Two papers by Columbia and Harvard researchers report for the first time that astrocytes (the most abundant non-neuronal cells in the central nervous system), which carry a mutated gene known to cause some cases of amyotrophic lateral sclerosis (ALS/Lou Gehrig's disease), induce motor neuron death. This indicates that astrocytes may contribute to ALS by releasing a toxic factor that damages neurons. These findings, posted online by Nature Neuroscience on April 15, suggest that developing an effective therapy for ALS would require overcoming the destructive effects of astrocytes and replacing the damaged motor neurons, possibly by transplanting motor neurons derived from embryonic stem cells.

Results of two studies funded by Project A.L.S. and appearing in today's advance online publication of Nature Neuroscience demonstrate that embryonic stem cells may provide a new tool for studying disease mechanisms and for identifying drugs to slow ALS, also known as Lou Gehrig's disease.

Both studies were completed by researchers participating in an ongoing collaboration with the Project A.L.S./Jenifer Estess Laboratory for Stem Cell Research, the world's first and only privately funded laboratory focused exclusively on stem cells and ALS.

Grandparents of adopted grandchildren relate to them as an integral part of the family – just as they relate to their biological grandchildren. This was revealed in research conducted at the University of Haifa School of Social Work. This research is unique in the field in that it evaluated adoptive relationships from the viewpoint of grandparents; previous research examined relationships from the viewpoint of parents and children.

A study by U.S. and Australian researchers is helping dispel the 40-year-old "thrifty genotype theory," which purports that certain minority groups are genetically prone to diabetes.

The study, co-authored by UC Irvine anthropologist Michael Montoya, along with an epidemiologist and population geneticist, analyzed existing genetic studies published across a variety of disciplines. The team found no evidence to support the widely held thrifty genotype theory, which suggests that cycles of feast and famine early in human history created a gene that helps the body use scarce nutrients – a gene that leads to obesity and diabetes in comfortable, sedentary modern lifestyles.

Researchers have discovered how a defect in a single master gene disrupts the process by which several genes interact to create myelin, a fatty coating that covers nerve cells and increases the speed and reliability of their electrical signals.

The discovery has implications for understanding disorders of myelin production. These disorders can affect the peripheral nervous system—the nerves outside the brain and spine. These disorders are known collectively as peripheral neuropathies. Peripheral neuropathies can result in numbness, weakness, pain, and impaired movement. They include one of the most common genetically inherited disorders, Charcot-Marie-Tooth disease, which causes progressive muscle weakening.

Ancient aquatic amphibians developed the ability to feed on land before completing the transition to terrestrial life, researchers from Harvard University report this week in the Proceedings of the National Academy of Sciences.

Their work is based on analysis of the skulls of the first amphibians, which arose 375 million years ago, and their fish ancestors. The shapes of the junctions between adjacent skull bones -- termed "sutures" -- in the tops of these fish and amphibian skulls reveal how these extinct animals captured prey, say authors Molly J. Markey and Charles R. Marshall.