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      Depression: Evolutionary New Neural Circuitries Are Still Adjusting for Cognition

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          Abstract

          Depression can be both normal and abnormal, and the balance of its expression determines the behavioral outcome/diagnosis. It is a complex pathophysiology based on a heterogeneous syndrome whose etiology is diverse as well. Within the context of a central nervous system, the nervous system blueprint can be found in single cells (sensory, motor, and integrative processes). These consolidated functions provide for novel coping strategies for survival. The maintenance and evolvement of this system into a central nervous system is based on conserving these functions, including chemical messengers and functionality in having specific cells mediate these primordial functions. Additionally, this neural coping strategy provides advantages for DNA. Thus, with different neural cells at work, pathways/networks would evolve, producing more complex behaviors and become a very critical phenomenon for future advances. This evolvement has taken over 1 billion years to develop. In so doing, as with any new programming (e.g., cognition), errors will occur. Given the widespread qualities of depression, it is surmised that this abnormality, and other psychiatric disorders, may emerge due to inherent neural weaknesses related to cognition being a recent evolutionary development.

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          The Selfish Gene

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            Is Open Access

            Neuroplasticity Underlying the Comorbidity of Pain and Depression

            Acute pain induces depressed mood, and chronic pain is known to cause depression. Depression, meanwhile, can also adversely affect pain behaviors ranging from symptomology to treatment response. Pain and depression independently induce long-term plasticity in the central nervous system (CNS). Comorbid conditions, however, have distinct patterns of neural activation. We performed a review of the changes in neural circuitry and molecular signaling pathways that may underlie this complex relationship between pain and depression. We also discussed some of the current and future therapies that are based on this understanding of the CNS plasticity that occurs with pain and depression.
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              Pathophysiology of depression: do we have any solid evidence of interest to clinicians?

              Due to the clinical and etiological heterogeneity of major depressive disorder, it has been difficult to elucidate its pathophysiology. Current neurobiological theories with the most valid empirical foundation and the highest clinical relevance are reviewed with respect to their strengths and weaknesses. The selected theories are based on studies investigating psychosocial stress and stress hormones, neurotransmitters such as serotonin, norepinephrine, dopamine, glutamate and gamma-aminobutyric acid (GABA), neurocircuitry, neurotrophic factors, and circadian rhythms. Because all theories of depression apply to only some types of depressed patients but not others, and because depressive pathophysiology may vary considerably across the course of illness, the current extant knowledge argues against a unified hypothesis of depression. As a consequence, antidepressant treatments, including psychological and biological approaches, should be tailored for individual patients and disease states. Individual depression hypotheses based on neurobiological knowledge are discussed in terms of their interest to both clinicians in daily practice and clinical researchers developing novel therapies.
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                Author and article information

                Journal
                Med Sci Monit Basic Res
                Medical Science Monitor Basic Research
                Medical Science Monitor Basic Research
                International Scientific Literature, Inc.
                2325-4394
                2325-4416
                2015
                30 September 2015
                : 21
                : 213-215
                Affiliations
                MitoGenetics, LLC, Farmingdale, NY, U.S.A.
                Author notes
                Corresponding Author: George B. Stefano, e-mail: George.Stefano@ 123456MitoGenetics.com
                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                Article
                895991
                10.12659/MSMBR.895991
                4596351
                26420361
                6bd57be8-497a-4862-b23d-4acfd3127edd
                © Med Sci Monit, 2015

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License

                History
                : 29 July 2015
                : 17 September 2015
                Categories
                Hypothesis

                depression,evolution, molecular,molecular biology,repetitive sequences, nucleic acid,serotonin

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