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        gravitational waves generated during inflation. The researchers believe the signal they detected was cosmic in origin and did not come from

        Schizophrenia, which affects 1 in 100 people
        worldwide and an estimated 2.4 million
        Americans, exacts tremendous social costs and
        great human suffering. Drugs can calm the inner voices,
        delusions and hallucinations, but few patients recover
        fully, and there is no cure. Nor are there predictive
        tests or internal markers for the disease — it must be
        diagnosed by outward signs alone.
        But this problem is at last yielding
        to progress on the genetic front.
        In July, an international
        consortium of schizophrenia
        researchers, mounting what
        it calls the largest biological
        experiment in the history of
        psychiatry, reported 108 regions
        in the genome associated with
        schizophrenia. Two dozen of
        these genetic links had been
        recorded before, but more than
        80 were new. Neuroscientists
        now have many more avenues
        for exploring the biological
        underpinnings of the disorder.
        Originally thought to stem from
        bad parenting, schizophrenia tends to cluster in families,
        implicating DNA. The risk of the disease rises the closer
        one is related to a patient. Until recently, gene scans were
        unsuccessful in turning up links to schizophrenia.
        “When we started, we got a lot of things wrong,”
        says Patrick Sullivan, a geneticist and psychiatrist at
        the University of North Carolina. “We had no clear
        fix on the problem. What was the best study design?
        How many samples did we need? Also, in the ’80s,
        genotyping [reading DNA’s sequence of letters] was
        really expensive. Every time a new technology came
        along, we gave it a shot, but schizophrenia was way
        more complicated than we thought.”
        Sullivan is principal investigator for the
        Psychiatric Genomics Consortium, which includes
        “nearly everyone in the world who’s working on
        schizophrenia,” he says. The consortium’s broadscale
        analyses included 35 research groups that have
        integrated genetic samples from a total of 150,000
        subjects — 37,000 of whom have schizophrenia and
        113,000 healthy controls. The unprecedentedly large
        sample allows a glimpse of the genetic basis of the
        disease that smaller, earlier studies didn’t have the
        statistical power to see. The specific method employed
        was a genome-wide association study, or GWAS.
        Because DNA’s code varies slightly from person to
        person, GWAS seeks to identify the places where a
        schizophrenic’s genome differs from a healthy person or
        from another schizophrenic. The genotyping technology
        can distinguish a million possible
        sequences across each sample, the
        goal being to show the variants that
        are more prevalent in the patients
        than in healthy subjects.
        The good news from the study was
        that many of the variants associated
        with the disorder made biological
        sense. Some, for example, pointed to
        genes that expressed themselves in
        brain cells, or that involved immune
        function, a previously established
        connection. Another important
        hit was at DRD2, the gene for the
        dopamine receptor, which is targeted
        by antipsychotic drugs. The bad
        news — which really wasn’t news
        to the investigators — was that the
        variants were fairly common in the population, but their
        effect was weak. They weren’t blockbuster genes like
        those for cystic fibrosis or Huntington’s disease, single
        flaws making for straightforward predictions. The risk
        of schizophrenia to someone who carries one of these
        markers is increased by as little as one-tenth of a percent.
        Thomas Insel, director of the National Institute of
        Mental Health, describes schizophrenia as polygenic,
        meaning that genes probably act in networks to produce
        it. “The genome works like a symphony, not like a
        soloist,” he says. “If you line up these [variants] and
        determine the likely function of the genes, do they tell the
        same story?” The next task will be to engineer neurons
        in cell cultures so that they manifest one or more of the
        variants. “Does this alter any aspect of how neurons
        develop or how they fire?” Insel wants to know.
        “The goal of this work is to understand the
        neurobiology,” Sullivan stresses. “So the molecular
        basis is polygenic. Are we going to sit back and
        cry because schizophrenia didn’t turn out like we
        hoped it would? It’s complicated. That’s the scientific
        challenge.” 

        2017-11-25 2:06 PM Comentarii 0 Vizitator Schizophrenia Study Finds New Genet

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