Evidence map›Paper›PMID 40574425›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Long Term High-Salt Diet Induces Cognitive Impairments via Down-Regulating SHANK1.

Cuiping Guo, Yuanyuan Li, Wensheng Li, Tongrui Wu, Yi Liu, Yacoubou Abdoul Razak Mahaman, Jianzhi Wang, Rong Liu, Wei Liu, Hui Shen and 1 more

Abstract read
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In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. 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. Long Term High-Salt Diet Induces Cognitive Impairments via Down-Regulating SHANK1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

11 authors.

Cuiping GuoInstitutes of Biomedical Sciences, School of Medicine, Hubei Key Laboratory of Cognitive and Affective Disorders, Jianghan University, Wuhan, 430056, China.
Yuanyuan LiLaboratory of Neurobiology, School of Basic medicine, Tianjin Medical University, Tianjin, 300070, China.
Wensheng LiDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Tongrui WuLaboratory of Neurobiology, School of Basic medicine, Tianjin Medical University, Tianjin, 300070, China.
Yi LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Yacoubou Abdoul Razak MahamanDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jianzhi WangInstitutes of Biomedical Sciences, School of Medicine, Hubei Key Laboratory of Cognitive and Affective Disorders, Jianghan University, Wuhan, 430056, China.
Rong LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Wei LiuDepartment of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Hui ShenLaboratory of Neurobiology, School of Basic medicine, Tianjin Medical University, Tianjin, 300070, China.
Xiaochuan WangInstitutes of Biomedical Sciences, School of Medicine, Hubei Key Laboratory of Cognitive and Affective Disorders, Jianghan University, Wuhan, 430056, China.ORCID https://orcid.org/0009-0004-5067-043X

Funding

Department of Science and Technology of Hubei Province 2022-72-18National Natural Science Foundation of China 82330041National Natural Science Foundation of China 92049107
6 · The paper itself

Abstract

High-salt (HS) diet is an established risk factor for cognitive impairment, but the underlying mechanisms remain unclear. This study reveals that HS diet reduces SHANK1, a key postsynaptic scaffolding protein, via downregulation of the PKA/CREB pathway, leading to synaptic dysfunction and cognitive deficits in rats. RNA sequencing of HS-fed rat hippocampi showed downregulation of cAMP signaling and SHANK1 expression. Pharmacological inhibition of PKA/CREB reduced SHANK1 levels and impaired dendritic structure and synaptic function, while PKA activation restored CREB activity and SHANK1 expression, reversing HS-induced deficits. Notably, CREB activation is essential for SHANK1 regulation, as a CREB mutant (S133A) blocked the effects of PKA activation, and a constitutively active CREB (S133D) prevented SHANK1 downregulation. These findings highlight the PKA/CREB/SHANK1 pathway as a potential therapeutic target for HS-induced cognitive dysfunction.

Indexed as

Cognitive DysfunctionNerve Tissue ProteinsSodium Chloride, DietaryAnimalsCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinDisease Models, AnimalDown-RegulationHippocampusMaleRatsRats, Sprague-DawleySignal TransductionCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinNerve Tissue ProteinsSodium Chloride, Dietarycognitive deficitshigh‐salt dietPKA/CREBSHANK1synaptic dysfunction

Identifiers

PMID40574425
PMCPMC12463032

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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.