ReviewNeurotoxicity research2008
Clinical perspectives on the genetics of schizophrenia: a bottom-up orientation.
Review in Neurotoxicity research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Metabolic Parameters in Patients with Prader-Willi Syndrome and DiGeorge Syndrome with Respect to Psychopathological Manifestation.Neuropsychiatric disease and treatment · 2020Article
- Copy number variants in a sample of patients with psychotic disorders: is standard screening relevant for actual clinical practice?Neuropsychiatric disease and treatment · 2012Article
- Contrasting monosymptomatic patients with hallucinations and delusions in first-episode psychosis patients: a five-year longitudinal follow-up study.Psychopathology · 2011Article
- Focusing on symptoms rather than diagnoses in brain dysfunction: conscious and nonconscious expression in impulsiveness and decision-making.Neurotoxicity research · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phenomenology has been the reference point that investigators have used in their efforts to understand schizophrenia. Although symptoms and signs are crucial for the diagnosis of schizophrenia, there is an ongoing debate since Kraepelin attempted to group symptoms to understand the etiology of schizophrenia. Several operational criteria have been developed to establish the diagnosis of schizophrenia, making it obvious that there are no precise symptomatological boundaries. There is little clear indication which of the systems is valid for genetic and other biological research. Despite the enormous effort to find a linkage between schizophrenia and one or more loci, the results are far from conclusive. Another approach is the search for candidate genes of which DICS1 and 22q11 deletion syndrome are examples. In all studies into the genetic underpinnings of schizophrenia, however, the clinical vantage point is neglected in that a broad clinical phenotype with respect to, e.g., developmental issues, symptoms and comorbidity is narrowed down to one categorical diagnosis. This is illustrated by the lack of exclusion criteria in genetic studies and by the occurrence of schizophrenia-like psychoses in a broad array of genetic syndromes. In case of 22q11 deletion syndrome, the psychotic symptoms emerge in the context of brain anomalies, a plethora of somatic abnormalities and specific neurocognitive deficits. Prader-Willi syndrome is a hypothalamic disorder in which psychotic symptoms may occur that resemble schizophrenia. It is concluded that not only schizophrenia is a highly variable disease but that the genetic samples are even much more heterogeneous.
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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.