Evidence map›Paper›PMID 30887246›Full record

ArticleNeuroscience bulletin2019

Circular HDAC9/microRNA-138/Sirtuin-1 Pathway Mediates Synaptic and Amyloid Precursor Protein Processing Deficits in Alzheimer's Disease.

Yanjun Lu, Lu Tan, Xiong Wang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 2% of its field
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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.

  1. Pooled it
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  16. Opioid-Induced Regulation of Cortical Circular-International journal of molecular sciences · 2025
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  19. Circular RNAs in Brain Physiology and Neurologic Diseases.Advances in experimental medicine and biology · 2025
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44 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Yanjun LuDepartment of Laboratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Lu TanKey Laboratory for Molecular Diagnosis of Hubei Province, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430014, China.
Xiong WangDepartment of Laboratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. tjhwangxiong@163.com.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synaptic dysfunction and abnormal processing of amyloid precursor protein (APP) are early pathological features in Alzheimer's disease (AD). Recently, non-coding RNAs such as microRNAs (miRNAs) and circular RNAs (circRNAs) have been reported to contribute to the pathogenesis of AD. We found an age-dependent elevation of miR-138 in APP/PS1 (presenilin-1) mice. MiR-138 inhibited the expression of ADAM10 [a disintegrin and metalloproteinase domain-containing protein 10], promoted amyloid beta (Aβ) production, and induced synaptic and learning/memory deficits in APP/PS1 mice, while its suppression alleviated the AD-like phenotype in these mice. Overexpression of sirtuin 1 (Sirt1), a target of miR-138, ameliorated the miR-138-induced inhibition of ADAM10 and elevation of Aβ in vitro. The circRNA HDAC9 (circHDAC9) was predicted to contain a miR-138 binding site in several databases. Its expression was inversely correlated with miR-138 in both Aβ-oligomer-treated N2a cells and APP/PS1 mice, and it co-localized with miR-138 in the cytoplasm of N2a cells. CircHDAC9 acted as a miR-138 sponge, decreasing miR-138 expression, and reversing the Sirt1 suppression and excessive Aβ production induced by miR-138 in vitro. Moreover, circHDAC9 was decreased in the serum of both AD patients and individuals with mild cognitive impairment. These results suggest that the circHDAC9/miR-138/Sirt1 pathway mediates synaptic function and APP processing in AD, providing a potential therapeutic target for its treatment.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsFemaleHippocampusHistone DeacetylasesHumansMaleMiceMice, TransgenicMicroRNAsMiddle AgedRepressor ProteinsRNA, CircularAmyloid beta-Protein PrecursorHdac9 protein, mouseHistone DeacetylasesMicroRNAsMIRN138 microRNA, mouseRepressor ProteinsRNA, CircularSirt1 protein, mouseSirtuin 1Alzheimer’s diseaseCircular RNAMemorymicroRNASirtuin-1Synapse

Identifiers

PMID30887246
PMCPMC6754481
OpenAlexW2922418290

What OpenQuestion holds

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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.