Evidence map›Paper›PMID 34277597›Full record

ArticleFrontiers in cell and developmental biology2021

The Synaptic Vesicle Protein 2A Interacts With Key Pathogenic Factors in Alzheimer's Disease: Implications for Treatment.

Yanyan Kong, Lin Huang, Weihao Li, Xuanting Liu, Yinping Zhou, Cuiping Liu, Shibo Zhang, Fang Xie, Zhengwei Zhang, Donglang Jiang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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  14. Connectivity Mapping Using a NovelFrontiers in molecular neuroscience · 2022
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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

16 authors at 6 institutions in 2 countries.

Yanyan KongPET Center, Huashan Hospital, Fudan University, Shanghai, China.
Lin HuangLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Weihao LiLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Xuanting LiuLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Yinping ZhouLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Cuiping LiuLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Shibo ZhangLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Fang XiePET Center, Huashan Hospital, Fudan University, Shanghai, China.
Zhengwei ZhangPET Center, Huashan Hospital, Fudan University, Shanghai, China.
Donglang JiangPET Center, Huashan Hospital, Fudan University, Shanghai, China.
Weiyan ZhouPET Center, Huashan Hospital, Fudan University, Shanghai, China.
Ruiqing NiInstitute for Biomedical Engineering, ETH Zurich, University of Zurich, Zurich, Switzerland.
Chencheng ZhangDepartment of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Bomin SunDepartment of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jiao WangLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Yihui GuanPET Center, Huashan Hospital, Fudan University, Shanghai, China.
Shanghai University · CNFudan University · CNHuashan Hospital · CNRuijin Hospital · CNShanghai Jiao Tong University · CNUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD), a serious neurodegenerative disease, is pathologically characterized by synaptic loss and dysfunction. Synaptic vesicle protein 2A (SV2A) is an indispensable vesicular protein specifically expressed in synapses and can be used as a biomarker for synaptic density. We found that the expression of SV2A was down-regulated in the hippocampus of AD patients, yet the relation of SV2A to other hallmarks of AD pathology such as amyloid precursor protein (APP), β-amyloid (Aβ), and Tau protein is not thoroughly clear. In addition, SV2A colocalized with APP and was down-regulated at Aβ deposition. Moreover, we found that SV2A deficiency leads to a simultaneous increase in Aβ and Tau hyperphosphorylation, while SV2A overexpression was associated with downregulation of β-site APP cleaving enzyme 1 and apolipoprotein E genes. In addition, evidence gained in the study points to the phosphatidylinositol 3-kinase signaling pathway as a possible mediator in SV2A regulation influencing the incidence and development of AD. With limited effective diagnostic methods for AD, a close interplay between SV2A and AD-related proteins demonstrated in our study may provide novel and innovative diagnostic and therapeutic opportunities.

Indexed as

Alzheimer’s diseaseAβneurodegenerationPI3K signaling pathwaysynaptic vesicle protein 2ATau

Identifiers

PMID34277597
PMCPMC8282058
OpenAlexW3183745470

What OpenQuestion 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 OpenQuestion graph.