Webster, R. December 8, 20112models and human genetic association studies has found that the dopamine, glutamate, and
-amino butyric acid (GABA) neurotransmitter pathways do not function appropriately in personswith schizophrenia. In particular, the interneurons in the prefrontal cortex, which are critical tomemory and higher executive functions, are incapable of properly suppressing cortical neuronactivity, which is essential for normal adult cognitive performance
. This mayexplain why a full manifestation of symptoms typically does not appear until late adolescence.There is also a characteristic age of onset for schizophrenia. First diagnosis incidencepeaks around 15 years of age for both males and females, and declines gradually to almost zeroby late middle age (Abel, Drake, and Goldstein, 2010). This does not preclude the possibility of schizophrenia emerging late in life, but the chances are reduced by one third after the age of 55(Narrow, Rae, Robins, and Regier, 2002). Growing older is therefore a protective factor againstschizophrenia. Late onset disease due to hereditary factors is also protective, since members of these families have a lower risk of developing symptoms (Svensson et al, 2011). In addition, if symptoms do manifest late in life they are typically less severe.
Mechanism of Schizophrenia
A large number of research studies over the past two decades have shown that braindevelopment in children who eventually develop schizophrenia is altered early in life
Imaging studies have revealed delayed anatomical maturation and corticalthinning consistent with below average intellectual abilities. Psychiatric symptoms consistentwith a diagnosis of schizophrenia, such severe attention deficit disorder, hallucinations, andsuicidal or homicidal tendencies, can appear as early as 6 years of age (Freedman, 2003, p.1747). These findings are all consistent with schizophrenia being caused by altered braindevelopment early in life, whether due to genetic or inflammatory causes.
The main risk factors for schizophrenia is a family history, a spontaneous geneticmutation during early fetal development or earlier, or exposure to an infectious agent duringgestation. About 80% of all schizophrenia cases can be explained by a family history of thedisease. The remaining 20% are due to spontaneous genetic mutations, infection-inducedinflammation, and other unknown causes.Current estimates suggest approximately 1.25 million Americans can expect to developschizophrenia in their lifetime. Of these, 1 million will have a family history of the disease. Theremaining 0.25 million represents 0.08% of the U.S. population, therefore the lifetime risk of schizophrenia in the absence of a disease family history is 1 in 1250.These risks are reduced by a number of factors, including a family history of late onsetschizophrenia, growing older, an absence of psychiatric symptoms during childhood, living in arural setting, staying close to the
place of birth, or living in a developing or third worldeconomy.The advances that have been made over the past two decades in our understanding of schizophrenia make the use of a schizophrenia diagnosis during state-run persecution campaignsproblematic, especially in countries where its citizenry have access to high quality medical care.