Evidence map›Paper›PMID 40830578›Full record

ArticleMolecular psychiatry2026

α7 nicotinic acetylcholine receptor, activated glia, and cognitive impairment in schizophrenia: a dual-tracer PET study.

Tomoyasu Wakuda, Masamichi Yokokura, Yasuhiro Magata, Chie Suzuki, Chihiro Murayama, Takafumi Goto, Taishi Tamayama, Yosuke Kameno, Toshiki Iwabuchi, Takashi Isobe and 5 more

Abstract read
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In one paragraph

Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

15 authors.

Tomoyasu Wakuda *Department of Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan.ORCID http://orcid.org/0000-0002-1924-8167
Masamichi Yokokura *Department of Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Yasuhiro MagataMolecular Imaging Laboratory, Division of Preeminent Bioimaging Research, Institute of Photonics Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Chie SuzukiMolecular Imaging Laboratory, Division of Preeminent Bioimaging Research, Institute of Photonics Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.ORCID http://orcid.org/0000-0002-7997-1955
Chihiro MurayamaDepartment of Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Takafumi GotoDepartment of Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Taishi TamayamaDepartment of Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Yosuke KamenoDepartment of Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Toshiki IwabuchiUnited Graduate School of Child Development, Osaka University, Kanazawa University, Hamamatsu University School of Medicine, Chiba University and University of Fukui, Suita, Japan.ORCID http://orcid.org/0000-0003-1747-8222
Takashi IsobeCentral Research Laboratory, Hamamatsu Photonics K. K., Hamamatsu, Japan.ORCID http://orcid.org/0009-0007-1523-3703
Yuya OnishiCentral Research Laboratory, Hamamatsu Photonics K. K., Hamamatsu, Japan.ORCID http://orcid.org/0000-0001-9715-4636
Tatsuhiro TeradaBiofunctional Imaging Laboratory, Division of Preeminent Bioimaging Research, Institute of Photonics Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.ORCID http://orcid.org/0000-0002-0783-5508
Nori TakeiUnited Graduate School of Child Development, Osaka University, Kanazawa University, Hamamatsu University School of Medicine, Chiba University and University of Fukui, Suita, Japan.
Yasuomi OuchiBiofunctional Imaging Laboratory, Division of Preeminent Bioimaging Research, Institute of Photonics Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.ORCID http://orcid.org/0000-0002-1795-0614
Hidenori YamasueDepartment of Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan. yamasue@hama-med.ac.jp.ORCID http://orcid.org/0000-0002-2748-6317

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) JP16K10186MEXT | Japan Society for the Promotion of Science (JSPS) JP19K08070
6 · The paper itself

Abstract

The α7 nicotinic acetylcholine receptor (nAChR) plays a crucial role in cognitive function, and its dysfunction has been proposed as a primary pathophysiological factor in schizophrenia. Although the α7 nAChR is expressed in both neuronal and activated glial cells, its association with activated glia and its role in the pathophysiology of schizophrenia remain uncertain. Therefore, we investigated α7 nAChR availability and activated glia evaluated with 18 kDa translocator protein (TSPO) levels in individuals with schizophrenia, and further examined their association and relationships to cognitive impairment. Nineteen individuals with schizophrenia, no smoking history or use of anticholinergic or benzodiazepine medications for at least 6 months, and 20 age- and sex-matched healthy controls underwent [

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorCognition DisordersNeurogliaSchizophreniaAcetamidesAdultBrainCognitive DysfunctionFemaleHumansMaleMiddle AgedPositron-Emission TomographyPyrazolesPyridinesPyrimidinesAcetamidesalpha7 Nicotinic Acetylcholine ReceptorN-(2-methoxybenzyl)-N-(4-phenoxypyridin-3-yl)acetamidePyrazolesPyridinesPyrimidinesReceptors, GABATSPO protein, human

Identifiers

PMID40830578

What OpenQuestion holds

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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.