The researchers used DNA micro-arrays to survey white blood cells genes from 14 people.

They examined in detail which genes might be involved and assessed their level of social interaction using a scoring system; six scored in the top 15 percent of the UCLA Loneliness Scale, the others scored in the bottom 15 percent.

They then looked at the genetic activity in their white blood cells and tried to compare the results.

The UCLA research discovered that certain genes are more active in people who feel socially isolated which may make them more vulnerable to illness.

The researchers found 209 gene transcripts differentially expressed between the two groups, 78 were over-expressed and 131 were under-expressed.

Those over-expressed in lonely individuals were involved in immunity and inflammation, while those under-expressed involved antiviral responses and antibody production.

Other research has shown quite clearly that there are links between lack of social support and illnesses such as heart disease.

The scientists say social isolation has a biological impact on the activity of the genes and affects some of the most important basic internal processes.

Dr. Steven Cole, who led the study, says the study shows the biological impact of social isolation.

He says the differences found were not connected to other factors such as age, wealth or health of the people involved, but were specifically connected to their feelings of social isolation and were unconnected to the size of the person's social network.

Dr. Cole says what appears to matter is not how many people you know, but how many you feel really close to over time.

He hopes in future that the gene profile he has identified might help doctors develop effective therapies to ease loneliness.

The study is published in Genome Biology.

N-cofilin also controls the fate of neural stem cells, which are involved in development of the cortex. In its absence more stem cells stop to self-renew and instead start differentiating. This imbalance depletes the pool of neuronal progenitors so that fewer cells can be made to build a complete and functional cortex. The study provides the first proof that proteins affecting actin filament dynamics are involved in neuronal migration disorders.

This might have implications for humans, too, says Gian Carlo Bellenchi from Witke's lab. Like many other cytoskeletal proteins n-cofilin is conserved between mice and humans and it is likely to play a similar role in the development of the human cortex.

This makes the gene encoding n-cofilin an interesting candidate that might be mutated in neuronal disorders such as lissencephaly and other forms of mental retardation.

The mouse model is a powerful tool to further investigate the roles n-cofilin and the actin cytoskeleton play in stem cell physiology and cell migration. Our studies also identified n-cofilin as a potential target molecule that might allow to interfere with stem cell function in diseases where stem cell division has derailed, concludes Christine Gurniak from Witke's group.

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