Neuroprogressive processes in major depressive disorder (MDD) can occur in association with recurrent episodes. The primary biological underpinnings are mediated by increases in the levels of immune-inflammation, tryptophan catabolites, mitochondrial dysfunction, and oxidative and nitrosative stress. Such biochemical alterations may be driven by changes in many peripheral and central sites, including in the gut, as well as by early developmental priming, such as prenatal stressors and breastfeeding consequences. As such, the conceptualization of MDD is shifted from simple psychological and central biochemical models to one that includes whole body processes over a developmental timescale. This provides a model that better integrates wider bodies of data relevant to the aetiology and course of MDD, and which therefore underpins the neuroprogressive processes that can occur over the course of MDD. This also significantly challenges current MDD (and wider psychiatric) classification by shifting classification to one based on biological processes rather than one based on subjective phenomenology.
Once original scientific results are published the author has the "intellectual property" and may claim ownership. Discovery credit is one of the most important "rewards" for scientists and thus incorrect credits undermine the reward system of science. Scientists who publish should therefore give proper credit and acknowledge the primary sources. Failure to do so is regarded as "citation negligence", "the disregard syndrome", "citation amnesia", "plagiarism by omission", "bibliographic plagiarism" or "citation plagiarism", and may range from an unconscious or conscious "failure to credit a prior discoverer so as to give an improper impression of priority" to "the appropriation of another person's ideas or results without given proper credit". False discovery credit is considered to be "a menace to honest science", "a serious transgression" or "intellectual theft, be it intentional or not". This paper describes some examples of citation amnesia showing that scientists often fail to credit prior sources and give false discovery credit to other scientists. One example is the association between major depression and activated immuno-inflammatory pathways, a discovery by European groups and published in many papers since 1990. Now, 25 years later, it is commonplace that these theories are credited to secondary American sources whose work in "the last decade", did or did not examine these pathways in major depression. This gives an improper impression of priority of American-based scientists. Here it is proposed that this citation amnesia and plagiarism reinforced the wrong science and had negative effects on the development of immune-inflammatory biomarkers and new immune-related treatments for depression. It is concluded that journal editors should improve their citation standards to guarantee correct assignment of discovery credit for example by demanding a signed pledge from the authors that correct citations to the primary sources were made.
Multiple Sclerosis (MS) is a chronic autoimmune disease characterized by neuroinflammation, demyelination and neuroaxonal degeneration affecting >2 million people around the world. MS is often accompanied by psychiatric comorbidities such as major depressive disorder (MDD), which presents a lifetime prevalence of around 50% in MS patients. Experimental Autoimmune Encephalomyelitis (EAE) is an animal model extensively used to study MS. EAE mimics the autoimmune nature of MS, as well as its inflammatory and demyelinating mechanisms also presenting predictive validity. There are important similarities between EAE and MS-associated depression (MSD). The mechanisms shared by these disorders include peripheral inflammation, neuroinflammation, mitochondrial dysfunctions, oxidative stress, nitrosative stress, lowered antioxidant defenses, increased bacterial translocation into the systemic circulation, and microglial pathology. Although the role of the immune-inflammatory system in MDD has been established in the 1990's, only few studies addressed immune pathways as a major determinant of depressive-like behavior in EAE. Therefore, in the present study we aimed at revising the current literature on EAE as an animal model to investigate the comorbidity between MS and MDD. In this regard, we revised the current literature on behavioral alterations in EAE, the possible mechanisms involved in this comorbidity and the potential and limitations of using this animal model to study depressive-like behavior.
Patients with treatment-resistant major depression had a significantly higher percentage of helper CD4+ T cells and immature double positive CD4+CD8+ T cells in their blood, and higher CD4+/CD8+ ratio than healthy controls. These results suggest activation of T helper immuno-response and disturbance in thymus function in these patients.
