This approach presumes that what we now call “depression” or “sch

This approach presumes that what we now call “depression” or “schizophrenia” are, in fact, many different disorders with distinct underlying biological causes that require different treatments. While this approach is not ready for clinical use,

Y-27632 datasheet it demonstrates the extent to which mental disorders are now addressed as brain disorders, or, more specifically, as brain circuit disorders. Across brain disorders, whether primarily neurologic or psychiatric, there is an increasing recognition that behavioral symptoms are late manifestations of disease. This insight for Alzheimer’s, Parkinson’s, schizophrenia, and autism represents a fundamental shift in emphasis, similar to the shift in the treatment of atherosclerosis and hypertension before they cause ischemic heart disease or stroke. This preemptive approach focuses on early detection of brain changes and the development of early interventions that can prevent or forestall neurodegenerative or neurodevelopmental disorders.

What about new treatments? Basic science has yielded several new molecular targets that have become the basis of new therapies. For neurological disorders, the past two decades have brought breakthroughs in the treatment of migraine (triptans; Lipton, 2011), multiple sclerosis (beta interferon, copolymer, fingolimide, and difumarate; Stankiewicz et al., 2013), acute stroke (tissue plasminogen activator), and a number of new agents for epilepsy, including rapamycin for epilepsy in tuberous sclerosis (Krueger et al., 2013). For mental disorders, we have seen the development of second-generation antipsychotics and antidepressants, with different side effect profiles but little improvement in efficacy over the medications of 1988. There have been few

novel targets in this space, in part because of the limited understanding of the pathophysiology of neurodevelopmental disorders, relative to the progress on neurodegenerative Urease diseases (Hyman, 2012). One hopeful discovery is the relatively recent insight that antidepressant effects can be achieved within hours rather than weeks (Martinowich et al., 2013). The observation that ketamine resolves even treatment-refractory depression in less than 24 hr has changed our expectations for the development of new antidepressants. Basic science has also yielded insights about circuitry that have been translated into new, effective therapies. Modulation of circuits through deep brain stimulation (DBS) has proven to be effective for movement disorders including Parkinson’s disease, essential tremor, and dystonia (Miocinovic et al., 2013). Development of DBS surgery for Parkinson’s disease resulted from decades of basic science studies of basal ganglia circuitry in nonhuman primates (DeLong and Wichmann, 2007). More recently, DBS in the subcallosal cingulate region, identified as metabolically hyperactive in patients with severe drug-resistant depression, showed dramatic antidepressant effects (Holtzheimer et al.

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