Schizophrenia: From Nash to Neurotransmitters

This paper reflects the research and thoughts of a student at the time the paper was written for a course at Bryn Mawr College. Like other materials on Serendip, it is not intended to be "authoritative" but rather to help others further develop their own explorations. Web links were active as of the time the paper was posted but are not updated.

Contribute Thoughts | Search Serendip for Other Papers | Serendip Home Page

Biology 202

2006 First Web Paper

On Serendip

Schizophrenia: From Nash to Neurotransmitters

Stephanie Pollack

The disease schizophrenia often causes people to think of Russell Crowe's character John Nash in the film A Beautiful Mind. Schizophrenia is a serious mental disorder, which affects about one percent of the human population (1). Like most victims of schizophrenia, the brilliant mathematician John Nash, developed the disease in his early adulthood (2). The onset of schizophrenia in early adulthood establishes that brain development remains underway during this period. However, John Nash's genius is uncharacteristic of schizophrenics; most are of average intelligence, and often experience a declining IQ as the disease progresses (1). Schizophrenia impacts not only the victim, but all those around him. The schizophrenic often has trouble holding a job and leading a normal, independent life, frequently having difficulty dealing with the challenges of daily living (2).

Usually, the symptoms of schizophrenia are severe at the start of the disease and then continue "to worsen and improve in cycles known as relapses and remissions" (8). Schizophrenia varies in its severity and can be categorized into four classes: Paranoid schizophrenia, Disorganized schizophrenia, Catatonic schizophrenia and Undifferentiated schizophrenia (8). Paranoid schizophrenia is the most common form and causes sufferers to believe they are being persecuted and to hear imaginary voices (7). These delusions and hallucinations are examples of positive symptoms, or symptoms absent in people without schizophrenia (8). Negative symptoms, or the lacking of particular normal behaviors in people with schizophrenia, include antisocial behavior and poor personal hygiene (8).

Presently, treatments for schizophrenia blend therapy with prescription medications (antipsychotics) which help to alleviate the more stereotypic symptoms of the disease, such as paranoid delusions and hallucinations (2). Electric shock treatment, an older method of treatment, is rarely used today (8). Drugs that treat schizophrenia work to manipulate the expression of symptoms "by neuroreceptor antagonism." (3)

Recent studies have shown that schizophrenia can be a precisely diagnosed disease with evident "changes in brain structure and function" (2). On average, schizophrenics tend to have smaller brains than their normal counterparts (1). Aside from size, individuals with schizophrenia have anatomically distinct brains from unaffected individuals, raising the question of whether changes in brain structure cause schizophrenia or if schizophrenia causes changes in brain structure. Schizophrenics "have abnormalities in the prefrontal, temporal, and anterior cingulate regions" of the brain, which are areas that help direct cognition and emotion (2). Additionally, memory loss brought on "by lesions of the frontal lobe... [is] evident in schizophrenia and may account for the cardinal symptoms of disorganization in thinking, planning and expressing thoughts" (2).

Scientists have come to realize that no one part of the brain is solely responsible for schizophrenia. Schizophrenia, like normal behavior, involves the combined effort of the entire brain, and the interruption of normal function results from the interactions of multiple brain regions (1). Schizophrenia is a complex disorder that is believed to have a genetic basis. The disease is not caused by a single gene defect, rather it is polygenic, or brought about by multiple genes acting together (6). This genetic predisposition is combined with environmental factors to yield the disorder. Such environmental factors include "obstetric complications, intrauterine abnormalities, and viruses" (2). Polygenetic forces may account for the wide range of symptoms across schizophrenic patients (1).

Interestingly, the drug amphetamine mimics the symptoms found in schizophrenic patients in normal individuals (5). Additionally, when schizophrenic patients are given amphetamine, their schizophrenic symptoms often worsen (5). Consequently, amphetamine must interact with neurotransmitters in the brain to elicit such similar symptoms. Researchers have been on the hunt for which neurotransmitter in particular gives way to schizophrenic behavior.

Dopamine is an important neurotransmitter in the central nervous system and its receptors are linked to "a number of neuropathological disorders such as Parkinson's disease and schizophrenia" (3). The "dopamine theory" suggests that the symptoms associated with schizophrenia are correlated with "excess dopamine release in important brain regions" (1). Therefore, an increased level of dopamine receptors in schizophrenic patients can be used to help diagnose the disease (3). The dopamine hypothesis can be extended to the limbic system, which directs emotion and cognition (4). These areas of behavior are clearly altered in those suffering from schizophrenia. The limbic system "is richly innervated by noradrenic and dopaminergic neurons", and thus demonstrates how malfunctioning dopamine receptors can influence schizophrenic behavior (4).

Although this evidence is quite convincing, new data has indicated that the neurotransmitter glutamate may play a more active role than that of dopamine (1). Glutamate can be found in nearly all areas of the brain and would be a better candidate to explain schizophrenia's variety of symptoms (1). While glutamate is important in signaling all over the brain, dopamine's significance is confined to only certain parts of the brain (1).

Clearly, the intricacies of the roles of neurotransmitters in the brain are not yet fully understood. Continued research in this area will lead to the development of more effective drugs to combat the devastating disease of schizophrenia.


1) Javitt, D.C. & Coyle, J.T., Decoding Schizophrenia, Scientific American, January 2004, Vol. 290 Issue 1, p48-55.

2) Workshop on Schizophrenia

3) A Peripheral Marker for Schizophrenia: Increased Levels of D3 Dopamine Receptor mRNA in Blood Lymphocytes

4) Schizophrenia: Elevated Cerebrospinal Fluid Norepinephrine

5) Phenylethylamine in Paranoid Chronic Schizophrenia

6) Schizophrenia: Genetic Tools for Unraveling the Nature of a Complex Disorder

7), Classification of Schizophrenia

8), Mental Health: Schizophrenia

| Course Home | Serendip Home |

Send us your comments at Serendip

© by Serendip 1994- - Last Modified: Thursday, 23-Feb-2006 15:50:05 EST