Evidence map›Paper›PMID 41090516›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

NEAT1 Promotes Epileptogenesis in Tuberous Sclerosis Complex.

Suhui Kuang, Tinghong Liu, Zhirong Wei, Jinshan Xu, Jiayi Han, Jiaqi Wang, Feng Zhai, Yiran Tian, Shuli Liang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. NEAT1 Promotes Epileptogenesis in Tuberous Sclerosis Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    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

9 authors.

Suhui KuangFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Tinghong LiuFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Zhirong WeiFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Jinshan XuFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Jiayi HanFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Jiaqi WangFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Feng ZhaiFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Yiran TianFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Shuli LiangFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.ORCID https://orcid.org/0000-0002-7292-745X

Funding

Joint Basic-Clinical Laboratory of Pediatric Epilepsy and Cognitive Development 3-1-013-03National Natural Science Foundation of China 82071448Natural Science Foundation of Beijing Municipality L222078
6 · The paper itself

Abstract

The primary neurological manifestations of tuberous sclerosis complex (TSC) are intractable epilepsy and intellectual impairment. Current treatment outcomes remain limited. Investigating the role of the epigenetic long non-coding RNA NEAT1 in TSC-related epilepsy and cognition is essential. RNA sequencing analysis of clinical tissue samples revealed that NEAT1 is differentially expressed in epileptogenic versus non-epileptogenic tubers and enriched in the PI3K-AKT signaling pathway. To prove and further investigate the functional role suggested by the earlier transcriptomic and pathway enrichment analyses, NEAT1-overexpression and NEAT1-knockdown TSC2 conditional knockout (CKO) mouse models, as well as TSC2-KO cell models, are established. In vivo experiments demonstrated that NEAT1 knockdown reduced seizure frequency and improved spatial learning and working memory. Cellular analyses in TSC model further revealed that NEAT1 significantly regulates the PI3K/AKT/mTOR signaling pathway, neurotransmitter receptor balance, and outward potassium currents. Specifically, NEAT1 overexpression excessively activated the mTORC1 signaling, leading to changes in 4E-BP1 and S6K and abnormal cell proliferation. Moreover, NEAT1 overexpression contributed to an imbalance in excitatory neurotransmitter receptors and outward potassium currents, resulting in neuronal hyperexcitability, whereas NEAT1 knockdown has the opposite effect. This study provides new insights into the transcriptional regulation of TSC-related epilepsy, highlighting the therapeutic potential of NEAT1.

Indexed as

EpilepsyRNA, Long NoncodingTuberous SclerosisAnimalsDisease Models, AnimalHumansMaleMiceMice, KnockoutSignal TransductionTuberous Sclerosis Complex 2 ProteinNEAT1 long non-coding RNA, humanNEAT1 long non-coding RNA, mouseRNA, Long NoncodingTuberous Sclerosis Complex 2 ProteinepilepsyepileptogenesisLncRNA NEAT1PI3K/AKT/mTORtuberous sclerosis complex

Identifiers

PMID41090516
PMCPMC12767121

What Socratic 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 Socratic graph.