It’s happened to all of us at one time or another: You’re walking through a crowd, and suddenly a face seems incredibly familiar — so much so that you do a double-take. Who is that? How do you know them? You have no idea, but something about their face nags at you. You know you’ve seen it before.

The reason you know that face is in part because of your perirhinal cortex. This is an area of the brain that helps us to determine familiarity, or whether we have seen an object before. A new study of brain cells in this area finds that firing these neurons at one frequency makes the brain treat novel images as old hat. But firing these same neurons at another frequency can make the old new again.

“Novelty and familiarity are both really important,” says study coauthor Rebecca Burwell, a neuroscientist at Brown University in Providence, R.I. “They are important for learning and memory and decision making.” Finding a cache of food and knowing it is new could be useful for an animal’s future. So is recognizing a familiar place where the pickings were good in the past.

But knowing that something is familiar is not quite the same thing as knowing what that thing is. “You’re in a crowd and you see a familiar face, and there’s a feeling,” Burwell explains. “You can’t identify them, you don’t know where you met them, but there’s a sense of familiarity.” It’s different from recalling where you met the person, or even who the person is. This is a sense at the base of memory. And while scientists knew the perirhinal cortex was involved in this sense of familiarity, how that feeling of new or old was coded in the brain wasn’t fully understood.

When exposed to something new, groups of brain cells in the perirhinal cortex fire quickly, at a rate of about 30 pulses per second, or hertz. As the object gets familiar, this oscillation — or pattern of firing from a group of brain cells — decreases, to around 11 Hz. To investigate just how this change affects an animal’s sense of novelty, Burwell and her colleagues infected brain cells in rats’ perirhinal cortex with a virus containing a light-activated channel. When the cells were exposed to blue light, they would fire. The frequency of the blue light stimulation determined how quickly the brain cells fired.

Then, the researchers took advantage of rats’ natural tendency to look longer at novel objects, and showed them images of, say, cloverleaves, swans or bunnies. In the presence of a familiar bunny, the rats spent less time looking at the picture. After all, they had seen that animal before.

But when the scientists stimulated the rats’ brains at 30 Hz, the rats looked longer at the bunny, as if seeing it for the first time. Conversely, when presented with a new image, such as a cloverleaf, the rats stared at it for longer than they gazed at a familiar swan shape. But when their perirhinal cortex was stimulated at 11 Hz, the rats didn’t find cloverleaves so fascinating. The new object had suddenly become familiar, Burwell and her colleagues report September 30 in the Journal of Neuroscience.

The results suggest that novelty and familiarity are two sides of the same brain cells. Turn them down, and even the new is boring and old. Turn them up and the old is new again. Many other studies have associated these oscillations with specific kinds of recognition memory, says Howard Eichenbaum, a neuroscientist at Boston University. But this study goes beyond association, he notes, and actually gets at a cause, showing that specific frequencies cause rats to treat an object as new or old.

“It’s a very neat paper,” says John Aggleton, a neuroscientist at Cardiff University in Wales. “And there’s a parallel to what’s going on in humans. We know in fMRI, if you repeat [images] you get decreased activity in the perirhinal cortex, and we know in animals if you look at expression of genes you get a decrease in activity. All of these come together in a very neat way.” He says this study indicates the signals of activity are “not a by-product, but a key component” of how we process the old and the new.

So the next time you see a face in the crowd, and you know that person is familiar, thank the brain cells in your perirhinal cortex. But when you can’t remember their name or how know you them? Well, I’m afraid the rest of your brain is to blame.

BALTIMORE — Molecular tests may be able to distinguish homosexual from heterosexual men, a small study of twins suggests.

Chemical modifications to DNA that change the activity of genes without changing the genes’ information differ between homosexual and heterosexual men, researchers from UCLA David Geffen School of Medicine have discovered. Results of the unpublished study on the link between these modifications, called epigenetic tags, and sexual orientation were presented October 8 at the annual meeting of the American Society of Human Genetics. Comparing one type of epigenetic tag known as DNA methylation in pairs of twins in which one brother is gay and the other straight revealed patterns that distinguish one group from the other about 67 percent of the time, computational geneticist Tuck Ngun and colleagues say.

The work already has provoked controversy, with some scientists questioning its methodology and others worried about how the research could be used. Some are concerned that the research could be misinterpreted as one step in an effort to “cure” homosexuality. Nothing could be further from the researchers’ intentions, say Ngun and Eric Vilain, the geneticist who heads the research group. “None of us see homosexuality as a disorder or something to be fixed,” Ngun said. “We’re just interested in what makes us tick.”

Very little is known about how human sexual preferences of any type arise, Vilain adds. That’s especially true on a biological level. “Our research is not about homosexuality,” he says. “It’s about understanding sexual attraction, the biology of desire.”

Previous studies have found tentative genetic links to male sexual orientation, but no one has identified a “gay gene” or genes. Still, the development of sexuality seems to have origins early in life, maybe even stemming from cues in the womb. For instance, for each biological older brother a man has, his likelihood of being homosexual rises by 33 percent. That finding has been replicated in several studies and could indicate that some condition in the womb sets epigenetic marks, which later influence preference of sexual partners.

