Evidence map›Paper›PMID 40448997›Full record

ArticleCell reports2025

Cell-death pathways and tau-associated neuronal vulnerability in Alzheimer's disease.

Gen Lin, Sarah E Chancellor, Taekyung Kwon, Maya E Woodbury, Astrid Doering, Aicha Abdourahman, Rachel E Bennett, Fan Liao, Timothy Pastika, Joseph Tamm and 16 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
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

26 authors.

Gen LinAbbVie Pte Ltd, North Buona Vista Road #19-01, Singapore 138588, Singapore.
Sarah E ChancellorAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA. Electronic address: sarah.chancellor@abbvie.com.
Taekyung KwonAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Maya E WoodburyAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Astrid DoeringAbbVie Deutschland GmbH & Co. KG, Knollstraße, 67061 Ludwigshafen, Germany.
Aicha AbdourahmanAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Rachel E BennettDepartment of Neurology, Harvard Medical School, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Fan LiaoAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Timothy PastikaAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Joseph TammAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Nandini RomanulAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Kiran YanamandraAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Miwei HuDepartment of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Karen ZhaoAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Matthew P FroschDepartment of Neurology, Harvard Medical School, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Yelena GrinbergAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Huan LiDepartment of Neurology, Harvard Medical School, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Sudeshna DasDepartment of Neurology, Harvard Medical School, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Tammy DellovadeAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Eric H KarranAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Robert V TalanianAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA.
Knut BiberAbbVie Deutschland GmbH & Co. KG, Knollstraße, 67061 Ludwigshafen, Germany.
Alberto Serrano-PozoDepartment of Neurology, Harvard Medical School, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Janina S RiedAbbVie Deutschland GmbH & Co. KG, Knollstraße, 67061 Ludwigshafen, Germany.
Xavier LangloisAbbVie Inc., Cambridge Research Center, 200 Sidney Street, Cambridge, MA 02139, USA. Electronic address: xavier.langlois@abbvie.com.
Bradley T HymanDepartment of Neurology, Harvard Medical School, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA. Electronic address: bhyman@mgh.harvard.edu.

Funding

Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI STEVEN E ARNOLD · 2019 to 2026
$36.5M
Microvascular Stress as a Pathway to Neurodegeneration in Alzheimer'sR01AG071567 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Rachel Elise Bennett · 2022 to 2026
$2.1M
Astrocyte Reaction in Alzheimer's DiseaseK08AG064039 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI SERRANO-POZO, ALBERTO · 2019 to 2023
$837k
NIA NIH HHS K08 AG064039NIA NIH HHS P30 AG062421NIA NIH HHS R01 AG071567
6 · The paper itself

Abstract

Neuronal loss is the ultimate driver of neural system dysfunction in Alzheimer's disease (AD). We used single-nucleus RNA sequencing and neuropathological phenotyping to elucidate mechanisms of neurodegeneration in AD by identifying vulnerable neuronal populations and probing for their differentially expressed genes. Evidenced by transcriptomic analyses and quantitative tau immunoassays of human AD and non-AD brain tissue, we identified a neuronal population especially vulnerable to tau pathology. Multiplexed immunohistochemistry and in situ hybridization (CBLN2 and LINC00507) validated the presence of the tau-vulnerable neuronal population and revealed a propensity of this population to bear tau pathology. Differentially expressed genes associated with phospho-tau pathology in these neurons revealed genes involved in apoptosis, cell-component dissociation (e.g., autophagosome maturation and actin filament depolymerization), and regulation of vesicle-mediated transport.

Indexed as

Alzheimer DiseaseNeuronstau ProteinsAgedAged, 80 and overBrainCell DeathFemaleHumansMaletau ProteinsAlzheimer’s diseaseCP: Neurosciencemultiplex FISH/IHCneurodegenerationphospho-tau ELISAselective vulnerabilitysingle-nucleus RNA-seqtau pathology

Identifiers

PMID40448997
PMCPMC12312735

What OpenQuestion holds

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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.