Evidence map›Paper›PMID 42190665›Full record

ArticleCell reports. Medicine2026

CSNK2B gene replacement rescues autism-related phenotypes and establishes translational EEG biomarkers.

Chaodong Ding, Xiaqing Wang, Yiting Yuan, Yuefang Zhang, Yixin Hu, Changhe Wang, Ailian Du, Zilong Qiu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Chaodong DingDepartment of Neurology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: dingchaodong@shsmu.edu.cn.
Xiaqing WangDepartment of Neurology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yiting YuanDepartment of Neurology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuefang ZhangDepartment of Neurology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yixin HuDepartment of Neurology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Changhe WangDepartment of Neurology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ailian DuDepartment of Neurology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: 734001737@shsmu.edu.cn.
Zilong QiuDepartment of Neurology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China; MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: qiuzilong@shsmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Variants in CSNK2B cause neurodevelopmental disorders with autism and epilepsy, but therapeutic evidence and translatable biomarkers remain limited. We generate Csnk2b haploinsufficient mice that recapitulate key disease features, including social and cognitive deficits, anxiety-like behavior, spontaneous seizures, cortical abnormalities, and reduced inhibitory interneurons. Early postnatal, brain-wide gene replacement improves survival and rescues structural, behavioral, and seizure phenotypes. Treatment also normalizes brain activity signatures linked to circuit function, including theta and gamma power, power ratios, interregional coherence, and gamma-band directional connectivity. These findings show that reduced Csnk2b dosage disrupts cortical development and network synchronization but can be corrected after birth. They also identify a compact set of noninvasive brain activity biomarkers with potential value for target engagement, dose selection, and longitudinal monitoring in future gene therapy studies.

Indexed as

Autistic DisorderCasein Kinase IIElectroencephalographyAnimalsBiomarkersBrainDisease Models, AnimalFemaleGenetic TherapyHaploinsufficiencyHumansMaleMicePhenotypeSeizuresBiomarkersCasein Kinase IIautismCsnk2b(+/−) miceCSNK2B mutationsepilepsygene therapy

Identifiers

PMID42190665
PMCPMC13293933

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.