PMC:3649690 / 32354-34408 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/3649690","sourcedb":"PMC","sourceid":"3649690","source_url":"http://www.ncbi.nlm.nih.gov/pmc/3649690","text":"14. Conclusion\nDepression is a complex neuropsychiatric disease with a poorly defined etiology. While hosts of antidepressant drugs do exist, they are often inefficacious. Elucidating the neural underpinnings of depression and fully understanding the pleiotropic effects of current antidepressant compounds, beyond their role in modulating monoaminergic neurotransmission, are necessary for the development of more effective drugs. The potential role of neurogenesis, both its decline with the occurrence of depression and its enhancement by chronic treatment with antidepressant drugs and therapies, has provided a promising avenue for research. Though significant findings have been made relating neurogenesis to the effective treatment of depression, large gaps in our understanding still exist. To this end, the role of synaptic proteins and cell adhesion molecules, including PSA-NCAM, in the etiology and treatment of depression should also be investigated. As with neurogenesis, PSA-NCAM is reduced in depressed patients and in models of depression, while chronic antidepressant treatment increases expression of PSA-NCAM. Importantly however, PSA-NCAM mediates multiple facets of neural plasticity, including neurogenesis and synaptic plasticity, in addition to mediating effects of neurotrophic factors, such as BDNF. PSA-NCAM therefore functions at the confluence of many forms of neural plasticity, and its mechanisms bridge several theories of depression: monoamine, neurogenic, and neurotrophic. This review has focused on the potential roles of neurogenesis and PSA-NCAM in depression; however many other proteins are associated with neural plasticity and depression [29, 182, 183]. Given the limitations in the understanding of the genesis of depression and current antidepressant treatments, continued research into the exact contribution of adult neurogenesis and the potential roles of proteins associated with neural plasticity and the continued perusal of a broader, neural plasticity hypothesis of depression are certainly 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