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In the Waiting Room

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In the Waiting Room OUTLOOK AUTISM have become good at stealing drugs developed for other disorders,” jokes Hardan. But even second-hand drugs are better than nothing, given how disruptive these behaviours can be. STRIKING A BALANCE ‘Irritability’ may sound like a minor failing, but the behaviours it encompasses — mood UNC ASPIRE RESEARCH PROGRAM UNC ASPIRE RESEARCH swings, aggression and self-harming — can be debilitating and dangerous to people with autism and their caregivers. That’s why irritability is a primary target for pharma- ceuticals in ASDs. Two antipsychotic drugs, aripiprazole (marketed as Abilify by Otsuka Pharmaceuticals) and risperidone are now in widespread use in people with ASDs. “These drugs are effective in 60–70% of children and adolescents that have significant irrit- ability,” says Christopher J. McDougle, direc- tor of the Lurie Center for Autism at Massa- chusetts General Hospital in Boston. Both drugs, however, come with side effects. Jer- emy Veenstra-VanderWeele, a child psychia- trist and researcher at Vanderbilt University Medical Center in Nashville, Tennessee, has determined that aripiprazole and risperidone frequently induce drowsiness and weight gain, and he cautions against prescribing these drugs unless symptoms are severe. “When you’re using a medicine in a seven-year-old A seven-year-old boy with autism is given oxytocin nasally to see if it alters his sociability. child that increases their body weight by 10% over the course of a couple of months, that TREATMENTS potentially changes the way their metabolism is going to work down the line,” he says, not- ing the chance for increased risk of metabolic syndrome or cardiovascular disease. In the waiting Many clinicians prescribe anti-depressants from the selective-serotonin reuptake inhibi- tor (SSRI) family, such as fluoxetine (Pro- zac) and citalopram, to treat ASD patients, room despite scant evidence supporting their use. Randomized controlled trials have shown that SSRIs may reduce compulsive, After years of making do with drugs developed for other repetitive behaviour in adults with autism, but conditions, doctors and scientists are eagerly pursuing have no observed effect on these symptoms in children and adolescents. But these trials drugs that target the social symptoms of autism. did not examine social anxiety, a symptom for which some doctors have observed improve- ments in children with SSRIs. McDougle, who BY MICHAEL EISENSTEIN That desperation is borne of the limited pioneered the study of SSRIs for ASDs while success achieved in developing drugs to treat working at Yale University School of Medicine hy would any parent feed their child autism. “When I give a lecture on medication, in the 1990s, believes factors related to age- worm eggs? In Stewart Johnson’s I usually start by saying that I won’t be talking associated brain development may also limit case, it was because he believed he about the state of pharmacology in autism, but their use. “One reason some children didn’t Whad stumbled across a promising treatment about the miserable state of pharmacology in get better was that they couldn’t tolerate even for the symptoms of his teenage son’s autism autism,” says Antonio Hardan, a child psychia- low starting doses,” he says. “They became after limited success with other treatments. trist at Stanford University School of Medicine much more irritable, agitated and aggressive.” Although he is not a professional scientist, in California. In fact, no drugs are approved by Since the value of both SSRIs and anti- his bold experiment with porcine whipworm the US Food and Drug Administration (FDA) psychotics is based largely on the extent to (Trichuris suis) ova has culminated in a formal for autism per se, although a handful of medi- which they enable children with autism to par- clinical trial spearheaded by a leading autism cations approved for ticipate in school, caregivers must weigh the research centre. However, Johnson’s story also “Talking about other psychiatric indi- potential medical benefits and adverse effects tells of the desperation felt by many parents immune stuff cations have proven carefully. “If we’re putting kids to sleep, even to find something — anything — that might was considered useful in mitigating if their aggression is down, we haven’t actu- improve the lives of children with autism spec- fringe and some of the symp- ally facilitated their psycho-educational inter- trum disorders (ASDs). funky.” toms of ASDs. “We vention,” says Evdokia Anagnostou, a child S14 | NATURE | VOL 491 | 1 NOVEMBER 2012 AUTISM OUTLOOK ACTIVATING THE AUTISTIC BRAIN Functional MRI images from a small, preliminary study (7 participants) show that the administration of oxytocin could potentially change brain patterns in a way that would reduce the symptoms of autism. Insula Precuneus (self-awareness and Temporal parietal junction Medial prefrontal cortex OXYTOCIN (memory and perception of social cues) (attention, self-perception (decision-making and consciousness) and theory of mind) social