Four-year-old conjoined twins, sharing a linked thalamus:

Adding to the conundrum, of course, are their linked brains, and the mysterious hints of what passes between them. The family regularly sees evidence of it. The way their heads are joined, they have markedly different fields of view. One child will look at a toy or a cup. The other can reach across and grab it, even though her own eyes couldn’t possibly see its location. “They share thoughts, too,” says Louise. “Nobody will be saying anything,” adds Simms, “and Tati will just pipe up and say, ‘Stop that!’ And she’ll smack her sister.” While their verbal development is delayed, it continues to get better. Their sentences are two or three words at most so far, and their enunciation is at first difficult to understand. Both the family, and researchers, anxiously await the children’s explanation for what they are experiencing. (#)

Schizophrenia & MS: endogenous retroviruses?

Through this research, a rough account is emerging of how HERV-W could trigger diseases like schizophrenia, bipolar disorder, and MS. Although the body works hard to keep its ERVs under tight control, infections around the time of birth destabilize this tense standoff. Scribbled onto the marker board in Yolken’s office is a list of infections that are now known to awaken HERV-W—including herpes, toxoplasma, cytomegalovirus, and a dozen others. The HERV-W viruses that pour into the newborn’s blood and brain fluid during these infections contain proteins that may enrage the infant immune system. White blood cells vomit forth inflammatory molecules called cytokines, attracting more immune cells like riot police to a prison break. The scene turns toxic.

In one experiment, Perron isolated HERV-W virus from people with MS and injected it into mice. The mice became clumsy, then paralyzed, then died of brain hemorrhages. But if Perron depleted the mice of immune cells known as T cells, the animals survived their encounter with HERV-W. It was an extreme experiment, but to Perron it made an important point. Whether people develop MS or schizophrenia may depend on how their immune system responds to HERV-W, he says. In MS the immune system directly attacks and kills brain cells, causing paralysis. In schizophrenia it may be that inflammation damages neurons indirectly by overstimulating them. “The neuron is discharging neurotransmitters, being excited by these inflammatory signals,” Perron says. “This is when you develop hallucinations, delusions, paranoia, and hyper-suicidal tendencies.”

The first, pivotal infection by toxoplasmosis or influenza (and subsequent flaring up of HERV-W) might happen shortly before or after birth. That would explain the birth-month effect: Flu infections happen more often in winter. The initial infection could then set off a lifelong pattern in which later infections reawaken HERV-W, causing more inflammation and eventually symptoms. This process explains why schizophrenics gradually lose brain tissue. It explains why the disease waxes and wanes like a chronic infection. And it could explain why some schizophrenics suffer their first psychosis after a mysterious, monolike illness.

The infection theory could also explain what little we know of the genetics of schizophrenia. One might expect that the disease would be associated with genes controlling our synapses or neurotransmitters. Three major studiespublished last year in the journal Nature tell a different story. They instead implicate immune genes called human leukocyte antigens (HLAs), which are central to our body’s ability to detect invading pathogens. “That makes a lot of sense,” Yolken says. “The response to an infectious agent may be why person A gets schizophrenia and person B doesn’t.” (#)