Describe and Evaluate Biological Explanations of Schizophrenia

AO1

THE GENETIC BASIS OF SCHIZOPHRENIA

  • SCHIZOPHRENIA RUNS IN THE FAMILY: GREATER GENETIC SIMILARITY between FAMILY MEMBERS associates with the LIKELIHOOD of BOTH DEVELOPING SCHIZOPHRENIA – 100% GENES with MONOYGOTIC and 50% SIBLING à GOTTESMAN: shows the link through META-ANALYSIS of 40 studies = IDENTICAL TWINS: 48% / DIZYGOTIC: 17%
  • CANDIDATE GENES: POLYGENIC ( not determined by a SINGLE gene – 108) and AETIOLOGICALLY HETEROGENEOUS (DIFFERENT COMBINATIONS of factors can lead to different conditions) à RIPKE ET AL: LARGE-SCALE combining PREVIOUS DATA from ‘GENOME-WIDE’ (a complete set of DNA) studies of schizophrenia, compared genetic makeup of 37,000 patients and 113,000 CONTROLS = 108 genes associated with HIGHER RISK

DOPAMINE HYPOTHESIS

  • NEUROTRANSMITTERS – brain’s CHEMICAL MESSENGERS
  • HYPERDOPAMINE in the SUBCORTEX: ORIGINAL VERSION, HIGH levels of ACTIVITY of DOPAMINE in the SUBCORTEX e.g. EXCESS of DOPAMINE RECEPTORS in the BROCA’S AREA (speech production)
  • HYPODORAMINERGIA in the CORTEX: MORE RECENT, GOLDMAN-RAKIC ET AL show how LOW LEVELS in the PRE-FRONTAL (thinking and decision-making) create NEGATIVE SYMPTOMS

NEURAL CORRELATES OF SCHIZOPHRENIA

  • The MEASUREMENT of the STRUCTURE of the BRAIN that CORRELATE with an EXPERIENCE
  • NEGATIVE SYMPTOMS: AVOLITION (loss of MOTIVATION) + MOTIVATION involves the ANTICIPATION of the REWARD and the VENTRAL STRIATUM is believed to be involved with this à JUCKEL: LOWER LEVELS of activity than in the CONTROLS and saw a NEGATIVE CORRELATION between ACTIVITY LEVELS in the V.S and THE SEVERITY OF OVERALL NEGATIVE SYMPTOMS

= ACTIVITY in the V.S is a NEURAL CORRELATE

  • POSITIVE SYMPTOMS: ALLEN ET AL scanned BRAINS of PAITIENTS and compared to CONTROL GROUP = LOWER ACTIVATION LEVELS in the SUPERIOR TEMPORAL GYRUS and the ANTERIOR CINGULATE GYRUS in the HALLUCINATION GROUP = MORE ERRORS

= LOW activity in these areas is a NEURAL CORRELATE OF AUDITORY HALLUCINATIONS

AO3

  • MULTIPLE SOURCES OF EVIDENCE: GROTTESMAN: genetic similarity and shared risk of schizophrenia, ADOPTION STUDIES (TIENARI ET AL): children of SUFFERERS are STILL at a HIGH RISK even if adopted into FAMILIES WITH NO HISTORY
  • THE CORRELATION-CAUSATION PROBLEM: DOES the UNUSUAL activity in the region of the brain CAUSE the SYMPTOM or OTHER EXPLANATIONS? e.g. correlation with V.S + negative symptoms – could be something in the V.S or the negative symptoms CAUSING the LESSER INFORMATION in the V.S
  • PSYCHOLOGICAL ENVIRONMENT: ENVIRONMENT FACTORS have an important role like psychological ones – FAMILY FUNCTIONING DURING CHILDHOOD – probability of getting schizophrenia, even if you are a MONOZYGOTIC TWIN, is 50%
  • MIXED EVIDENCE FOR DOPAMINE HYPOTHESIS: DOPAMINE AGONISTS like AMPHETAMINES = INCREASE LEVELS of DOPAMINE and ANTI-PSYCHOTIC DRUGS = DECREASE of DOPAMINE levels = important role

BUT some say it doesn’t provide a full explanation à RIPKE ET AL: some genes code for production of OTHER NEUROTRANSMITTERS = others, like GLUTAMATE, are important