judgment) ILANIT GORDON, YALE CHILD STUDY CENTER CHILD STUDY ILANIT GORDON, YALE Cingulate cortex (cognitive and R R emotional behavior) Superior temporal sulci Inferior temporal sulci (responds to voice and PLACEBO gaze of others) R R neurologist at the Bloorview Research Institute on an ambitious five-year study of 300 children FXS is caused by mutations in the gene in Toronto, Canada. and adolescents to examine whether extended encoding a protein that regulates the produc- treatment with oxytocin confers measurable tion of other proteins involved in neuron sig- THE HEART OF THE MATTER improvements in social function. nalling. Bear and colleagues discovered that No medications target the core symptoms One of the biggest obstacles confronting the protein produced by the mutated gene of autism, which include attention deficit, clinical studies of oxytocin — and, indeed, represses a glutamate receptor called mGluR5. abnormal social behaviour and poor ability to any treatment of ASD’s core symptoms — is Bear hypothesized that the neurological communicate. Accordingly, when a potential the lack of robust, reproducible measure- symptoms of FXS might arise from overactive treatment option for these symptoms is ident- ments of social deficits and improvements in mGluR5, so his group studied animal models ified, it grabs the community’s attention. For those deficits. “Social behaviour is so com- of FXS to test this theory1. “We took fragile example, extensive research in both animals plicated, and trying to measure changes in it X mice and engineered them to have 50% of and humans has identified a prominent role is really tricky,” says McDougle. This is espe- the normal level of mGluR5, with the predic- for the hormone oxytocin in behaviours asso- cially true for early-stage experimental drugs, tion that this would correct multiple aspects ciated with trust, empathy and attachment — which target neurological pathways with of the disease, and it did,” says Bear. “That was emotions commonly impaired in people with unclear contributions to ASD and in which a powerful proof of principle.” ASDs. At least half-a-dozen clinical trials are the therapeutic effects are likely to be weaker Since then, numerous drug candidates underway to test whether oxytocin affects than for approved drugs such as risperidone. have been identified that can potentially cor- these traits in people with ASDs. Furthermore, the inclusivist definition of rect mGluR5-associated deficits — Novartis, The Swiss pharmaceutical company Novartis autism as a spectrum of disorders overlooks Swiss drug giant Roche, and Seaside Thera- makes a nasal oxytocin spray, Syntocinon, and very real differences. “Autism is a heterogene- peutics, based in Cambridge, Massachusetts, this is the primary mode of delivery in devel- ous disorder, and it’s very unlikely that you’re and co-founded by Bear, all have agents in opment. Veenstra-VanderWeele cautions that going to find a compound that’s effective in clinical trials. Mouse models of FXS have the benefits remain unclear. “Kids with ASD the treatment of social deficits in all kids with proven useful in testing these candidates, are having oxytocin squirted up their noses, autism,” says Hardan. as they directly mimic the genetic and cel- and we need to know if that makes any sense,” lular-scale defects seen in FXS, even if they he says. Early studies have shown modest FRAGILE X MARKS THE SPOT do not always recapitulate the full spectrum improvements — for example, an increased Some of the most exciting progress has of behavioural and social symptoms. Most tendency to make eye contact or elevated activ- emerged from work focused on ASDs with encouragingly, a collaboration between Bear’s ity in social centres of the brain. But most of a clearly defined genetic cause. For example, team and Lothar Lindemann’s research group these investigations have looked at the impact research by Mark Bear, a neuroscientist at at Roche has discovered that mGluR5 inhibi- of single doses in small numbers of patients. the Massachusetts Institute of Technology in tors can even repair FXS-associated symp- A new round of larger-scale initiatives should Cambridge, has shown that defects in brain toms in grown mice2 — suggesting that the help clarify both the efficacy and the long- signalling mediated by the neurotransmitter window for repairing cognitive damage may term safety of oxytocin use. For example, a glutamate appear to be critical to the patho- be far wider than expected. “That’s something treatment network funded by the US National physiology of fragile X syndrome (FXS), an we wouldn’t have imagined 10 years ago,” says Institutes of Health through its Autism Cent- inherited disability in which patients often Veenstra-VanderWeele, who was not involved ers of Excellence programme is set to embark manifest autistic-like social deficits. in the study. 1 NOVEMBER 2012 | VOL 491 | NATURE | S15 OUTLOOK AUTISM Novartis has published data from a phase II as illuminate autism’s still-mysterious aeti- “One-quarter of the people in our study group trial of its mGluR5 inhibitor, AFQ056.
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