Evidence map›Paper›PMID 35882228›Full record

ArticleNeuron2022

Molecular signatures underlying neurofibrillary tangle susceptibility in Alzheimer's disease.

Marcos Otero-Garcia, Sameehan U Mahajani, Debia Wakhloo, Weijing Tang, Yue-Qiang Xue, Samuel Morabito, Jie Pan, Jane Oberhauser, Angela E Madira, Tamara Shakouri and 7 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuron, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 2 pooled it
23.6field-weighted citation impact, top 1% 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

157 citing papers in PubMed, 2 syntheses or guidelines pooled it, 204 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Transcriptomic Signatures of Microglial Phagocytosis Reveal Diagnostic Markers and Immune Landscape in Alzheimer's Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

97 more citing papers are in PubMed but not listed here.

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

17 authors at 3 institutions in 2 countries.

Marcos Otero-GarciaDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Sameehan U MahajaniDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Debia WakhlooDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Weijing TangDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Yue-Qiang XueDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Samuel MorabitoMathematical, Computational and Systems Biology Program, University of California, Irvine, CA 92697, USA; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697, USA.
Jie PanDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Jane OberhauserDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Angela E MadiraDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Tamara ShakouriDepartment of Pathology, University of California, Los Angeles, CA 90095, USA.
Yongning DengDepartment of Pathology, University of California, Los Angeles, CA 90095, USA; Department of Neurology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Thomas AllisonDepartment of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.
Zihuai HeDepartment Neurology and Neurological Sciences and Quantitative Sciences Unit, Department of Medicine, Stanford University, Stanford, CA 94305, USA.
William E LowryDepartment of Molecular Cell and Developmental Biology, Broad Center for Regenerative Medicine and Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.
Riki KawaguchiDepartment of Psychiatry and Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90095, USA.
Vivek SwarupInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697, USA; Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, USA.
Inma CobosDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: icobos@stanford.edu.
Stanford University · USUniversity of California, Los Angeles · USUniversity of California, Irvine · US

Funding

Stanford Alzheimer's Disease Research CenterAdmin Supp: Developing iPSC models for AD and PDP30AG066515 · NIA · STANFORD UNIVERSITY · PI Jennifer Kaci Fairchild · 2020 to 2026
$29.0M
Oligodendrocyte heterogeneity in Alzheimer' s diseaseRF1AG071683 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI SWARUP, VIVEK, ZHANG, JING · 2021 to 2024
$2.2M
Resolving selective vulnerability and disease progression in human Alzheimer's brain via single-cell RNA-seqR01AG059848 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COBOS, INMA · 2018 to 2022
$2.0M
Oligodendrocyte heterogeneity in Alzheimer' s diseaseR01AG071683 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI SWARUP, VIVEK · 2024 to 2025
$1.2M
NIA NIH HHS P30 AG066515NIA NIH HHS R01 AG059848NIA NIH HHS R01 AG071683NIA NIH HHS RF1 AG071683
6 · The paper itself

Abstract

Tau aggregation in neurofibrillary tangles (NFTs) is closely associated with neurodegeneration and cognitive decline in Alzheimer's disease (AD). However, the molecular signatures that distinguish between aggregation-prone and aggregation-resistant cell states are unknown. We developed methods for the high-throughput isolation and transcriptome profiling of single somas with NFTs from the human AD brain, quantified the susceptibility of 20 neocortical subtypes for NFT formation and death, and identified both shared and cell-type-specific signatures. NFT-bearing neurons shared a marked upregulation of synaptic transmission-related genes, including a core set of 63 genes enriched for synaptic vesicle cycling. Oxidative phosphorylation and mitochondrial dysfunction were highly cell-type dependent. Apoptosis was only modestly enriched, and the susceptibilities of NFT-bearing and NFT-free neurons for death were highly similar. Our analysis suggests that NFTs represent cell-type-specific responses to stress and synaptic dysfunction. We provide a resource for biomarker discovery and the investigation of tau-dependent and tau-independent mechanisms of neurodegeneration.

Indexed as

Alzheimer DiseaseNeurofibrillary TanglesBiomarkersBrainHumanstau ProteinsBiomarkerstau Proteinsamyloidbiomarkersdementianeurodegenerationneuropathologyselective vulnerabilitysingle-cell RNA-seqsingle-nucleus RNA-seqtauopathiestranscriptomics

Identifiers

PMID35882228
PMCPMC9509477
OpenAlexW4287881862

What OpenQuestion holds

Textmetadata
LicenceTDM
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.