2. Genetic Hypothesis:
Schizophrenia tends to run in families, but no single gene is thought to be responsible.
It’s more likely that different combinations of genes make people more vulnerable to the condition. However, having these genes doesn’t necessarily mean you’ll develop schizophrenia.
Evidence that the disorder is partly inherited comes from studies of twins. Identical
twins share the same genes.
In identical twins, if one twin develops schizophrenia, the other twin has a one in two chance of developing it, too. This is true even if they’re raised separately.
In non-identical twins, who have different genetic make-ups, when one twin develops schizophrenia, the other only has a one in seven chance of developing the condition.
While this is higher than in the general population, where the chance is about 1 in
100, it suggests genes aren’t the only factor influencing the development of
3. Specific genes:-
According to, Meta-analysis of genetic linkage studies strong evidence of susceptibility for schizophrenia has found on loci 13q, 22q11-12 and 8p21-22. According to evidence for susceptibility many other loci is also there (Badner ; Gershon, 2002; DeLisi, Crow, et al., 2002; Levinson, Lewis, ; Wise, 2002; Lewis et al., 2003; Tandon, Keshavan, ; Nasrallah, 2008).
In some individuals in the development of schizophrenia some rare specific genetic aberrations have been implicated. These are microdeletions of part of chromosome 22q11.2, which leads to a 20-fold increase in risk for schizophrenia (Bassett et al., 2005), and deletions in 1q21.1, 15q11.2, and 15q13.3 (Stefansson et al., 2008). These microdeletions accounts for up to 2% of schizophrenia (Bassett, et al., 2005).
In rare causes of schizophrenia other genes implicated include Val66Met (Gratacòs et al., 2007), GAD1 (Straub et al., 2007), and DISC1 (disrupted in schizophrenia 1) (Hennah, Thompson, Peltonen, ; Porteous, 2006). Furthermore, Neuroregulin 1 (NRG1), COMPT (catechol-O-methyl-transferase), ALC6A3, DRD3, DTNBP1 (dysbindin) and SLC184 are implicated in schizophrenia (Duan et al., 2007; Nicodemus et al., 2007; Riley et al., 2009; Tan et al., 2007).
4. Neurotransmitter Dysfunction Hypotheses:
Dopamine is a neurotransmitter which is important in the pathology of schizophrenia. Drugs that block dopamine receptors, specifically D2 receptors (Carlsson, Carlsson, ; Milsson, 2004), have an ameliorating effect on symptoms of schizophrenia (Creese, Burt, ; Snyder, 1996), and those that increase the action of dopamine exacerbate symptoms (Snyder, 1972).
B. Serotonin, glutamate and ?-aminobutyric acid:
Cerebral serotonin imbalances have been implicated in schizophrenia. Second
generation antipsychotics are, amongst other actions, serotonin antagonists (Meltzer, Matsubara, ; Lee, 1989), and are more effective for treatment resistant schizophrenia than typical antipsychotics (Bondolfi et al., 1998). Serotonin antagonists have also proved effective in the treatment of negative symptoms (Duinkerke et al., 1993). However, the exact mechanism via which serotonin plays a role in schizophrenia is not fully understood (Duncan, Zorn, ; Lieberman, 1999).
Another neurotransmitter that has been implicated in schizophrenia is glutamate. This hypothesis was drawn from the ability of glutamate agonists, such as Ketamine, to produce quasi psychotic symptoms in the normal population and in people with schizophrenia (Malhotra et al., 1996, 1997).
The inhibitory neurotransmitter ?-aminobutyric acid (GABA) has also been
proposed to play a role in schizophrenia. Post-mortem studies of the brains of people with schizophrenia have found abnormalities in the GABA neurotransmitter system in the frontal lobes (Benes, Vincent, Marie, ; Khan, 1996; Sherman, Davidson, Baruah, Hegwood, ; Waziri, 1991). GABA plays an important function in working memory, and it has been proposed that these GABA reductions may be linked to deficits in working memory found in schizophrenia (Lewis, Hashimoto, ; Volk, 2005; Lewis, Volk, ; Hashimoto, 2004; Volk ; Lewis, 2002).