Week 3 Flashcards by Colleen Quigley

The Finnish Adoptive Family Study of Schizophrenia

Finnish Adoptive Family Study of Schizophrenia

A nationwide study in Finland comparing the mental health of adopted offspring of schizophrenic mothers with those of non-schizophrenic biological parents, focusing on the interaction between genetic vulnerability and adoptive rearing environments.

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The Finnish Adoptive Family Study of Schizophrenia

Genetic Vulnerability

The predisposition to develop a disorder due to inherited genetic factors, potentially activated by environmental influences.

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The Finnish Adoptive Family Study of Schizophrenia

Adoptive Index Group

Offspring of schizophrenic biological mothers placed in adoptive families, used as a study group to assess genetic and environmental influences on mental health.

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The Finnish Adoptive Family Study of Schizophrenia

Adoptive Control Group

Offspring of non-schizophrenic biological parents placed in adoptive families, serving as a comparison group in the study.

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The Finnish Adoptive Family Study of Schizophrenia

Psychosis

A severe mental disorder characterized by impaired thoughts and emotions, often associated with hallucinations or delusions.

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The Finnish Adoptive Family Study of Schizophrenia

Family Mental Health Rating

A classification system used to assess the overall mental health of adoptive families, ranging from “healthy” to “severely disturbed.”

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The Finnish Adoptive Family Study of Schizophrenia

Gene-Environment Interaction

The hypothesis that genetic predispositions and environmental factors, such as family dynamics, interact to influence the development of mental disorders like schizophrenia.

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The Finnish Adoptive Family Study of Schizophrenia

Rigid-Syntonic Family

A family system that views its coping strategies as adequate despite evidence of dysfunction, characterized by low overt anxiety, unresolved conflicts, and blurred boundaries.

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The Finnish Adoptive Family Study of Schizophrenia

Severe Family Disturbance

A family environment marked by high anxiety, unclear boundaries, and frequent use of primitive defenses like projective identification and splitting.

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The Finnish Adoptive Family Study of Schizophrenia

Adoptive Family Dynamics

The interactions, boundaries, and overall emotional environment provided by adoptive parents, which can influence the mental health of adopted children.

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The Finnish Adoptive Family Study of Schizophrenia

MMPI (Minnesota Multiphasic Personality Inventory)

A psychological test used in the study to independently assess the mental health of adopted offspring without bias from clinical family ratings.

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The Finnish Adoptive Family Study of Schizophrenia

Borderline Case

In this study, a broader classification encompassing severe personality disorders that do not meet the criteria for psychosis but indicate significant mental health challenges.

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The Finnish Adoptive Family Study of Schizophrenia

Healthy Family Rearing

A family environment with low anxiety, clear boundaries, and effective conflict resolution, proposed as a protective factor against developing schizophrenia in genetically predisposed individuals.

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The Finnish Adoptive Family Study of Schizophrenia

Schizophrenia Spectrum Disorders

A range of mental health conditions with shared features of thought disturbances, emotional dysregulation, and impaired reality testing.

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The Finnish Adoptive Family Study of Schizophrenia

Interaction Hypothesis

The theory that schizophrenia emerges due to the combined effects of genetic predisposition and a disturbing rearing environment.

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The Finnish Adoptive Family Study of Schizophrenia

Genetic Influence

Offspring of schizophrenic mothers had higher rates of severe mental disturbances (28.6%) compared to control offspring (16.5%).

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The Finnish Adoptive Family Study of Schizophrenia

Environment’s Role

No psychotic or borderline cases were observed in offspring reared in healthy or mildly disturbed adoptive families, but such cases significantly increased in severely disturbed families.

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The Finnish Adoptive Family Study of Schizophrenia

Gene-Environment Interaction

Genetic vulnerability combined with a disturbed adoptive family environment increased the likelihood of severe mental illness.

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The Finnish Adoptive Family Study of Schizophrenia

Protective Factors

Healthy family environments acted as a buffer against the development of schizophrenia, even in genetically predisposed individuals.

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Effect of Adolescent-Onset Cannabis Use on Adult Psychosis

Cannabis and Psychosis Relationship

Cannabis use during adolescence is associated with a modest risk of developing psychotic symptoms, such as hallucinations and delusions, and may contribute to clinically significant schizophrenia. The majority of cannabis users do not develop psychosis, suggesting potential genetic vulnerability.

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Effect of Adolescent-Onset Cannabis Use on Adult Psychosis

Gene-Environment Interaction (G x E)

The interplay between genetic predisposition and environmental factors, such as cannabis use, in influencing the development of psychotic disorders.

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Effect of Adolescent-Onset Cannabis Use on Adult Psychosis

COMT Gene

A gene located on chromosome 22q11 that produces the enzyme catechol-O-methyltransferase, involved in dopamine metabolism. The COMT Val158Met polymorphism has been linked to differences in psychosis susceptibility.

Effect of Adolescent-Onset Cannabis Use on Adult Psychosis

Val158Met Polymorphism

A genetic variation in the COMT gene where valine (Val) is substituted with methionine (Met) at position 158. This affects COMT enzyme activity and dopamine regulation in the brain.

