Most of you probably assume that your genes stay put – that they stay where they started on the chromosome. But that’s not always the case. Small pieces of our DNA can relocate and proliferate in other areas of the genome.

They’re called retrotransposons or “jumping genes”. We don’t fully understand their function, but studies suggest they play contradicting roles in normal brain development and neuropsychiatric diseases.

People with Louis-Bar syndrome, a neurological motor disease, have higher levels of a jumping gene called L1. So do people with a form of autism called Rett. And now the same has been found in people with schizophrenia.

A recent study found people with schizophrenia had more of these jumping genes. They’re even higher in schizophrenics exposed to certain environments. For example, fetuses with malnutrition are more likely to develop schizophrenia. Nearly half of our genome consists of jumping genes which can be silent, reproduce, or alter the activities of nearby genes. But problems can arise when jumping genes overexpress.

But what causes L1 levels to go up? Could it be environmental factors? To find out, researchers injected pregnant lab rats with a molecule that simulates a viral infection. Indeed those offspring had elevated levels of L1.

In studies with macaques, L1 was also higher in those that were exposed to a hormone that increases the risk of schizophrenia. We can’t conclude yet that L1 jumping causes these diseases.

More studies are needed not only to answer this question but to understand how jumping genes might affect our cognitive development.


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