Dietary Salt Linked to Autoimmune Diseases
Salt in food may increase the risk of autoimmune diseases, according to provocative results reported this week in Nature. Immunobiologist David Hafler of the Yale School of Medicine and colleagues determined that a pinch of salt triggered cultures of unspecialized T cells to produce large numbers of destructive TH17 cells, which have been implicated in diseases such as psoriasis, rheumatoid arthritis, and multiple sclerosis. They also showed that a salt-rich diet makes mice more susceptible to experimental autoimmune encephalomyelitis (EAE), a rodent illness similar to multiple sclerosis.
A salt connection also crystallized when computational biologist Aviv Regev of the Broad Institute in Cambridge, immunologist Vijay Kuchroo of Harvard Medical School in Boston, and colleagues pieced together the molecular circuit that controls specialization of TH17 cells. An influential gene was SGK1, which helps cells manage sodium levels. And mice on high-salt rations developed a milder form of EAE if they lacked SGK1. The work doesn't establish that salt drives human autoimmune diseases, but "the stage is set to do precise experiments to test the hypothesis," Kuchroo says.
Tweet, Shriek: On the Origin of Language
The complex amalgam that is human language had humble beginnings: An analysis of bird songs and monkey calls suggests that it may have evolved from a combination of simpler systems.
Our language has two layers: the words we use (the lexical structure) and how we organize those words (the expression structure). We're the only animal to combine the two, but some animals do use one or the other. Vervet monkeys use different alarm calls for different predators—a lexical structure with no grammar. And although nightingales can sing up to 200 different melodies, the individual notes have no meaning—an expression structure with no words.
Similar preexisting systems could have combined to form human language, researchers posited online last month in Frontiers in Psychology. "Evolution can work in different ways, and one way would be that existing mechanisms are combined into something new," says Johan Bolhuis, a biologist at Utrecht University in the Netherlands who was not involved with the study. Still, he cautions, "we simply don't know enough about the evolution of all these systems to know if that is really the case." http://scim.ag/langevol
Shared Genetics Could Drive Psychiatric Disorders
Finding genes behind psychiatric disorders has been a struggle, but a massive new study of about 60,000 cases and controls offers additional clues. The study took an unusual tack, lumping together five conditions generally considered to be distinct. Lo and behold, it found a handful of gene variants shared by all of the disorders. Reporting last week in The Lancet, the researchers, part of a collaboration called the Psychiatric Genomics Consortium, describe three variants that correlate with autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia. A fourth gene variant surfaced more often in people with either bipolar disorder or schizophrenia than in controls. Two variants are linked to calcium channels, which help cells communicate.
The Lancet report is the largest yet to dig for genes underlying these conditions. As is common in so-called genome-wide association studies, the variants raise risk only slightly, by about 10%. But some researchers say that identifying them adds to growing evidence that psychiatric conditions, even those that present very differently in patients, might share common molecular causes that could help better define and treat them.