Science and Medical Engineering, Southeast University, Nanjing, 210009, China.
Ming-Hu HanDepartment of Pharmacological Sciences, Department of Neuroscience, Center for Affective Neuroscience, and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Zhijun ZhangDepartment of Neurology, Affiliated Zhongda Hospital, School of Medicine, Institution of Neuropsychiatry, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, Jiangsu 210096, China.
Zhongda Hospital Southeast University · CNState Key Laboratory of Digital Medical EngineeringAllen Institute for Brain Science · USChinese Academy of Sciences · CNNanjing University of Chinese Medicine · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence suggests that dysfunction of the visual cortex may be involved in major depressive disorder (MDD). However, the underlying mechanisms remain unclear. We previously established that combined magnetic stimulation system treatment (c-MSST) resulted in an antidepressant effect in mice. In the present study, we found that V1-targeted c-MSST induced significant antidepressant effects in chronic unpredictable mild stress (CUMS)- and lipopolysaccharide (LPS)-treated mice. Proteomic screening investigation and repeatable validation revealed that expression of the V1 neuronal ATP-binding cassette transporter A1 (ABCA1) and apolipoprotein A-1 (ApoA1) was downregulated in CUMS mice, an effect that was normalized by c-MSST. Neuron-specific knockdown of ABCA1 in V1 blocked c-MSST's antidepressant effects. Mechanistically, CUMS reduced dendritic spine density and long-term plasticity in V1, and these deficits were reversed by c-MSST. V1-targeted c-MSST was found to induce rapid antidepressant effects that are mediated by alterations in synaptic plasticity via the ABCA1/ApoA1 signaling pathway in V1.

Indexed as

Cellular neuroscienceMolecular neuroscienceTechniques in neuroscience

Identifiers

PMID35479414
PMCPMC9036135
OpenAlexW4223942307

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.