another psychotic break.) Their once-a-day dose failed, too. “I think the company’s pharmacologists were smart enough to know all this,” Freedman said, “but their marketing people rule how they make drugs. And so, they sort of were doomed to failure.”
Freedman saw the experience as an object lesson in how pharmaceutical companies work. “It was disappointing, because I think they could have gotten a good drug out of what they were doing.” After all that promise, he was back where he started. To jump-start the α7 receptor and strengthen the brain’s ability to process information, Freedman would have to find another way.
CHAPTER 33
2000
State University of New York at Stony Brook
It had been a decade since Lynn DeLisi first met the Galvin family, and she was still steadfastly collecting families, still acquiring DNA, in hopes of finding a genetic abnormality that helped explain schizophrenia. She wasn’t having much luck, and neither was anyone else. In 1994, The New England Journal of Medicine published a survey of schizophrenia research that concluded that very little had been learned about schizophrenia and no headway had been made in its treatment. All the doctors could do, it seemed, was what they’d been doing for years: prescribe medication and hope for the best. This, for a disease that the editor of Nature had a few years earlier called “arguably the worst disease affecting mankind, even AIDS not excepted.’’
In 1995, however, DeLisi’s work attracted the attention of a well-funded investor: Sequana Therapeutics, a privately held pharmaceutical company that would eventually partner with Parke-Davis to develop schizophrenia drugs. Sequana’s director of genetics, Jay Lichter, was clear about what DeLisi had to offer: “Dr. DeLisi and her collaborators have assembled one of the largest collections of families whose members include one or more sibling pairs with schizophrenia,” he said. Sequana thought DeLisi had an inside track on finding a genetic link to the illness—the advance everyone was waiting for. In return, the company offered DeLisi access to the most sophisticated genetic-analysis equipment available—technology “beyond the practical capabilities of a small laboratory,” she said. “As a result, we expect to move much more quickly.”
With DeLisi in charge, the company funded the largest single-investigator multiplex family study to date, studying the linkages of about 350 different markers spread throughout the genome. The Galvin family’s DNA was part of that study. DeLisi seemed poised for a breakthrough. But within a few years, she, like Robert Freedman, learned the hard way about the vagaries of the marketplace. In 2000, Parke-Davis was bought by Pfizer. Almost right away, DeLisi learned that Pfizer was canceling DeLisi’s project. All work would stop immediately. And all the genetic material she had accumulated at Parke-Davis, including the Galvin family’s DNA, would remain the property of Pfizer—unavailable for DeLisi to use, unless she found another company willing to fund the project.
Why was Pfizer not interested in DeLisi’s family research? She had been making slow progress, that was true. But in research, you only have to go fast if someone else is outrunning you.
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THE HUMAN GENOME Project was a highly publicized effort to map out and understand the structure, organization, and function of every single human gene—the entire DNA blueprint for building a human. The project started in the 1980s at the U.S. Department of Energy, which engaged in a sort of friendly competition with NIH to raise money for the effort. In 1990, the project launched in earnest with an estimated $3 billion in funding. This was like a moon shot for biology. If the project could successfully diagram the human genome, nothing about the study of virtually any genetic disease would be the same—even complex diseases like schizophrenia.
Before the Human Genome Project, Lynn DeLisi and others had been working with the understanding that if you wanted to go looking for the genetic mutations for schizophrenia, the easiest place to find them was in families like the Galvins. That their linkage studies had proved to be unfruitful so far, they thought, was evidence of how complicated the illness was. The alternative—searching for schizophrenia mutations by studying the genetic code of the general population—had seemed ludicrous. All that changed, however, with the Human Genome Project.
Human beings have more than twenty thousand genes that, by