Epigenetic marks have been shown to influence behaviors in rodents such as maternal care and drug addiction (SN: 5/24/08, p. 14). Whether and how these marks are involved in human behavior is still a matter of intense debate, says Peng Jin, a human geneticist at Emory University in Atlanta. Exploring whether they are associated with sexual preference isn’t unreasonable, Jin says, he’s just not sure the researchers have gone about it correctly. He also doubts that a study of less than 100 men has the statistical power to predict sexual orientation.

Ngun and colleagues measured DNA methylation levels in the saliva of 37 pairs of identical twins in which one twin self-identified as homosexual and the other as heterosexual. Another 10 pairs of twins in which both were gay also participated in the study. A computer program dubbed the FuzzyForest algorithm examined data from half of the gay and straight twins to learn how their DNA methylation patterns differed from each other. The initial round of training found 6,134 spots in the genome where the twins differed, but together those sites could correctly identify gay twins in the remaining pairs only 44 percent of the time. Narrowing down the number of sites to nine improved accuracy to 64 percent.

Further analysis involved the set of 10 pairs of gay twins. The researchers asked the computer program to pick out the spots that were different in the mixed orientation twins, but the same in the gay twins. That left five sites that could correctly identify 67 percent of gay twins in the test group.

Some of the regions may be involved in controlling activity of two genes: CIITA, which regulates activity of some immune system genes, and KIF1A, a gene involved in the transport of communication molecules in the brain.

The study raises many issues. Scientists question whether the finding will hold up in larger groups of unrelated people. Also, the computer algorithm hasn’t been tested on other datasets, raising concerns about whether the method is valid.  

Vilain agrees that the study has limitations. “We’re looking at the wrong tissue at the wrong time,” he laments. The right tissue would be the brain, and ideally, researchers would be able to track DNA methylation changes over time from fetal stages on. Such research is not ethical in humans, so the team measured DNA methylation patterns in saliva taken from adult men, long after their sexual orientation had been determined. “There were no other choices,” he says.

DNA methylation patterns in saliva may not accurately reflect what is going on in the brain where behavior is controlled, Jin says. Saliva is not good material for epigenetic studies, he adds. The types of cells present in saliva can change dramatically depending on when and what a person has eaten and other factors. Different mixes of cells in the saliva would probably have different DNA methylation patterns that could further confuse the results. Blood would have been a more stable material to examine, although it also doesn’t always match what happens in the brain.

Vilain says his work has “zero clinical application.” This is not molecular gaydar, it’s simply a statistical measure that epigenetic marks differ between men of opposite sexual orientations, he says.

Whether the epigenetic changes are a determining factor in sexual orientation or a result of differing experiences in life, the study can’t determine, he says. But it may offer invaluable insight to the development of human sexuality, says pharmacologist Margaret McCarthy of the University of Maryland in College Park. "This study provides a major step forward in our understanding of how the brain can be affected by factors outside of the genome,” she said in a statement to the Genetic Expert News Service. “Regardless of when, or even how, these epigenetic changes occur, their findings demonstrates a biological basis to partner preference.”

Elephants’ genetic instruction books include a hefty chapter on fighting cancer.

The massive mammals have about 20 copies of TP53, a gene that codes for a potent tumor-blocking protein, researchers analyzing elephant DNA report October 8 in JAMA. Humans have just one copy of TP53.

An extra dose (or 19) of the anticancer gene may explain why elephants have unusually low cancer rates, say Joshua Schiffman, a pediatric oncologist at the University of Utah in Salt Lake City, and colleagues.

Schiffman’s team pored over 14 years of animal autopsy data from the San Diego Zoo, and a separate database that included detailed info on 644 elephant deaths. Based on those data, the team calculated that just 4.8 percent of elephants die of cancer. For humans, that number is anywhere from 11 to 25 percent.

Elephants’ extra genes could help keep defective cells from morphing into tumors, the researchers suggest.

A Liberian woman contracted Ebola in March by having sex with a survivor of the viral disease, researchers report. Using studies of both people’s viral genomes and of the people’s contacts with any other possible sources of the virus, the researchers conclude that the woman’s disease represents the first known case of sexual transmission of Ebola.

People ordinarily catch the often-deadly virus through direct contact with blood or other body fluids.

In this case, the two people had unprotected sex six months after the man got Ebola, and 155 days after his second blood test showed him to be clear of the virus. The genomes of the Ebola virus from the man’s semen and woman’s blood were not only practically identical but also different from all other Western African Ebola viruses that had been sequenced, researchers report October 14 in the New England Journal of Medicine.

Also appearing in the journal is a preliminary report that genetic material from Ebola viruses can persist in semen nine months after infection.

Both findings suggest that Ebola remains in certain parts of the body long after the blood is clear of the virus. However, in an opinion piece that accompanies the two research reports, Armand Sprecher of Doctors Without Borders in Brussels notes that more than 17,000 people survived the West African Ebola outbreak. “If sexual transmission from survivors were an important means of disease propagation, we would have seen a number of cases by now,” he writes.