ArticleDialogues in clinical neuroscience2001
Genetic basis of cognitive disability.
Article in Dialogues in clinical neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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.
Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Homozygous Missense Variant in the N-Terminal Region of ANK3 Gene Is Associated with Developmental Delay, Seizures, Speech Abnormality, and Aggressive Behavior.Molecular syndromology · 2023Article
- The practice of genomic medicine: A delineation of the process and its governing principles.Frontiers in medicine · 2022Article
- Impact of the Olig Family on Neurodevelopmental Disorders.Frontiers in neuroscience · 2021Review
- Cognitive impairment in COPD: should cognitive evaluation be part of respiratory assessment?Breathe (Sheffield, England) · 2017Review
- Genetic variation and cognitive dysfunction in opioid-treated patients with cancer.Brain and behavior · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The importance of genetic influences on cognitive disability has been recognized for a long time, but molecular analysis has only recently begun to yield insights into the pathogenesis of this common and disabling condition. The availability of genome sequences has enabled the characterization of the chromosomal deletions and trisomies that result in cognitive disability, and mutations in rare single-gene conditions are being discovered. The molecular pathology of cognitive disability is turning out to be as heterogeneous as the condition itself, with unexpected complexities even in apparently simple gene-deletion syndromes. One remarkable finding from studies on X-linked mental retardation is that mutations in different small guanosine triphosphate (GTP)-binding proteins result in cognitive disability without other somatic features. Advances are also being made in cognitive disability with polygenic origins, such as dyslexia and autism. However, the genetic basis of mild intellectual disability has yet to be satisfactorily explained.
Indexed as
Identifiers
22034445PMC3181642W125030491What OpenQuestion holds
Registered trials
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.