Neuroinflammation: Mechanisms and Management (Contemporary Neuroscience)

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Clinical neurology is underpinned by knowledge of the neuroanatomy of the central and peripheral nervous system.

Frontiers | Monitoring the Neuroinflammatory Response Following Acute Brain Injury | Neurology

In order to diagnose, investigate and provide appropriate treatment we must first localize the lesion. In order to do this, a thorough knowledge of basic neuroanatomy is essential. This module will provide neuroanatomy video sessions followed by laboratory dissection of the human brain and spinal cord by students. The dissection course is complimented by a lecture series on functional neuroanatomy and functional neuroscience. This lecture course covers the basic anatomy and physiology that underpins our understanding of neurological disease.

Cerebrovascular disease is a common cause of death and disability. The brain and the immune system are the two major adaptive systems of the body. Two major pathways are involved in this cross-talk: the Hypothalamic-pituitary-adrenal axis HPA axis , and the sympathetic nervous system SNS , via the sympathetic-adrenal-medullary axis SAM axis. The activation of SNS during an immune response might be aimed to localize the inflammatory response.

The role of inflammation in the development of epilepsy

The body's primary stress management system is the HPA axis. The HPA axis responds to physical and mental challenge to maintain homeostasis in part by controlling the body's cortisol level.

Circulating immune cells such as macrophages , as well as glial cells microglia and astrocytes secrete these molecules. Cytokine regulation of hypothalamic function is an active area of research for the treatment of anxiety-related disorders. Cytokines mediate and control immune and inflammatory responses.

Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis. Like the stress response, the inflammatory reaction is crucial for survival. Systemic inflammatory reaction results in stimulation of four major programs: [18]. Common human diseases such as allergy , autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro-inflammatory versus anti-inflammatory and T helper Th1 versus Th2 cytokine balance.

Chronic secretion of stress hormones , glucocorticoids GCs and catecholamines CAs , as a result of disease, may reduce the effect of neurotransmitters , including serotonin , norepinephrine and dopamine , or other receptors in the brain, thereby leading to the dysregulation of neurohormones.

Through stimulation of these receptors, locally released norepinephrine, or circulating catecholamines such as epinephrine , affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells. Glucocorticoids also inhibit the further secretion of corticotropin-releasing hormone from the hypothalamus and ACTH from the pituitary negative feedback.

Under certain conditions stress hormones may facilitate inflammation through induction of signaling pathways and through activation of the Corticotropin-releasing hormone. This systemic or neuro-inflammation and neuroimmune activation have been shown to play a role in the etiology of a variety of neurodegenerative disorders such as Parkinson's and Alzheimer's disease , multiple sclerosis , pain, and AIDS -associated dementia.

However, cytokines and chemokines also modulate central nervous system CNS function in the absence of overt immunological, physiological, or psychological challenges. Although changes related to infectious disease and wound healing have provided the strongest evidence to date, the clinical importance of immunological dysregulation is highlighted by increased risks across diverse conditions and diseases.

For example, stressors can produce profound health consequences. In one epidemiological study, all-cause mortality increased in the month following a severe stressor — the death of a spouse. Researchers have suggested that these changes are beneficial if they are of limited duration, [22] but when stress is chronic, the system is unable to maintain equilibrium or homeostasis ; the body remains in a state of arousal, where digestion is slower to reactivate or does not reactivate properly, often resulting in indigestion.

Furthermore, blood pressure stays at higher levels. In one of the earlier PNI studies, which was published in , subjects were led to believe that they had accidentally caused serious injury to a companion through misuse of explosives. In the first meta-analysis by Herbert and Cohen in , [34] they examined 38 studies of stressful events and immune function in healthy adults. They included studies of acute laboratory stressors e. They found consistent stress-related increases in numbers of total white blood cells , as well as decreases in the numbers of helper T cells , suppressor T cells , and cytotoxic T cells , B cells , and natural killer cells NK.

These effects were consistent for short-term and long-term naturalistic stressors, but not laboratory stressors. In the second meta-analysis by Zorrilla et al. Using the same study selection procedures, they analyzed 75 studies of stressors and human immunity.

Naturalistic stressors were associated with increases in number of circulating neutrophils , decreases in number and percentages of total T cells and helper T cells, and decreases in percentages of natural killer cell NK cells and cytotoxic T cell lymphocytes. A study done by the American Psychological Association did an experiment on rats, where they applied electrical shocks to a rat, and saw how interleukin-1 was released directly into the brain. Interleukin-1 is the same cytokine released when a macrophage chews on a bacteria , which then travels up your vagus nerve , creating a state of heightened immune activity, and behavioral changes.

More recently, there has been increasing interest in the links between interpersonal stressors and immune function. For example, marital conflict, loneliness, caring for a person with a chronic medical condition, and other forms on interpersonal stress dysregulate immune function.

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Release of corticotropin-releasing hormone CRH from the hypothalamus is influenced by stress. Furthermore, stressors that enhance the release of CRH suppress the function of the immune system; conversely, stressors that depress CRH release potentiate immunity. Glutamate agonists , cytokine inhibitors, vanilloid-receptor agonists , catecholamine modulators, ion-channel blockers , anticonvulsants , GABA agonists including opioids and cannabinoids , COX inhibitors , acetylcholine modulators , melatonin analogs such as Ramelton , adenosine receptor antagonists and several miscellaneous drugs including biologics like Passiflora edulis are being studied for their psychoneuroimmunological effects.

For example, SSRIs , SNRIs and tricyclic antidepressants acting on serotonin , norepinephrine , dopamine and cannabinoid receptors have been shown to be immunomodulatory and anti-inflammatory against pro-inflammatory cytokine processes, specifically on the regulation of IFN-gamma and IL, as well as TNF-alpha and IL-6 through a psychoneuroimmunological process. These studies warrant investigation of antidepressants for use in both psychiatric and non-psychiatric illness and that a psychoneuroimmunological approach may be required for optimal pharmacotherapy in many diseases.

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The endocannabinoid system appears to play a significant role in the mechanism of action of clinically effective and potential antidepressants and may serve as a target for drug design and discovery. The increase in amygdalar CB 1 receptor binding following imipramine treatment is consistent with prior studies which collectively demonstrate that several treatments which are beneficial to depression, such as electroconvulsive shock and tricyclic antidepressant treatment, increase CB 1 receptor activity in subcortical limbic structures , such as the hippocampus , amygdala and hypothalamus.

And preclinical studies have demonstrated the CB 1 receptor is required for the behavioral effects of noradrenergic based antidepressants but is dispensable for the behavioral effect of serotonergic based antidepressants. Extrapolating from the observations that positive emotional experiences boost the immune system, Roberts speculates that intensely positive emotional experiences —sometimes brought about during mystical experiences occasioned by psychedelic medicines—may boost the immune system powerfully.

Research on salivary IgA supports this hypothesis, but experimental testing has not been done. From Wikipedia, the free encyclopedia. They also address the molecular, cellular, and therapeutic actions of first generation agents, as well as their potential clinical relevance to AIDS dementia, Alzheimer's disease, amyotropic lateral sclerosis ALS , Down's syndrome, Huntington's disease, multiple sclerosis, Parkinson's disease, and stroke. Neuroinflammation: Mechanisms and Management offers a remarkable new synthesis that will play a key role in developing the molecular targets now emerging in neuropharmacological drug design, and so lead to a new generation of drugs for neurologists to use in the treatment of a wide variety of both acute and chronic neurodegenerative disorders.

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Neuroinflammation - A Zimmerman, M.D.

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