Evidence map›Paper›PMID 38133681›Full record

ArticleActa neuropathologica2023

Loss of TDP-43 splicing repression occurs early in the aging population and is associated with Alzheimer's disease neuropathologic changes and cognitive decline.

Koping Chang, Jonathan P Ling, Javier Redding-Ochoa, Yang An, Ling Li, Stephanie A Dean, Thomas G Blanchard, Tatiana Pylyukh, Alexander Barrett, Katherine E Irwin and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Acta neuropathologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
10.9field-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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026
    Review
  5. Early axonal injury in fentanyl intoxication.Acta neuropathologica communications · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

14 authors at 5 institutions in 2 countries.

Koping ChangDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Jonathan P LingDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Javier Redding-OchoaDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Yang AnLaboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Ling LiDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Stephanie A DeanOffice of the Chief Medical Examiner, State of Maryland, Baltimore, MD, 21223, USA.
Thomas G BlanchardDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Tatiana PylyukhDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Alexander BarrettDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Katherine E IrwinDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Abhay MoghekarDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Susan M ResnickLaboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Philip C WongDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Juan C TroncosoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. troncoso@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · USNational Institute on Aging · USOffice of Chief Medical Examiner · USUniversity of Maryland, Baltimore · US

Funding

Research Education ComponentP30AG066507 · NIA · JOHNS HOPKINS UNIVERSITY · PI Corinne Pettigrew · 2020 to 2026
$29.3M
TDP-43 Proteinopathy in ALS-FTD: Mechanism, Target Validation and BiomarkerR01NS095969 · NINDS · JOHNS HOPKINS UNIVERSITY · PI PHILIP C WONG · 2016 to 2026
$2.4M
NIA NIH HHS P30AG066507NINDS NIH HHS R01 NS095969NINDS NIH HHS R01NS095969
6 · The paper itself

Abstract

LATE-NC, the neuropathologic changes of limbic-predominant age-related TAR DNA-binding protein 43 kDa (TDP-43) encephalopathy are frequently associated with Alzheimer's disease (AD) and cognitive impairment in older adults. The association of TDP-43 proteinopathy with AD neuropathologic changes (ADNC) and its impact on specific cognitive domains are not fully understood and whether loss of TDP-43 function occurs early in the aging brain remains unknown. Here, using a large set of autopsies from the Baltimore Longitudinal Study of Aging (BLSA) and another younger cohort, we were able to study brains from subjects 21-109 years of age. Examination of these brains show that loss of TDP-43 splicing repression, as judged by TDP-43 nuclear clearance and expression of a cryptic exon in HDGFL2, first occurs during the 6th decade, preceding by a decade the appearance of TDP-43+ neuronal cytoplasmic inclusions (NCIs). We corroborated this observation using a monoclonal antibody to demonstrate a cryptic exon-encoded neoepitope within HDGFL2 in neurons exhibiting nuclear clearance of TDP-43. TDP-43 nuclear clearance is associated with increased burden of tau pathology. Age at death, female sex, high CERAD neuritic plaque score, and high Braak neurofibrillary stage significantly increase the odds of LATE-NC. Faster rates of cognitive decline on verbal memory (California Verbal Learning Test immediate recall), visuospatial ability (Card Rotations Test), mental status (MMSE) and semantic fluency (Category Fluency Test) were associated with LATE-NC. Notably, the effects of LATE-NC on verbal memory and visuospatial ability are independent of ADNC. However, the effects of TDP-43 nuclear clearance in absence of NCI on the longitudinal trajectories and levels of cognitive measures are not significant. These results establish that loss of TDP-43 splicing repression is an early event occurring in the aging population during the development of TDP-43 proteinopathy and is associated with increased tau pathology. Furthermore, LATE-NC correlates with high levels of ADNC but also has an impact on specific memory and visuospatial functions in aging that is independent of AD.

Indexed as

Alzheimer DiseaseCognitive DysfunctionTDP-43 ProteinopathiesAgedAgingDementiaDNA-Binding ProteinsFemaleHumansLongitudinal StudiesDNA-Binding ProteinsCryptic exonsCryptic HDGFL2DementiaLATE-NCTDP-43 loss-of-functionTDP-43 neuronal inclusions

Identifiers

PMID38133681
OpenAlexW4390107055

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.