Evidence map›Paper›PMID 19636313›Full record

ArticleMolecular psychiatry2010

Dysregulation of kisspeptin and neurogenesis at adolescence link inborn immune deficits to the late onset of abnormal sensorimotor gating in congenital psychological disorders.

M Cardon, N Ron-Harel, H Cohen, G M Lewitus, M Schwartz

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In one paragraph

Article in Molecular psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Animal models of prenatal immune challenge and their contribution to the study of schizophrenia: a systematic review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012
    Pooled it
  2. Disorders of puberty and neurodevelopment: A shared etiology?Annals of the New York Academy of Sciences · 2024
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  10. Variants of the RELA gene are associated with schizophrenia and their startle responses.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
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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

5 authors at 3 institutions in 2 countries.

M CardonDepartment of Neurobiology, The Weizmann Institute of Science, Rehovot 76100, Israel.
N Ron-Harel
H Cohen
G M Lewitus
M Schwartz
Weizmann Institute of Science · ILBen-Gurion University of the Negev · ILMcGill University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropsychological syndromes including schizophrenia often do not manifest until late adolescence or early adulthood. Studies attributing a role in brain maintenance to the immune system led us to propose that malfunction of immune-dependent regulation of brain functions at adolescence underlies the late onset of such diseases/syndromes. One such function is sensorimotor gating, the ability to segregate a continuous stream of sensory and cognitive information, and to selectively allocate attention to a significant event by silencing the background (measured by prepulse inhibition; PPI). This activity is impaired in schizophrenia, as well as in several other neuropsychological diseases. Using a model of prenatal immune activation (maternal polyriboinosinic-polyribocytidylic acid (poly I:C) injection), often used as a model for schizophrenia, and in which abnormal PPI has a delayed appearance, we demonstrated a form of immune deficit in the adult offspring. Similar abnormal PPI with a delayed appearance was found in congenitally immune-deficient mice (severe combined immune deficient, SCID), and could be reversed by immune reconstitution. This functional deficit correlated with impairment of both hippocampal neurogenesis and expression of the gene encoding kisspeptin (Kiss1) that manifested at adulthood. Moreover, exogenous administration of a kisspeptin-derived peptide partially reversed the gating deficits in the SCID mice. Our results suggest that a form of congenital immune deficiency may be a key factor that determines manifestation of developmental neuropsychological disorders with onset only at early adulthood.

Indexed as

Acoustic StimulationAge FactorsAnalysis of VarianceAnimalsAnimals, NewbornBromodeoxyuridineCell DifferentiationCell ProliferationDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleHippocampusKisspeptinsLymphocytesMaleMental DisordersBromodeoxyuridineKiss1 protein, mouseKisspeptinsPeptidesPoly CPoly Gpoly G-poly CProteins

Identifiers

PMID19636313
OpenAlexW2010346966

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.