Sschizophrenia runs in families. Weak evidence for genetic link due to families sharing environment but systematic investigations do show greater genetic similarity is associated developing the disease.
Found as genetic similarity increase so does probability of sharing schizophrenia. If both parents have the disease for example, then there is a 46% chance for the child to develop it.
Investigated 57 schizophrenic patients. If a monozygotic twin had schizophrenia, there was a 42% chance their twin would also have schizophrenia. If the twin was dizygotic, the concordance rate dropped to 9%.
Found through adoption studies that although the biological parent was not in close contact with the child, there was a genetic development of schizophrenia in the child.
Individual genes are believed to be associated with risk of inheritance. Polygenic as it requires a number of combinations and factors to work. Aetiologcially heterogenous as different combination of factors can lead to contracting schizophrenia.
Neurotransmitters are chemical messengers of the brain that appear to work differently in people with schizophrenia. Dopamine is particularly involved.
High levels of dopamine in the subcortex. Excess dopamine. E.g: dopamine receptors in Broca's area associated with poverty of speech and auditory hallucinations.
Patterns of structure or activity in the brain that occur in conjunction with an experience and are associated with specific cognitive functions, emotions, behaviors, or conscious experience.
Avolition. Ventral striatum believed to be involved in the anticipation of a reward, caused by motivation. Juckel et al measured activity levels in the ventral striatum in schizophrenia patients and found lower levels of activity than in the control.
Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group compared to control. Reduced activity in these two areas of the brain is neural correlate of auditory hallucination.