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Abstract. According to the World Health Organization, major depression will become the leading cause of disability worldwide by the year 2030. Despite extensive research into the mechanisms underlying this disease, the rate, prevalence and disease burden has been on the rise, particularly in the industrialized world. Epidemiological studies have shown biological and biochemical differences in disease characteristics and treatment responses in different age groups. Notable differences have been observed in the clinical presentation, co-prevalence with other diseases, interaction with the immune system and even in the outcome. Thus, there is an increased interest in characterizing these differences, particularly in terms of contribution of different factors, including age, cytokines and immunotherapy. Research into the possible mechanisms of these interactions may reveal novel opportunities for future pharmacotherapy. The aim of the present review is to document recent literature regarding the impact of inflammatory mechanisms on the pathophysiology of the depressive disorder.

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S audi Arabia spends 5.1% of its gross domestic product (GDP) on education and 4.7% of GDP on health, with the result that there are 2.39 physicians per 1000 population, which is highest in the Middle East and comparable to the United States (2.59), the United Kingdom (2.81) and the United Arab Emirates (2.39). 1 The literacy rate in Saudi Arabia is 94.7%. Research and development have been prioritized in the Saudi Vision 2030 program with ambitious goals set to attain an international standard in higher education. A goal of Saudi Vision 2030 is that at least five Saudi universities be among the top 200 universities in the world by 2030. 2 The 2020 Times Higher Education World University Ranking includes seven Saudi universities among the 1400 universities of the world. This ranking criterion takes into account important parameters of research productivity namely teaching, research, citations, industry outcome and international outlook. 3 King Abdulaziz University (KAU), the number 1 university in Saudi Arabia, has reached a world ranking in the 201-250 universities group. KAU is followed by Alfaisal University that is ranked in the 251-300 group. King Saud University (KSU) and King Saud bin Abdulaziz University for Health Sciences (KSAU-HS) are within the 501-600 rank√. KSAU-HS, a specialized health sciences university has been included in this ranking recently. 3 To ensure that a certain policy is producing the desired benefits, it is important to monitor and evaluate the programs. Productivity in the field of medical education and research can be measured by several variables. The

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The human gut microbiome has been implicated in a host of bodily functions and their regulation, including brain development and cognition. Neuroinflammation is a relatively newer piece of the puzzle and is implicated in the pathogenesis of many neurological disorders. The microbiome of the gut may alter the inflammatory signaling inside the brain through the secretion of short-chain fatty acids, controlling the availability of amino acid tryptophan and altering vagal activation. Studies in Korea and elsewhere highlight a strong link between microbiome dynamics and neurocognitive states, including personality. For these reasons, re-establishing microbial flora of the gut looks critical for keeping neuroinflammation from putting the whole system aflame through probiotics and allotransplantation of the fecal microbiome. However, the numerosity of the microbiome remains a challenge. For this purpose, it is suggested that wherever possible, a fecal microbial auto-transplant may prove more effective. This review summarizes the current knowledge about the role of the microbiome in neuroinflammation and the various mechanism involved in this process. As an example, we have also discussed the autism spectrum disorder and the implication of neuroinflammation and microbiome in its pathogenesis.

Electroconvulsive therapy (ECT) is an effective treatment for severe medication-resistant depression. However, ECT frequently results in episodic memory impairments, causing many patients to discontinue treatment. The objective of this study was to explore the functional connectivity underpinnings of ECT-induced episodic memory impairments. We investigated verbal episodic memory and intrinsic functional connectivity in 24 patients with depression (13F, 11M) before and after ECT, and 1 month after treatment. We used a novel individual-oriented approach to examine functional connectivity, and trained a linear support vector regression model to estimate verbal memory performance based on connectivity. The model identified a set of brain connections that can predict baseline verbal memory performance (r = 0.535, p = 0.026). Importantly, we found a nonoverlapping set of brain connections whose changes after ECT can track patients' verbal memory impairments (r = 0.613, p = 0.008). These connections mainly involve the frontoparietal control, default mode, and hippocampal networks, suggesting that ECT affects broad functional networks that are involved in memory performance. In contrast, functional connectivity defined using traditional group-level analyses was unable to estimate either baseline memory performance or post-ECT verbal memory impairments. A parallel analysis using the same strategy did not identify a connectivity marker for overall mood improvement, suggesting that functional connectivity changes related to depressive symptoms may be highly heterogenous. Our findings shed light on the mechanism through which ECT impairs episodic memory, and additionally underline the importance of accounting for interindividual variability in the investigation of functional brain organization in patients with depression.

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