Depression is a serious public health problem, and adolescence is an \'age of risk\' for the onset of Major Depressive Disorder. Recently, we and others have proposed neuroimmune network models that highlight bidirectional communication between the brain and the immune system in both mental and physical health, including depression. These models draw on research indicating that the cellular actors (particularly monocytes) and signaling molecules (particularly cytokines) that orchestrate inflammation in the periphery can directly modulate the structure and function of the brain. In the brain, inflammatory activity heightens sensitivity to threats in the cortico-amygdala circuit, lowers sensitivity to rewards in the cortico-striatal circuit, and alters executive control and emotion regulation in the prefrontal cortex. When dysregulated, and particularly under conditions of chronic stress, inflammation can generate feelings of dysphoria, distress, and anhedonia. This is proposed to initiate unhealthy, self-medicating behaviors (e.g. substance use, poor diet) to manage the dysphoria, which further heighten inflammation. Over time, dysregulation in these brain circuits and the inflammatory response may compound each other to form a positive feedback loop, whereby dysregulation in one organ system exacerbates the other. We and others suggest that this neuroimmune dysregulation is a dynamic joint vulnerability for depression, particularly during adolescence. We have three goals for the present paper. First, we extend neuroimmune network models of mental and physical health to generate a developmental framework of risk for the onset of depression during adolescence. Second, we examine how a neuroimmune network perspective can help explain the high rates of comorbidity between depression and other psychiatric disorders across development, and multimorbidity between depression and stress-related medical illnesses. Finally, we consider how identifying neuroimmune pathways to depression can facilitate a \'next generation\' of behavioral and biological interventions that target neuroimmune signaling to treat, and ideally prevent, depression in youth and adolescents.

The gut microbiota is indispensable for maintaining host health by enhancing the host\'s digestive capacity, safeguarding the intestinal epithelial barrier, and preventing pathogen invasion. Additionally, the gut microbiota exhibits a bidirectional interaction with the host immune system and promotes the immune system of the host to mature. Dysbiosis of the gut microbiota, primarily caused by factors such as host genetic susceptibility, age, BMI, diet, and drug abuse, is a significant contributor to inflammatory diseases. However, the mechanisms underlying inflammatory diseases resulting from gut microbiota dysbiosis lack systematic categorization. In this study, we summarize the normal physiological functions of symbiotic microbiota in a healthy state and demonstrate that when dysbiosis occurs due to various external factors, the normal physiological functions of the gut microbiota are lost, leading to pathological damage to the intestinal lining, metabolic disorders, and intestinal barrier damage. This, in turn, triggers immune system disorders and eventually causes inflammatory diseases in various systems. These discoveries provide fresh perspectives on how to diagnose and treat inflammatory diseases. However, the unrecognized variables that might affect the link between inflammatory illnesses and gut microbiota, need further studies and extensive basic and clinical research will still be required to investigate this relationship in the future.

Inflammatory bowel diseases are considered immune disorders with a complex genetic architecture involving constantly changing endogenous and exogenous factors. The rapid evolution of genomic technologies and the emergence of newly discovered molecular actors are compelling the research community to reevaluate the knowledge and molecular processes. The human intestinal tract contains intestinal human microbiota consisting of commensal, pathogenic, and symbiotic strains leading to immune responses that can contribute and lead to both systemic and intestinal disorders including IBD. In this review, we attempted to highlight some updates of the new IBD features related to genomics, microbiota, new emerging therapies and some major established IBD risk factors.

Myasthenia gravis is an autoimmune disorder characterized by the presence of autoantibodies against the acetylcholine receptor present in the post-synaptic membrane of the neuromuscular junction impairing the muscle contraction and causing the patient suffering from the disorder to develop a myriad of muscular defects ranging from drooping of eyelids, blurred or double vision, shortness of breath, difficulty in swallowing, as well as weakness of limbs and arms. Myasthenia gravis is known as the disease of old men and young women but in contrast to the global scenario, in India, myasthenia gravis was found to be predominant in males with the ratio of 2.70:1. Though the disorder has been studied for centuries, the true reason for disease and its pathophysiology still eludes us. But recent advancement in molecular biology and diagnostic tools has enabled us to identify many targets for pharmacotherapy as well as for early diagnosis. Thus, improving the patient\'s morbidity and quality of life. In this article, we are discussing the recent advancements made in diagnosis and therapy of the disease.

Although many caspase inhibitors have been patented, caspase inhibitors have not entered the market due to their toxicity and poor pharmacokinetic profile.
In this article, we review patents (2013-2015) for peptide and non-peptide caspase inhibitors and their compositions.
Noteworthy patents include a peptidic caspase-2 inhibitor for nasal administration and a peptidomimetic caspase-6 inhibitor that can be administered via several routes for the treatment of neurodegenerative diseases. Furthermore, caspase-1 inhibitors for contact dermatitis and inflammation, cardiovascular diseases, and liver diseases and a caspase-3 inhibitor for cerebral stroke have been patented. Of particular interest is the novel use of tyrosine kinase inhibitors (sunitinib and its derivatives) for the prevention and treatment of age-related ocular diseases via inhibition of the caspase-3, dual-leucine zipper kinase (DLK) and leucine zipper-bearing kinase (LZK) pathways. However, for effective clinical application of caspase inhibitors, novel peptidic and nonpeptidic caspase inhibitors with lower toxicity and improved efficacy should be developed via structural modifications, and further animal studies and preclinical and clinical trials are needed. In addition, the poor pharmacokinetic properties of classic caspase inhibitors may be improved by using advanced drug delivery systems that employ liposomes, polymers, and nanoparticles through effective administration routes.