Congenital anomalies in relatives of schizophrenic probands may indicate a retinoid pathology

@article{Goodman1996CongenitalAI,
  title={Congenital anomalies in relatives of schizophrenic probands may indicate a retinoid pathology},
  author={Ann B. Goodman},
  journal={Schizophrenia Research},
  year={1996},
  volume={19},
  pages={163-170}
}
  • A. Goodman
  • Published 1 May 1996
  • Medicine, Psychology
  • Schizophrenia Research
Physical manifestations of neurodevelopmental disruption: are minor physical anomalies part of the syndrome of schizophrenia?
TLDR
Research findings on MPAs indicate that these minor anomalies are indeed part of some schizophrenia syndromes, representing a stable systemic or physical set of manifestations of the underlying neurodevelopmental processes that lead to the illness.
Structural variants in the retinoid receptor genes in patients with schizophrenia and other psychiatric diseases
  • Jinong Feng, Jiesheng Chen, S. Sommer
  • Psychology, Medicine
    American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics
  • 2005
TLDR
It is concluded that structural variants in the RAR/RXR and NURR1 genes do not play a major role in the etiology of schizophrenia.
Finding Genes Underlying Schizophrenia Retinoid and Thyroid Hormone Hypotheses
TLDR
The study failed to identify any of the described mutations in patients or controls, but these negative results do not exclude altered expression of nuclear receptors in schizophrenia or the presence of other mutations.
Three independent lines of evidence suggest retinoids as causal to schizophrenia.
  • A. Goodman
  • Medicine, Psychology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1998
TLDR
A close causal relationship between retinoids and the underlying pathophysiological defects in schizophrenia is suggested and new treatment modalities to alter the downstream expression of the dopamine receptors and other genes that are targets of retinoid regulation, and that are thought to be involved in schizophrenia are suggested.
Neurobiology of schizophrenia
Schizophrenia is a common chronic and disabling brain disease of unknown etiology, pathogenesis, and mechanism. Whether schizophrenia represents a single disorder of markedly variable expression or a
Low maternal retinol as a risk factor for schizophrenia in adult offspring
Neurodevelopmental risk factors in schizophrenia.
TLDR
The high prevalence of minor physical anomalies among schizophrenic subjects supports the neurodevelopmental theory of the etiology of schizophrenia, since they suggest either genetically or epigenetically controlled faulty embryonic development of structures of ectodermal origin like brain and skin.
Certain Aspects Of Teratological Effects Of Retinoids On Skin Of Swiss Albino Mice .
TLDR
In the present study effects of different doses on skin on different development stages of swiss albino mice are studied.
...
...

References

SHOWING 1-10 OF 51 REFERENCES
Chromosomal locations and modes of action of genes of the retinoid (vitamin A) system support their involvement in the etiology of schizophrenia.
  • A. Goodman
  • Medicine, Psychology
    American journal of medical genetics
  • 1995
TLDR
The knowledge about the transport, delivery, and action of retinoids is related to what is presently known about the pathology of schizophrenia, with particular reference to the dopamine hypothesis, neurotransmitters, the glutamate hypothesis, retinitis pigmentosa, dermatologic disorders, and craniofacial anomalies.
Elevated risks for amyotrophic lateral sclerosis and blood disorders in Ashkenazi schizophrenic pedigrees suggest new candidate genes in schizophrenia.
  • A. Goodman
  • Medicine, Psychology
    American journal of medical genetics
  • 1994
Among relatives of Ashkenazi schizophrenic probands the rate of amyotrophic lateral sclerosis was 3/1,000, compared to expected population rates of approximately 2/100,000. Relative risk of bleeding
Animal models for human craniofacial malformations.
TLDR
Human and animal studies indicate that cleft lips of multifactorial etiology may be generically susceptible because of small MNP)s or other MNP developmental alterations, such as those found in A/J mice, that make prominence contact more difficult.
Medical conditions in Ashkenazi schizophrenic pedigrees.
  • A. Goodman
  • Psychology, Medicine
    Schizophrenia bulletin
  • 1994
TLDR
The hypothesis posed is that the increased prevalence among the Ashkenazim of the rare lysosomal enzyme disorders, Tay Sachs disease (TDS), caused by low levels of hexosaminidase A, and Gaucher's disease (GD), might contribute to the demonstrated increased vulnerability to schizophrenia in this ethnic group.
Congenital malformations and structural developmental anomalies in groups at high risk for psychosis.
TLDR
The inferred genetic risk for psychosis does not appear to be associated with greater rates of early somatic developmental anomalies, suggesting that early developmental anomalies do not represent an expression of genetic influence toward psychosis.
Prenatal origin of schizophrenia in a subgroup of discordant monozygotic twins.
TLDR
It is concluded that some cases of adult-onset schizophrenia are associated with prenatal events, which may include neurodevelopmental abnormalities or specific insults such as anoxia or infectious agents.
Familial, obstetric, and other clinical correlates of minor physical anomalies in schizophrenia.
TLDR
Minor physical anomalies indicate early dysmorphogenesis in schizophrenia, particularly in males, which appears to be associated more reliably with genetic rather than obstetric factors and with cognitive impairment.
Minor physical anomalies in schizophrenia patients, bipolar patients, and their siblings.
TLDR
When viewed within a vulnerability-stress model, the results are consistent with the theory that MPAs may reflect early, largely extra-genetic, stressful events.
Retinoic acid and craniofacial development: Molecules and morphogenesis
TLDR
This article proposes that the amount of RA reaching the nucleus in different embryonic tissues is modulated by a mechanism involving three cytoplasmic binding proteins for retinol (CRBP I) and retinoic acid (CRABP I and II).
...
...