Schizophrenia as a pseudogenetic disease: A call for more gene-environmental studies

  title={Schizophrenia as a pseudogenetic disease: A call for more gene-environmental studies},
  author={E Fuller Torrey and Robert H. Yolken},
  journal={Psychiatry Research},
New Insights Regarding Diagnosis and Medication for Schizophrenia Based on Neuronal Synapse–Microglia Interaction
The hypothesis that excessive synaptic pruning plays a role in the development of schizophrenia is introduced and a strategy for diagnosis and medication based on modulation of the interaction between microglia and synapses is suggested.
Toxoplasma gondii Seropositivity Interacts with Catechol-O-methyltransferase Val105/158Met Variation Increasing the Risk of Schizophrenia
Evidence is provided that the catechol-O-methyltransferase (COMT) Val105/158Met genotype modifies the risk for schizophrenia conferred by T. gondii infection, with it being higher in those individuals with the Met/Met phenotype, intermediate in heterozygous, and lower in those with the Val/Val phenotype.
Association Between Childhood Green Space, Genetic Liability, and the Incidence of Schizophrenia.
The results suggest that risk of schizophrenia is associated additively with green space exposure and genetic liability, and provide no support for an environment-gene interaction between NDVI and schizophrenia.
Infection with Toxoplasma gondii increases the risk of psychiatric disorders in Taiwan: a nationwide population-based cohort study
It is revealed that Toxoplasma gondii infection in Taiwan significantly increases the risk for developing bipolar disorder, depression and anxiety, but not for schizophrenia and other psychiatric disorders.
Failed regeneration and inflammation in schizophrenia: two sides of the same coin?
This review summarizes key arguments speaking for or against the two hypotheses leading to a concept with both aspects position side by side of schizophrenia.
Neuroinflammation and oxidative stress in schizophrenia: are these opportunities for repurposing?
This narrative review throws light on the large-scale evidence pointing toward neuroinflammation and oxidative stress as key etiopathological markers that merit further consideration in SCZ, and may even be the basis for devising novel pharmacotherapies for SCZ.
Social preference is maintained in mice with impaired startle reflex and glutamate/D-serine imbalance induced by chronic cerebral toxoplasmosis
It is concluded that behavioral and cognitive aspects are maintained even though severe neural damage is observed by chronic infection of C57Bl/6 mice with the ME-49 strain, and the startle amplitude is reduced in the infected animals.
Dysfunctional family functioning in high socioeconomic status families as a risk factor for the development of psychiatric disorders in adoptees: the Finnish Adoptive Family Study of Schizophrenia
It was showed that in HSES families, dysfunctional family processes and HR for schizophrenia increased the likelihoods for the development of psychiatric disorders in adoptees.


The role of genetics in the etiology of schizophrenia.
Twin studies of schizophrenia: from bow-and-arrow concordances to star wars Mx and functional genomics.
The five newest studies since 1995 from Europe and Japan have confirmed earlier findings on the genetic basis of clinical heterogeneity within schizophrenia and provided further insights into non-inherited factors that contribute to the multifactorial etiology of this disorder.
After GWAS: searching for genetic risk for schizophrenia and bipolar disorder.
Ten years ago it was widely expected that the genetic basis of common disease would be resolved by genome-wide association studies (GWAS), large-scale studies in which the entire genome is covered by
Are we overestimating the genetic contribution to schizophrenia?
  • E. Torrey
  • Psychology, Medicine
    Schizophrenia bulletin
  • 1992
Although genetics remains as the single most clearly defined etiological factor in schizophrenia, the question remains whether the authors are overestimating the magnitude of the genetic contribution.
The complement system: a gateway to gene-environment interactions in schizophrenia pathogenesis
The complement system could be used as one of the ‘staging posts’ for a variety of focused studies of schizophrenia pathogenesis, including GEI studies of the C4A/C4B repeat polymorphisms in relation to inflammation-related or infectious processes, animal model studies and tests of hypotheses linked to autoimmune diseases that can co-segregate with schizophrenia.
Thinking About Schizophrenia in an Era of Genomic Medicine.
  • D. Weinberger
  • Psychology, Medicine
    The American journal of psychiatry
  • 2019
Genetic discoveries about human brain development and neuropsychiatric syndromes have changed the landscape of psychiatric research. The genotyping of hundreds of thousands of individuals has
Schizophrenia, psychiatric genetics, and Darwinian psychiatry: an evolutionary framework.
This article conceptualizes schizophrenia in a compensatory advantage framework whereby incomplete penetrance of the full disorder, or alternatively, the inheritance of risk alleles insufficient in number to manifest as the classic clinical syndrome, may manifest as a behavioral phenotype with adaptive advantages (eg, creative behavior or novel illuminating ideas).