Biological Explanations of Schizophrenia

There will be a significantly higher concordance rate in onset of Sz for monozygotic twins compared with dizygotic twins.

Risk of schizophrenia depends on genes shared MZ twins: 48% DZ twins (one effected parent): 17% 2 parents: 46%However: Concordance is not 100% in MZ so other factors must play a part.

MZ twins: concordance of 26.5% DZ: 0%Strongly supports a genetic link.

Twins rare and only 1% of Mz twins will have Sz so...(small studies) No same diagnostic criteria so it is hard to compare results Different definitions for MZ and DZ Concordance rates calculated in different ways

155 adopted children with schizophrenic parents Compared with children with non-schizophrenic parents 10% with schiz parents developed it 1% of other non-schiz developed it It is likely there is a genetic component

Dopamine neurons fire too easily/ too often Abnormally high number of D₂ receptors.

Supported by studies on effects of drugs:Phenothiazines (Blocks dopamine synapses)Clozapine (Also blocks dopamine receptors)L-Dopa (used for Parkinsons - increases dopamine and leads to similar effects to Sz)ALSOPost Mortems show increased dopaminePET scans - Wong etal found 2x dopamine in Sz brain not using drugs compared to Sz with drugs.

Neuroimaging hasnt provided evidenceDrugs do not have the same effects on all people Post-mortem shows that schiz' that hadnt received anti-psychotics had normal levelsMost post mortems are on Sz who used drugs. Hard to know whether ^ dopamine cause or effect

Torrey (2002), Schiz have 15% larger ventricles Could be result of poor brain development/ tissue damage

Copolov + Crook (2000), meta-analysis showed overlap between schiz and non-schiz sizes Lyon et al (1981), as dose of medication increased so did ventricles (so, did Sz cause change or the drugs?)Abnormalities are not found in all sufferers.

Type 1: genetically inherited. Associated with dopamine dysfunction + possitive symptoms. Responds to antipsychotic medication. Type 2: neurodevelopmental disorder. Pre-natal/ Perinatal insults. Poor premorbid functioning. Negative symptoms. Doesnt respond wel to drugs.

Have genetic predisposition, but only develops after significant psychological stressors

Doesn't take into account other factors. Biology trying to find specific explanations even to single genetic level (however, biologists do accept importance of other factors)

Diathesis-stress model is accepted by most biologists Predisposition-but may not get it.