Evidence map›Paper›PMID 41689153›Full record

ArticleCNS neuroscience & therapeutics2026

SATB1 Exhibits a Protective Role in HAmylin-Oligomer-Induced Neuronal Damage and Cognition Decline.

Yuan Xing, Wei Zhang, Zuxiao Yang, Xia Qin, Ting Zhou, Nan Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in CNS neuroscience & therapeutics, 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

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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. 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

6 authors.

Yuan XingNeuromedical Technology Innovation Center of Hebei Province, Department of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Wei ZhangDepartment of Pharmacology, Institution of Chinese Integrative Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Zuxiao YangDepartment of Pharmacology, Institution of Chinese Integrative Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Xia QinDepartment of Pharmacology, Institution of Chinese Integrative Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Ting ZhouDepartment of Neurology, Xinqiao Hospital, The Army Medical University (Third Military Medical University), Chongqing, China.
Nan ZhangNeuromedical Technology Innovation Center of Hebei Province, Department of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.ORCID 0009-0007-9365-751X

Funding

Hebei Province Government-funded Excellent Talents Project in Clinical Medicine ZF2023029Postdoctoral Science Foundation project of the Chongqing Natural Science Foundation CSTB2023NSCQ-BHX0119Science and Technology Research Project of Hebei Colleges BJK2023072The Key Research and Development Program of Heibei Province 23377708D
6 · The paper itself

Abstract

aimsAmylin is a hormone secreted by pancreatic β cells, and oligomerized human amylin (hAmylin) has shown neurotoxicity in mice. However, the effect of hAmylin oligomers on cognitive ability and the underlying mechanisms remains unexplored.

methodsIn this study, hAmylin oligomers were bilaterally injected into the hippocampus of mice.

resultsInspiringly, hAmylin-mice displayed obvious cognition decline and neuronal damages in the hippocampal dentate gyrus (DG) area. Thus, hippocampal tissues were collected for mRNA-seq analysis, which identified the upregulation of transcription factor SATB Homeobox 1 (SATB1) in the hippocampus of hAmylin mice. Using behavioral experiments and histopathological analyses, the promoting effect of SATB1 knockdown on cognition decline and neuronal damage in hAmylin mice was determined. In vitro, SATB1 expression was reduced in primary hippocampus neurons after hAmylin oligomer incubation. SATB1 overexpression inhibited hAmylin-induced mitochondrial dysfunction and neuronal apoptotic deaths, while SATB1 knockdown exhibited opposite effects. SATB1 transcriptionally activated AKT serine/threonine kinase 3 (AKT3) by binding to its promoter region, and AKT3 accounted for SATB1-mediated protection against hAmylin-induced mitochondrial dysfunction and neuronal injury.

conclusionIn summary, this study highlights the novel role of SATB1 in hAmylin oligomer-induced neuronal damage and cognition decline via AKT3.

Indexed as

Cognition DisordersHippocampusMatrix Attachment Region Binding ProteinsNeuronsAnimalsApoptosisCells, CulturedHumansMaleMiceMice, Inbred C57BLProto-Oncogene Proteins c-aktMatrix Attachment Region Binding ProteinsProto-Oncogene Proteins c-aktSatb1 protein, mouseAKT3cognitive abilityhAmylin oligomersneuronal apoptosisSATB1

Identifiers

PMID41689153
PMCPMC12904839

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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.