Research Report: Scripps Research Institute team finds surprising view of brain formation

Lynne Friedmann is a science writer based in Solana Beach.

By Lynne Friedmann

As the human brain develops, newly formed nerve cells travel from their place of origin to different brain regions where they connect to one another to form the intricate circuits and networks responsible for various brain functions. Anything that disrupts the course of this nerve cell migration results in an improperly formed brain often with devastating consequences.

Researchers had long known that newly formed nerve cells crawl along a particular type of cell in the brain, called a glial cell, which acts as a cellular guide for the nerve cells.

Researchers at The Scripps Research Institute report on a study focused on a protein called “reelin.” They found reelin to be a key player in the migration of new nerve cells to the neocortex, the part of the brain responsible for higher-order functions, such as language and movement. Unexpectedly, researchers also found that reelin affects this migration process independent of glial cells. The findings have implications for understanding a host of diseases, including some forms of mental retardation, epilepsy, schizophrenia, and autism.

The study appears in the journal Neuron.News release at http://bit.ly/gpynm9.

Finding key to nicotine addiction

Scientists from the Florida campus of The Scripps Research Institute (TSRI) have identified a pathway in the brain that regulates an individual’s vulnerability to the addictive properties of nicotine.

Nicotine is the major addictive component of tobacco smoke, and nicotine acts in the brain by stimulating proteins called nicotinic acetylcholine receptors (nAChRs). These nAChRs are made up of different types of subunits. One of these subunits (α5 subunit) was the focus of the TSRI study that examined that receptor’s response to nicotine in the brain. The scientists found that animal models with a genetic mutation inhibiting α5 consumed far more nicotine than normal. This effect could be reversed by boosting the subunit’s expression. Thus, the findings suggest a new target for anti-smoking therapies.

The findings appear in the journal Nature. News release at http://bit.ly/gDg0yK.

Breast cancer metastasis culprit identified

When doctors discover high concentrations of regulatory T cells in the tumors of breast cancer patients, the prognosis is often grim — though why exactly has long been unclear.

Research at the UCSD School of Medicine suggests these regulatory T cells — whose job is to help mediate the body’s immune response – produce a protein (known as RANKL) that appears to hasten and intensify the spread of breast cancer to distant organs and, in doing so, dramatically increase the risk of death.

In the study, mice with breast cancer were more likely to develop metastatic lung cancer due to elevated levels of RANKL. The scientists also determined that interfering with the ability of RANKL to interact with cancer cells seemed to block tumor progression, and may represent a potential target for drug therapy.

The findings are reported in the journal Nature. News release at http://bit.ly/fNNpT3.

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Posted by Staff on Feb 23, 2011. Filed under Columns, Editorial Columns, Health & Science, Research Report. You can follow any responses to this entry through the RSS 2.0. You can leave a response or trackback to this entry

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