The Neurobiology of Depression and Anxiety: How Do We Change from Models of Drug Efficacy to Understanding Mood and Anxiety Disorders?
Current treatments for depression and anxiety disorders are only effective in approximately half of the patient population. Effective treatments have negative side-effects including sexual dysfunction, weight gain and gastrointestinal problems. Furthermore, even when patients achieve remission, they often need to increase dosage or change treatment across their lifetime as efficacy weakens. The majority of treatments being used today are based on the monoamine hypothesis of depression, a theory of depression that was based on the effectiveness of drugs discovered by chance to alleviate the symptoms of depression. This chapter provides an overview of the neurobiology of depression and anxiety disorders within the context of drug discovery. The chapter starts with what we currently know about these disorders through the lens of the monoamine hypothesis of depression. We then provide a background into the animal models of depression and anxiety that are being used to understand the underlying biology of these disorders and test new treatments. Work conducted using these animal models has directed human imagining and has provided us with new information about both the molecular and cellular mechanism of depression and anxiety as well as the neural circuitry controlling these disorders. Finally, we will conclude with a discussion of new treatments being developed based on empirical evidence about the neurobiology of depression and anxiety and the need to develop more personalized treatments in the future. It is hoped that these new drugs will be able to provide effective treatment for more people, with fewer negative side-effects.