Abstract
Despite recent advances in biological psychiatric research, antidepressants based on the monoamine hypothesis are still the mainstay of treatment for depression, despite their inadequate efficacy rates, and there are still no useful biomarkers for diagnosis, leading to frequent misdiagnosis. Therefore, it is desirable to develop new treatment and diagnostic methods for depression based on a new pathological hypothesis that can replace the monoamine hypothesis. One new pathological hypothesis that is attracting attention is the neurogenesis hypothesis, which proposes that treatment increases adult hippocampal neurogenesis, which has been reduced by depression. Although this hypothesis has been established by basic research, it is still unclear whether hippocampal neurogenesis is actually decreased in depressed patients because neurogenesis cannot be detected in living humans. In this article, we first provide an overview of adult hippocampal neurogenesis, and then introduce research findings that support the neurogenesis hypothesis of depression and point out some of its problems. Finally, we discuss ways to overcome the problems with the neurogenesis hypothesis.
