Evidence map›Paper›PMID 31001081›Full record

ArticleFrontiers in neuroscience2019

Elevated Plasma Levels of Drebrin in Glaucoma Patients With Neurodegeneration.

Yi-Jing Gan, Ai-Wu Fang, Chang Liu, Bai-Jing Liu, Feng-Mei Yang, Ji-Tian Guan, Chun-Lin Lan, Xiao-Dan Dai, Tong Li, Ying Cao and 8 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

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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

18 authors at 4 institutions in 2 countries.

Yi-Jing GanState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Ai-Wu FangState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Chang LiuState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Bai-Jing LiuState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Feng-Mei YangState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Ji-Tian GuanState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Chun-Lin LanState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Xiao-Dan DaiState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Tong LiState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Ying CaoState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Yun RanState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Xian-Hui GongState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Zi-Bing JinState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Ren-Zhe CuiDepartment of Ophthalmology, Affiliated Hospital of Yanbian University, Yanji, China.
Takeshi IwataDivision of Molecular and Cellular Biology, National Institute of Sensory Organs, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Jia QuState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Fan LuState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Zai-Long ChiState Key Laboratory of Ophthalmology, Optometry and Visual Science, The Eye Hospital of Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CNAffiliated Eye Hospital of Wenzhou Medical College · CNTokyo Medical Center · JPYanbian University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glaucoma is an optic neuropathy characterized by progressive degeneration of retinal ganglion cells (RGCs). Aberrations in several cytoskeletal proteins, such as tau have been implicated in the pathogenesis of neurodegenerative diseases, could be initiating factors in glaucoma progression and occurring prior to axon degeneration. Developmentally regulated brain protein (Drebrin or DBN1) is an evolutionarily conserved actin-binding protein playing a prominent role in neurons and is implicated in neurodegenerative diseases. However, the relationship between circulating DBN1 levels and RGC degeneration in glaucoma patients remains unclear. In our preliminary study, we detected drebrin protein in the plasma of glaucoma patients using proteomic analysis. Subsequently, we recruited a total of 232 patients including primary angle-closure glaucoma (PACG), primary open-angle glaucoma (POAG) and Posner-Schlossman syndrome (PS) and measured its DBN1 plasma levels. We observed elevated DBN1 plasma levels in patients with primary glaucoma but not in patients with PS compared to nonaxonopathic controls. Interestingly, in contrast to tau plasma levels increased in all groups of patients, elevated drebrin plasma levels correlated with retinal nerve fiber layer defect (RNFLD) in glaucoma patients. To further explore the expression of DBN1 in neurodegeneration, we conducted experiment of optic nerve crush (ONC) models, and observed increased expression of DBN1 in the serum as well as in the retina and then decreased after ONC. This result reinforces the potentiality of circulating DBN1 levels are increased in glaucoma patients with neurodegeneration. Taken together, our findings suggest that circulating DBN1 levels correlated with RNFLD and may reflect the severity of RGCs injury in glaucoma patients. Combining measurement of circulating drebrin and tau levels may be a useful indicator for monitoring progression of neurodegenerative diseases.

Indexed as

axonal degenerationDBN1glaucomaRGCsRNFLD

Identifiers

PMID31001081
PMCPMC6456690
OpenAlexW2935401618

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.