Evidence map›Paper›PMID 32727516›Full record

ArticleMolecular neurodegeneration2020

BIN1 protein isoforms are differentially expressed in astrocytes, neurons, and microglia: neuronal and astrocyte BIN1 are implicated in tau pathology.

Mariko Taga, Vladislav A Petyuk, Charles White, Galina Marsh, Yiyi Ma, Hans-Ulrich Klein, Sarah M Connor, Alexandra Kroshilina, Christina J Yung, Anthony Khairallah and 9 more

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.0field-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

34 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Science advances · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  10. Article
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  12. Review
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  14. Article
  15. Article
  16. Cell type-specific functions of Alzheimer's disease endocytic risk genes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Review
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

19 authors at 6 institutions in 1 country.

Mariko TagaCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Vladislav A PetyukPacific Northwest National Laboratory, Richland, WA, USA.
Charles WhiteCell Circuits Program, Broad Institute, Cambridge, MA, USA.
Galina MarshBiogen, 225 Binney St, Cambridge, MA, 02142, USA.
Yiyi MaCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Hans-Ulrich KleinCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Sarah M ConnorCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Alexandra KroshilinaCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Christina J YungCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Anthony KhairallahCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Marta OlahCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Julie SchneiderAlzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.
Kyle KarhohsImaging Platform, Broad Institute, Cambridge, MA, USA.
Anne E CarpenterImaging Platform, Broad Institute, Cambridge, MA, USA.
Richard RansohoffThird Rock Ventures, 29 Newbury Street, Suite 301, Boston, MA, 02116, USA.
David A BennettAlzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.
Andrea CrottiBiogen, 225 Binney St, Cambridge, MA, 02142, USA.
Elizabeth M BradshawCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA.
Philip L De JagerCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, 630 West 168th st, PH19-311, New York, NY, 10032, USA. pld2115@cumc.columbia.edu.ORCID 0000-0002-8057-2505
Broad Institute · USColumbia University · USBiogen (United States) · USRush University Medical Center · USHarvard University · USPacific Northwest National Laboratory · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI LEURGANS, SUE E. · 1991 to 2020
$49.1M
EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Pathway discovery, validation and compound identification for Alzheimer's disease - SupplementU01AG046152 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2013 to 2017
$13.6M
Convergence of myeloid susceptibility protein function in Alzheimer's diseaseRF1AG058852 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BRADSHAW, ELIZABETH M · 2018 to 2020
$2.9M
Identifying, validating and targeting AD susceptibility networks in monocytesR01AG048015 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DE JAGER, PHILIP L · 2014 to 2018
$1.9M
Influence of genotype on microglia phenotype and function in PDR01NS089674 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BRADSHAW, ELIZABETH M · 2015 to 2018
$1.4M
NIA NIH HHS P30 AG010161NIA NIH HHS R01 AG015819NIA NIH HHS R01 AG017917NIA NIH HHS R01 AG048015NIA NIH HHS RF1 AG058852NIA NIH HHS U01 AG046152NINDS NIH HHS R01 NS089674
6 · The paper itself

Abstract

backgroundIdentified as an Alzheimer's disease (AD) susceptibility gene by genome wide-association studies, BIN1 has 10 isoforms that are expressed in the Central Nervous System (CNS). The distribution of these isoforms in different cell types, as well as their role in AD pathology still remains unclear.

methodsUtilizing antibodies targeting specific BIN1 epitopes in human post-mortem tissue and analyzing mRNA expression data from purified microglia, we identified three isoforms expressed in neurons and astrocytes (isoforms 1, 2 and 3) and four isoforms expressed in microglia (isoforms 6, 9, 10 and 12). The abundance of selected peptides, which correspond to groups of BIN1 protein isoforms, was measured in dorsolateral prefrontal cortex, and their relation to neuropathological features of AD was assessed.

resultsPeptides contained in exon 7 of BIN1's N-BAR domain were found to be significantly associated with AD-related traits and, particularly, tau tangles. Decreased expression of BIN1 isoforms containing exon 7 is associated with greater accumulation of tangles and subsequent cognitive decline, with astrocytic rather than neuronal BIN1 being the more likely culprit. These effects are independent of the BIN1 AD risk variant.

conclusionsExploring the molecular mechanisms of specific BIN1 isoforms expressed by astrocytes may open new avenues for modulating the accumulation of Tau pathology in AD.

Indexed as

Adaptor Proteins, Signal TransducingAlzheimer DiseaseAstrocytesBrainHumansMicrogliaNeuronsNuclear ProteinsProtein Isoformstau ProteinsTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingBIN1 protein, humanNuclear ProteinsProtein Isoformstau ProteinsTumor Suppressor ProteinsAlzheimer’s diseaseAmyloidAstrocytesBIN1 isoformsMicrogliaNeuronsTau

Identifiers

PMID32727516
PMCPMC7389646
OpenAlexW3045809806

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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.