Brain-derived neurotropic factor/TrkB signaling in the pathogenesis and novel pharmacotherapy of schizophrenia.
The role of neurotropins, predominantly brain-derived neurotropic factor (BDNF), has been implicated in the pathophysiology as well as treatment outcome of schizophrenia. Both human and rodent studies indicate that the beneficial effects of antipsychotic drugs are mediated, at least in part, through BDNF and its receptor, TrkB. This review will discuss the available data on the levels of BDNF and TrkB in subjects with schizophrenia and in animals with and without conventional antipsychotics. The data concerning the impact of the antipsychotic drugs on BDNF/TrkB signaling will also be discussed. More importantly, this review will provide future perspective on BDNF/TrkB signaling as a novel molecular target to correct the pathogenesis and improve the long-term clinical outcome by treatments with conventional and adjunctive drugs.
Pillai
Anilkumar
A
Department of Psychiatry and Health Behavior, Medical College of Georgia, Medical Research Service Line, Veterans Affairs Medical Center, Augusta, GA 30904, USA. apillai@mail.mcg.edu
D000818:Animals; D014150:Antipsychotic Agents / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*; D019208:Brain-Derived Neurotrophic Factor / Q000502:physiology*; D006801:Humans; D020813:Receptor, trkB / Q000502:physiology*; D012559:Schizophrenia / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*
D014150:Antipsychotic Agents; D019208:Brain-Derived Neurotrophic Factor; D020813:Receptor, trkB