Cancer treatment has been transformed, at its root, by a transformational change in how it is classified. Those successes have not escaped the notice of researchers in other areas of biomedicine, and diseases including heart failure, asthma and polycystic ovarian syndrome are being looked at with an eye to subdividing them in ways that brings diagnostics into the molecular era.
Cancer treatment has been transformed, at its root, by a transformational change in how it is classified. These days, which organ a tumor arises in is often less important than its molecular drivers, which can be sensitive either to specific targeted treatments, or increase the chance that a tumor will respond to immunotherapy. Those successes have not escaped the notice of researchers in other areas of biomedicine, and diseases including heart failure, asthma and polycystic ovarian syndrome are being looked at with an eye to subdividing them in ways that brings diagnostics into the molecular era. Nowhere do those changes have greater potential than in disorders of the brain – in part because there is nowhere much to go but up as far as classifying neurological diseases goes.
Zynerba Pharmaceuticals Inc. in late May popped the lid off top-line data from the open-label phase II study called Bright with ZYN-002 in children and adolescents with autism spectrum disorder, and the findings drew adjectives from Wall Street such as “provocative” and “encouraging.”
Digital therapeutics have had a tough time gaining traction in the last few years. They’ve been hampered by sometimes reluctant payers, providers and regulators who lack familiarity with the approach, which typically employs an app or other technology to treat a patient by supporting behavioral adjustments.
Lowering levels of tau protein improved multiple symptoms of autism spectrum disorders (ASD) in two different mouse models of the disease, both of which are driven by hyperactivity of the mTOR PI3 kinase pathway.
Lowering levels of tau protein improved multiple symptoms of autism spectrum disorders (ASD) in two different mouse models of the disease, both of which are driven by hyperactivity of the mTOR PI3 kinase pathway.