Effect of Adolescent-Onset Cannabis Use on Adult Psychosis

Schizophreniform Disorder

A psychotic disorder characterized by symptoms such as hallucinations, delusions, disorganized speech, and negative symptoms lasting between one and six months. It was used as a diagnostic measure in the study.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Dopaminergic Dysregulation

An imbalance in dopamine activity within the brain, implicated in both schizophrenia and cannabis-related psychotic symptoms.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Adolescent-Onset Cannabis Use

Cannabis use beginning during adolescence (prior to age 18), which has been associated with a higher risk of psychosis, particularly among individuals with the Val/Val genotype.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Mesolimbic Dopamine Transmission

Increased dopamine activity in the mesolimbic pathway, often associated with the “positive” symptoms of psychosis, such as hallucinations and delusions.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Endophenotype

A measurable component or marker, such as impaired memory or attention, that links genetic predispositions to clinical symptoms of a disorder like schizophrenia.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Sensitive Period of Brain Development

A critical phase during adolescence when the brain is more vulnerable to environmental influences, such as cannabis use, potentially leading to long-term changes in mental health.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Diagnostic Interview Schedule (DIS)

A standardized psychiatric interview used to assess psychosis outcomes in the study, including symptoms such as hallucinations and delusions.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Hardy-Weinberg Equilibrium

A principle used to determine whether the frequencies of genotypes in a population are consistent with expected values, indicating no significant genetic drift or selection.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Environmental Pathogen

An external factor, like adolescent cannabis use, that interacts with genetic predispositions to increase the risk of developing a disorder, such as psychosis.

**Effect of Adolescent-Onset Cannabis Use on Adult Psychosis** Dopamine Transmission in Prefrontal Cortex

Lower dopamine activity in this brain region, linked to deficits in cognitive functions such as memory and attention, contributing to schizophrenia symptoms.

**The polygenic architecture of schizophrenia** Polygenic Risk Score (PRS)

A measure of an individual’s genetic predisposition to develop a specific disorder, calculated from the sum of risk alleles weighted by their effect sizes.

**The polygenic architecture of schizophrenia** Genome-Wide Association Study (GWAS)

A study that investigates the association of millions of genetic variants across the genome with a given phenotype by comparing genotypes of cases and controls.

**The polygenic architecture of schizophrenia** Dopamine Hypothesis of Schizophrenia

A theory suggesting that psychotic symptoms are linked to excess synaptic levels of dopamine, particularly in the striatum.

**The polygenic architecture of schizophrenia** Neurodevelopmental Model

A hypothesis that schizophrenia arises from genetic and environmental factors that disrupt normal brain development, leading to abnormal synaptic connectivity and function.

**The polygenic architecture of schizophrenia** Negative Correlation

In genetics, a relationship where increases in one trait are associated with decreases in another trait, such as the inverse genetic correlation between schizophrenia and cognitive traits.

**The polygenic architecture of schizophrenia** Synaptic Pruning

The process of eliminating redundant synapses in the brain during development; excessive pruning is thought to contribute to schizophrenia.

**The polygenic architecture of schizophrenia** Heritability of Schizophrenia

The proportion of variance in schizophrenia risk attributable to genetic factors, estimated at 64–81% based on twin and family studies.

**The polygenic architecture of schizophrenia** Antipsychotic Medications

Drugs that manage positive symptoms of schizophrenia by blocking dopamine D2 receptors but have limited effectiveness on negative symptoms and cognitive impairments.

**The polygenic architecture of schizophrenia** Genetic Pleiotropy

The phenomenon where a single genetic variant influences multiple phenotypes or traits.

**The polygenic architecture of schizophrenia** Cognitive Decline in Schizophrenia

A hallmark feature where cognitive impairments often precede the onset of psychosis and include deficits in memory, attention, and executive functioning.

**The polygenic architecture of schizophrenia** Complement System

A part of the immune system involved in synaptic pruning and implicated in schizophrenia through genetic studies of complement component 4 (C4) variants.

**The polygenic architecture of schizophrenia** Psychiatric Nosology

The classification of mental disorders, with current systems challenged by the overlapping genetic and clinical features of disorders like schizophrenia and bipolar disorder.

**Current Research on the Genetic Contributors to Schizophrenia** Genetic Contributors to Schizophrenia

Family, twin, and adoption studies estimate that genetic factors account for approximately 83% of schizophrenia’s liability, influenced by multiple genes and environmental factors.

**Current Research on the Genetic Contributors to Schizophrenia** Multifactorial Threshold (MFT) Model

A model suggesting that schizophrenia results from the additive effects of many genetic and environmental factors, with risk distributed on a continuum and a threshold for clinical diagnosis.

**Current Research on the Genetic Contributors to Schizophrenia** Linkage Studies

Genetic studies that use DNA markers to identify chromosomal regions associated with schizophrenia by examining the correlation of phenotypic resemblance with genetic similarity.

**Current Research on the Genetic Contributors to Schizophrenia** Genome-Wide Association Studies (GWAS)

A method that screens the genome using millions of single nucleotide polymorphisms (SNPs) to identify genetic variants associated with schizophrenia, revealing small-effect genes.

**Current Research on the Genetic Contributors to Schizophrenia** Single Nucleotide Polymorphisms (SNPs)

Variations in a single nucleotide base pair in the genome, used as markers in genetic studies to identify associations with diseases like schizophrenia.

**Current Research on the Genetic Contributors to Schizophrenia** Copy Number Variants (CNVs)

Structural genetic variations involving differences in the number of copies of DNA sequences; linked to a small percentage of schizophrenia cases.

**Current Research on the Genetic Contributors to Schizophrenia** Endophenotypes

Heritable traits or characteristics, such as neuropsychological deficits or brain imaging markers, that are intermediate between genetic risk factors and schizophrenia diagnosis.

**Current Research on the Genetic Contributors to Schizophrenia** Dark Heritability

The unexplained portion of genetic contribution to schizophrenia risk, hypothesized to result from numerous small-effect genetic variants or complex interactions among genes.

**Current Research on the Genetic Contributors to Schizophrenia** Epigenetic Effects

Environmental modifications to DNA, such as histone configuration or methylation patterns, that influence gene expression and may contribute to schizophrenia.