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Schizophrenia

Uni of Notts, Neurobiology of Disease, year 2, topic 8

TermDefinition
Prevalence & onset pattern of schizophrenia ~1% prevalence (~1 in 300), with earlier onset in males & a ~1.4:1 male:female ratio. Caused by diatheses-stress model. Unlikely to be cured but remission is possible
Dopamine changes in schizophrenia Increased dopamine in mesolimbic pathways & reduced dopamine in mesocortical (PFC) pathways
Cognitive deficits in schizophrenia Impaired memory, social cognition/cues, perception, & organisation
Diagnostic criteria for schizophrenia & impact on life expectancy ≥2 core symptoms (e.g. delusions, hallucinations) for ≥1 month. ~15–20 years reduced life expectancy, disproportionate burden compared to prevalence
Heritability in schizophrenia Risk increases with genetic relatedness, but ~60% of cases have no family history. More likely to develop neurodegenerative disorders
DISC1 Glutamatergic post-synaptic receptor. Regulates neuronal development, synapse formation, & signalling pathways affecting brain connectivity
COMT & D2 SNPs in schizophrenia Reduces dopamine metabolism & D2-like inhibitory effects. Polymorphisms can lead to thermoinstability, causing hyperdopaminergia
Environmental risks of schizophrenia: Prenatal & postnatal (particularly around adolescence) Prenatal: Maternal infection, poor nutrition, stress, & birth complications Developmental: Migration, social isolation, stress, & drug use (especially cannabis)
Cannabis on schizophrenia risk over 4 years Higher likelihood than other recreational drugs but susceptible individuals usually succumb within 4 years of using. If no effects have occured, the risk plateaus to the same as other recreational drugs
Typical antipsychotics mode of action Antagonise dopamine D2 receptors to reduce positive symptoms
Side effects result from D2 blockade in the nigrostriatal & tuberinfundibular pathways Nigrostriatal: Extrapyramidal symptoms (Parkinson-like involuntary movement disorders) Tuberoinfundibular: Removes inhibition of prolactin release leading to overrelease
Atypical antipsychotic side-effects compared to typical antipsychotics Less extrapyramidal effects but higher risk of metabolic side effects (weight gain, diabetes)
3rd generation antipsychotics & example High affinity D2/D3 & 5HT2A/5HT1A receptor partial agonists with less concerning side effects. E.g., aripiprazole & Brilaroxazine
Flaws of dopamine hypothesis (2 examples) ~30% of patients don’t respond to D2 antagonists, & negative/cognitive symptoms persist. Post-mortem findings difficult to interpret due to medication altering dopamine levels & receptor expression
Glutamate hypothesis NMDA receptor hypofunction on GABA interneurons reduces inhibition → excess glutamate activity
Evidence for glutamate hypothesis (drugs) NMDA antagonists like ketamine & PCP can induce psychosis-like symptoms in healthy individuals
Evidence for glutamate hypothesis (imaging) & downsides Reduced glutamate, GABA, & NMDA receptor availability in brain regions like anterior cingulate cortex & hippocampus. But studies run in small non-stratified cohorts due to expense
Inflammation hypothesis Correlation with schizophrenia & elevated cytokines & association with immune genes (e.g. Major Histocompatibility locus, codes for antigens)
Inflammation hypothesis potential therapies Drugs like Celecoxib may reduce neuroinflammation by inhibiting glial activation when combined with antipsychotics
Synaptic pruning hypothesis Excessive cortical pruning & insufficient subcortical pruning during adolescence disrupt circuits
Genetic & environmental effects on synaptic pruning hypothesis They alter glial-mediated pruning, potentially removing important synapses
Integrated hypothesis Early risk → abnormal synaptic pruning → cortical imbalance → dysregulated dopamine → negative & positive symptoms
Limitations of integrated hypothesis Doesn’t fully explain grey matter loss, dendritic changes, or if synaptic alterations occured before or after 1st psychotic break
Created by: Denny12
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