Evidence map›Paper›PMID 32719966›Full record

ReviewCellular and molecular neurobiology2021

The Mechanistic Role of Bridging Integrator 1 (BIN1) in Alzheimer's Disease.

Peirong Gao, Lingqi Ye, Hongrong Cheng, Honglei Li

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  12. Alzheimer's Disease: An Updated Overview of Its Genetics.International journal of molecular sciences · 2023
    Review
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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

4 authors at 1 institution in 1 country.

Peirong GaoDepartment of Neurology and Research Center of Neurology in Second Affiliated Hospital, and Key Laboratory of Medical Neurobiology of Zhejiang Province, Zhejiang University School of Medicine, 88 Jiefang Rd, Hangzhou, 310009, China.ORCID http://orcid.org/0000-0001-9507-0017
Lingqi YeDepartment of Neurology and Research Center of Neurology in Second Affiliated Hospital, and Key Laboratory of Medical Neurobiology of Zhejiang Province, Zhejiang University School of Medicine, 88 Jiefang Rd, Hangzhou, 310009, China.ORCID http://orcid.org/0000-0003-3472-8414
Hongrong ChengDepartment of Neurology and Research Center of Neurology in Second Affiliated Hospital, and Key Laboratory of Medical Neurobiology of Zhejiang Province, Zhejiang University School of Medicine, 88 Jiefang Rd, Hangzhou, 310009, China.ORCID http://orcid.org/0000-0002-6086-9643
Honglei LiDepartment of Neurology and Research Center of Neurology in Second Affiliated Hospital, and Key Laboratory of Medical Neurobiology of Zhejiang Province, Zhejiang University School of Medicine, 88 Jiefang Rd, Hangzhou, 310009, China. lihonglei@zju.edu.cn.ORCID http://orcid.org/0000-0002-3018-7297
Second Affiliated Hospital of Zhejiang University · CN

Funding

the National Natural Science Foundation of China 81500908
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the leading cause of dementia. The majority of AD cases are late-onset, multifactorial cases. Genome-wide association studies have identified more than 30 loci associated with sporadic AD (SAD), one of which is Bridging integrator 1 (BIN1). For the past few years, there has been a consensus that BIN1 is second only to APOE as the strongest genetic risk factor for SAD. Therefore, many researchers have put great effort into studying the mechanism by which BIN1 might be involved in the pathogenetic process of AD. To date, plenty of evidence has shown that BIN1 may participate in several pathways in AD, including tau and amyloid pathology. In addition, BIN1 has been indicated to take part in other relevant pathways such as inflammation, apoptosis, and calcium homeostasis. In this review, we systemically summarize the research progress on how BIN1 participates in the development of AD, with the expectation of providing promising perspectives for future research.

Indexed as

Adaptor Proteins, Signal TransducingAlzheimer DiseaseGenetic Predisposition to DiseaseHumansNuclear Proteinstau ProteinsTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingBIN1 protein, humanNuclear Proteinstau ProteinsTumor Suppressor ProteinsAlzheimer’s diseaseAmyloid pathologyBIN1Tau pathology

Identifiers

PMID32719966
PMCPMC11448648
OpenAlexW3045938554

What OpenQuestion holds

Textmetadata
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.