Partial Genetic Basis of Depression and Schizophrenia?

It is not enough to link a gene with a disease, statistically. One must also demonstrate how alterations in the gene can affect disease symptoms.

Steven Clapcote, David Porteous, John Roder, and colleagues reported their findings in the May 3, 2007 issue of the journal Neuron, published by Cell Press.

In their experiments, the researchers sought to explore the consequences of mutating a gene called "Disrupted in schizophrenia 1" (DISC1), which had been found in one family to be associated with schizophrenia, bipolar disorder, and major depression.

The researchers' theory was that different mutant variations of DISC1 might have different pathological effects. To test this theory, the researchers screened a large population of mouse mutants to isolate two with different mutations in DISC1.

They found that, indeed, one of the mutant mouse strains exhibited behavioral abnormalities and memory deficiencies resembling the symptoms of schizophrenia in humans. Additionally, these symptoms could be alleviated in the mice by antipsychotic drugs.

Similarly, the other mutant mouse strain showed behaviors that reflected depressive symptoms. These symptoms could be alleviated by an antidepressant, found the researchers.

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The DISC-1 gene has been studied by schizophrenia researchers for years. Many other genes have likewise been looked at due to associations with schizophrenia.

The task of explaining the developmental and physiological effects of the altered gene products in humans, and why these changes lead to schizophrenic symptoms, remains to be done.

It goes without saying that pharmacologic agents are often developed and marketed for a disease, long before a complete understanding of that disease is arrived at. Humans are impatient creatures, and "solve" many problems without understanding them. If you were bold, you might even call humans irrational.