Evidence map›Paper›PMID 25824303›Full record

ReviewMolecular psychiatry2015

Kraepelin revisited: schizophrenia from degeneration to failed regeneration.

P Falkai, M J Rossner, T G Schulze, A Hasan, M M Brzózka, B Malchow, W G Honer, A Schmitt

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PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Cannabis use and psychosis: a review of reviews.European archives of psychiatry and clinical neuroscience · 2020
    Pooled it
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  14. Cellular pathology in the limbic system in schizophrenia.European archives of psychiatry and clinical neuroscience · 2023
    Article
  15. Optical coherence tomography reveals retinal thinning in schizophrenia spectrum disorders.European archives of psychiatry and clinical neuroscience · 2023
    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

8 authors at 2 institutions in 2 countries.

P FalkaiDepartment of Psychiatry and Psychotherapy; Ludwig-Maximilians-University, Munich, Germany.
M J Rossner1] Department of Psychiatry and Psychotherapy; Ludwig-Maximilians-University, Munich, Germany [2] Max-Planck-Institute of Experimental Medicine, Goettingen, Germany.
T G SchulzeInstitute for Psychiatric Phenomics and Genomics; Ludwig-Maximilians-University, Munich, Germany.
A HasanDepartment of Psychiatry and Psychotherapy; Ludwig-Maximilians-University, Munich, Germany.
M M BrzózkaDepartment of Psychiatry and Psychotherapy; Ludwig-Maximilians-University, Munich, Germany.
B MalchowDepartment of Psychiatry and Psychotherapy; Ludwig-Maximilians-University, Munich, Germany.
W G HonerDepartment of Psychiatry; University of British Columbia, Canada.
A Schmitt1] Department of Psychiatry and Psychotherapy; Ludwig-Maximilians-University, Munich, Germany [2] Laboratory of Neuroscience (LIM27), Institute of Psychiatry, University of Sao Paulo, Sao Paulo, Brazil.
Genomics (United Kingdom) · GBLudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One hundred years after its conceptual definition as 'Dementia Praecox' by Emil Kraepelin, schizophrenia is still a serious psychiatric illness that affects young adults and leads to disability in at least half of patients. The key treatment issue is partial or non-response, especially of negative symptoms. The illness is also associated with different degrees of cognitive dysfunction, particularly in verbal and working memory; the resulting functional impairment may lead to unemployment and an inability to maintain stable relationships. Patients' cognitive dysfunction led Kraepelin to the assumption that schizophrenia is a form of juvenile dementia caused by a degenerative process of the human brain. Postmortem studies and a plethora of imaging studies do not support the notion of a degenerative process, but such a process is supported by the recently published, largest genome-wide association study on schizophrenia. More than a 100 hits were described, converging on pathways that have a significant role in dopamine metabolism in immune modulation, calcium signalling and synaptic plasticity. This review suggests that research should focus on animal models based on risk genes like transcription factor 4 and study the effects of exposure to environmental stressors relevant for schizophrenia. The use of relevant end points like pre-pulse inhibition or cognitive dysfunction will allow us to gain an understanding of the molecular pathways in schizophrenia and consequently result in improved treatment options, especially for the disabling aspects of this illness.

Indexed as

AnimalsCognition DisordersHistory, 19th CenturyHistory, 20th CenturyHistory, 21st CenturyHumansNerve DegenerationRegenerationSchizophrenia

Identifiers

PMID25824303
OpenAlexW2039625379

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.