Evidence map›Paper›PMID 31453805›Full record

ArticleeLife2019

Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity.

Oleksandr Yagensky, Mahdokht Kohansal-Nodehi, Saravanan Gunaseelan, Tamara Rabe, Saima Zafar, Inga Zerr, Wolfgang Härtig, Henning Urlaub, John Je Chua

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Hydrogen Sulfide Signaling in Neurodegenerative Movement Disorders.Handbook of experimental pharmacology · 2026
    Review
  3. Cystathionine γ-lyase is a major regulator of cognitive function through neurotrophin signaling and neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. G-Quadruplexes Abet Neuronal Burnout in ALS and FTD.Antioxidants (Basel, Switzerland) · 2025
    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

9 authors at 6 institutions in 3 countries.

Oleksandr YagenskyResearch Group Protein Trafficking in Synaptic Development and Function, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.
Mahdokht Kohansal-Nodehi *Department of Neurobiology, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.ORCID 0000-0002-3898-5197
Saravanan Gunaseelan *Interactomics and Intracellular Trafficking Laboratory, Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Tamara RabeDepartment of Genes and Behavior, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.
Saima ZafarBiomedical Engineering and Sciences Department, School of Mechanical and Manufacturing Engineering (SMME), National University of Sciences and Technology (NUST), Islamabad, Pakistan.
Inga ZerrClinical Dementia Center, Department of Neurology, German Center for Neurodegenerative Diseases, University Medical Center Göttingen, Göttingen, Germany.
Wolfgang HärtigPaul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.
Henning UrlaubResearch Group Bioanalytical Mass Spectrometry, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.
John Je ChuaResearch Group Protein Trafficking in Synaptic Development and Function, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.ORCID 0000-0002-5615-1014
Max Planck Institute for Biophysical Chemistry · DEGerman Center for Neurodegenerative Diseases · DEAgency for Science, Technology and Research · SGLeipzig University · DENational University of Singapore · SGUniversitätsmedizin Göttingen · DE

Funding

Deutsche Forschungsgemeinschaft CH 1385/1-1International Max Planck Research School for Molecular Biology ScholarshipMax-Planck-Gesellschaft Open-access funding
6 · The paper itself

Abstract

Alzheimer's disease is the most prevalent neurodegenerative disorder leading to progressive cognitive decline. Despite decades of research, understanding AD progression at the molecular level, especially at its early stages, remains elusive. Here, we identified several presymptomatic AD markers by investigating brain proteome changes over the course of neurodegeneration in a transgenic mouse model of AD (3×Tg-AD). We show that one of these markers, heme-binding protein 1 (Hebp1), is elevated in the brains of both 3×Tg-AD mice and patients affected by rapidly-progressing forms of AD. Hebp1, predominantly expressed in neurons, interacts with the mitochondrial contact site complex (MICOS) and exhibits a perimitochondrial localization. Strikingly, wildtype, but not Hebp1-deficient, neurons showed elevated cytotoxicity in response to heme-induced apoptosis. Increased survivability in Hebp1-deficient neurons is conferred by blocking the activation of the mitochondrial-associated caspase signaling pathway. Taken together, our data highlight a role of Hebp1 in progressive neuronal loss during AD progression.

Indexed as

Gene ExpressionAlzheimer DiseaseAnimalsDisease ProgressionHeme-Binding ProteinsHumansMiceMice, TransgenicProteomeHEBP1 protein, humanHeme-Binding ProteinsProteomeAlzheimer's diseaseHebp1humanmouseneuronneurosciencerat

Identifiers

PMID31453805
PMCPMC6739868
OpenAlexW2970000608

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Registered trials

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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.