Inflammatory bowel disease (IBD) is defined as a chronic intestinal inflammation that results from host-microbial interactions in a genetically susceptible individual. IBDs are a group of autoimmune diseases that are characterized by inflammation of both the small and large intestine, in which elements of the digestive system are attacked by the body's own immune system. This inflammatory condition encompasses two major forms, known as Crohn's disease and ulcerative colitis. Patients affected by these diseases experience abdominal symptoms, including diarrhea, abdominal pain, bloody stools, and vomiting. Moreover, defects in intestinal epithelial barrier function have been observed in a number of patients affected by IBD. In this review, we first describe the types and symptoms of IBD and investigate the role that the epithelial barrier plays in the pathophysiology of IBD as well as the major cytokines involved. We then discuss steps used to diagnose this disease and the treatment options available, and finally provide an overview of the recent research that aims to develop new therapies for such chronic disorders.

Alzheimer’s disease (AD) is a complex neurodegenerative disorder characterized by the progressive loss of neurons, which typically leads to severe impairments in cognitive functions including memory and learning. Key pathological features of this disease include the deposition of highly insoluble amyloid β peptide and the formation of neurofibrillary tangles (NFTs) in the brain. Over the past few years, mounting evidence has implicated sustained glial-mediated inflammation as a major contributor of the neurodegenerative processes and cognitive deficits observed in AD. However, despite tremendous effort in elucidating the molecular and cellular players involved in AD pathology, to date, there is no treatment that could prevent or cure this disease. Current treatments are only useful in slowing down the progression of AD and helping patients manage some of their behavioral and cognitive symptoms. A better understanding of the role of glial cells in the regulation of AD pathogenesis is needed as this could pave the way to new therapeutic strategies. This paper provides an overview of findings from both human and animal studies regarding the involvement of microglia and astrocytes in AD, and discusses potential avenues for therapeutic intervention.

Neurodegenerative diseases are the result of progressive loss of neurons and axons in the central nervous system (CNS), which can lead to cognition and motor dysfunction. It is well known that CNS inflammation and immune activation play a major role in the pathophysiology of neurodegenerative diseases. Although the blood-brain barrier (BBB) is able to protect the CNS from immune activation, it becomes more permeable during inflammation, which renders the brain vulnerable to infections. A better understanding of the interaction between inflammatory mediators, such as cytokines, and the activated immune response, including astrocytes and microglia, is critical for the development of new therapeutic strategies for neurodegenerative diseases. This review first describes the role of innate immune activation in neurodegenerative diseases and illustrates the factors that contribute to the communication between the CNS and the immune system. A closer look is given at the role of the BBB in inflammation and immunity, as well as at the animal models used to study inflammation in neurodegenerative diseases. Finally, this review outlines the key pathways and biological mechanisms involved in CNS diseases, with a particular focus on multiple sclerosis (MS), Parkinson's disease (PD), and Alzheimer's disease (AD).

Spinal cord injury affects more than 2.5 million people worldwide and can lead to paraplegia and quadriplegia. Anatomical discontinuity in the spinal cord results in disruption of the impulse conduction that causes temporary or permanent changes in the cord’s normal functions. Although axonal regeneration is limited, damage to the spinal cord is often accompanied by spontaneous plasticity and axon regeneration that help improve sensory and motor skills. The recovery process depends mainly on synaptic plasticity in the preexisting circuits and on the formation of new pathways through collateral sprouting into neighboring denervated territories. However, spontaneous recovery after spinal cord injury can go on for several years, and the degree of recovery is very limited. Therefore, the development of new approaches that could accelerate the gain of motor function is of high priority to patients with damaged spinal cord. Although there are no fully restorative treatments for spinal injury, various rehabilitative approaches have been tested in animal models and have reached clinical trials. In this paper, a closer look will be given at the potential therapies that could facilitate axonal regeneration and improve locomotor recovery after injury to the spinal cord. This article highlights the application of several interventions including locomotor training, molecular and cellular treatments, and spinal cord stimulation in the field of rehabilitation research. Studies investigating therapeutic approaches in both animal models and individuals with injured spinal cords will be presented.