Page - (000008) - in Advances in Neuroimmunology

viii Parkinson’s disease is also a topic of the review by Grimmig et al. [11]. This review focuses on the role of neuroimmunology and neuron-glia interactions in the pathophysiology of Parkinson’s disease in the context of aging. Pathological mechanisms are described along with potential therapeutic agents and strategies. Fractalkine, a protein constitutively expressed by neurons in the brain, and the antioxidant astaxanthin, a xanthophyll carotenoid that occurs naturally, are discussed as potential therapeutic agents. Three original articles in this Special issue focus on the role of neuroimmune factors in the actions of drugs of abuse on the brain. Recent studies have revealed that several abused drugs, including alcohol and morphine, induce glial cells of the brain, primarily astrocytes and microglia, to secrete neuroimmune factors [2,12,13]. Microglial activation and elevated secretion of neuroimmune factors are thought to contribute to neuronal damage and cognitive dysfunction associated excessive drug use and other pathological conditions [14]. The original article by Marshall et al. [15] reports results from studies on the effects of a binge pattern of alcohol exposure on microglial activation and expression of neuroimmune factors in the brain of rats. Differences in the consequences of single versus repetitive alcohol exposure on microglial activation are addressed. In the original article by Knapp et al. [16], studies are reported that examine the expression of neuroimmune mRNAs in the brain after treatment of rats to an experimental paradigm involving chronic alcohol exposure followed by alcohol withdrawal. Results from the alcohol exposure/withdrawn animals are compared to neuroimmune mRNA expression produced in rats by stress, which is a risk factor for alcohol relapse. Chang et al. [17] report effects of the bacterial endotoxin lipopolysaccharide (LPS) on expression of genes for proteins localized in multi-protein complexes called inflammasomes, which are important producers of neuroimmune factors and regulators of the inflammatory response. A number of different inflammasomes have been identified [18]. The studies focus on LPS-induced expression of genes for proteins housed in the inflammasomes in the context of morphine tolerance, which results from prolonged exposure to morphine. LPS is used in these studies to model invasion by a pathogen, which causes an inflammatory response. Morphine is known to affect the inflammatory response elicited by pathogens. A variety of inflammasome–related genes (e.g., for neuroimmune factors and downstream signaling partners) are examined in brains of morphine naïve rats and rats chronically exposed to morphine in these studies. The review article by Liu et al. [19] focuses on another brain glial cell, the oligodendrocyte, and injury that occurs to this brain cell during HIV-1 infection. Oligodendrocytes are responsible for axonal myelination, which is essential for normal neuronal and synaptic processes that mediate brain function. Oligodendrocytes also contribute to the immunology of the brain by producing a wide range of neuroimmune mediators [20]. Process and mediators involved in oligodendrocyte and myelin damage as a consequence of HIV-1 are discussed in this article. Nizamutdinov and Shapiro [21] provide a comprehensive review of the traumatic brain injury (TBI), and the role of neuroimmunity and peripheral immunity in the complex pathology of this condition. Traumatic brain injury is a broad area that encompasses many types of brain injury. A number of TBI experimental models are discussed along with mechanisms of neuropathology and the involvement of neuroimmunity. Neuroimmune factors have been reported to play a critical role in TBI outcomes. Donna Gruol Special Issue Editor References 1. Nistico, R.; Salter, E.; Nicolas, C.; Feligioni, M.; Mango, D.; Bortolotto, Z.A.; Gressens, P.; Collingridge, G.L.; Peineau, S. Synaptoimmunology—Roles in health and disease. Mol. Brain 2017, 10, 26.