Evidence map›Paper›PMID 35344853›Full record

ReviewSchizophrenia research2022

Neurodegenerative model of schizophrenia: Growing evidence to support a revisit.

William S Stone, Michael R Phillips, Lawrence H Yang, Lawrence S Kegeles, Ezra S Susser, Jeffrey A Lieberman

Abstract readReview
In one paragraph

Review in Schizophrenia research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 4 pooled it
–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

60 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. A frontotemporal dementia-like phenotype in schizophrenia: links to striatal dopamine and iron accumulation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Observational
  7. Article
  8. Review
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  12. Does neurodevelopmental load predict cognitive flexibility?Schizophrenia research. Cognition · 2026
    Article
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  14. Article
  15. Article
  16. Article
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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

6 authors.

William S StoneHarvard Medical School Department of Psychiatry at Beth Israel Deaconess Medical Center, Boston, MA, USA. Electronic address: wstone@bidmc.harvard.edu.
Michael R PhillipsShanghai Mental Health Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, Shanghai, China; Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA.
Lawrence H YangDepartment of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA; New York University College of Global Public Health, New York, NY, USA.
Lawrence S KegelesDepartment of Psychiatry, Columbia University, New York, NY, USA; New York State Psychiatric Institute, New York, NY, USA.
Ezra S SusserDepartment of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA.
Jeffrey A LiebermanDepartment of Psychiatry, Columbia University, New York, NY, USA.

Funding

Characterizing Cognition across the Lifespan in untreated psychosis in ChinaR01MH108385 · NIMH · NEW YORK UNIVERSITY · PI KESHAVAN, MATCHERI S., PHILLIPS, MICHAEL ROBERT · 2015 to 2019
$4.0M
Longitudinal trajectories in treated and untreated schizophreniaR01MH127631 · NIMH · NEW YORK UNIVERSITY · PI KESHAVAN, MATCHERI S., STONE, WILLIAM SETH · 2021 to 2023
$1.7M
NIMH NIH HHS R01 MH108385NIMH NIH HHS R01 MH127631
6 · The paper itself

Abstract

Multidimensional progressive declines in the absence of standard biomarkers for neurodegeneration are observed commonly in the development of schizophrenia, and are accepted as consistent with neurodevelopmental etiological hypotheses to explain the origins of the disorder. Far less accepted is the possibility that neurodegenerative processes are involved as well, or even that key dimensions of function, such as cognition and aspects of biological integrity, such as white matter function, decline in chronic schizophrenia beyond levels associated with normal aging. We propose that recent research germane to these issues warrants a current look at the question of neurodegeneration. We propose the view that a neurodegenerative hypothesis provides a better explanation of some features of chronic schizophrenia, including accelerated aging, than is provided by neurodevelopmental hypotheses. Moreover, we suggest that neurodevelopmental influences in early life, including those that may extend to later life, do not preclude the development of neurodegenerative processes in later life, including some declines in cognitive and biological integrity. We evaluate these views by integrating recent findings in representative domains such as cognition and white and gray matter integrity with results from studies on accelerated aging, together with functional implications of neurodegeneration for our understanding of chronic schizophrenia.

Indexed as

SchizophreniaWhite MatterAgingCognitionGray MatterHumansAccelerated agingChronic schizophreniaCognitionNeurodegenerative processesNeurodevelopmental hypothesisWhite matter

Identifiers

PMID35344853
PMCPMC9189010

What OpenQuestion holds

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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.