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Anti-Proteus activity of some South African medicinal plants : their potential for the prevention of rheumatoid arthritis

semanticscholar(2013)

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摘要
Introduction: The concept of an “immune privileged” CNS has been redefined to suggest that the CNS is a site of selective and modified immune reactivity [1]. The findings presented provide mechanistic and clinical evidence to suggest that phenotypes of neuropsychiatric disorders such as cognitive and affective dysfunction and neurodegeneration are influenced by pathological functional and morphological changes of the CNS induced by impaired immune functions, and by neuroinflammation in particular. Under immune challenged conditions such as Encephalitis and Multiple Sclerosis, inflammation in the CNS results in trafficking of B and T cells to the site of injury leading to impaired pathophysiological mechanisms relevant to neuropsychiatric disorders. Aim: This presentation will demonstrate the current understanding on the role of inflammation in neuropsychiatric disorders. Results: The activation of humoraland cell-mediated immunity is met with an upregulation of various inflammatory proteins such as cytokines and chemokines. It has been demonstrated that these immune cells traffic to various regions in the CNS including the hippocampus, a region regarded as essential for memory and learning. A chronic upregulation of such inflammatory proteins may result in dysfunction of key cytokine-mediated molecular mechanisms and neuronal–glial interactions that subserve synaptic plasticity and learning and memory processes in the brain. During pathological conditions microglial interact with neurons, possibly via P2x7 receptors, to induce a neuroinflammatory response characterized by an up-regulation of cytokines, such as, IL-1, IL-6 and TNF, which can then alter the function of cytokines in synaptic plasticity [2]. In addition, chronic inflammatory conditions in the CNS may lead to pathological morphological changes such as grey matter hypointensities and associated iron deposition in basal ganglia as seen in diseases like Multiple Sclerosis [3] associated with cognitive impairment and neuropsychiatric symptoms. Discussion: The above described mechanisms provide insight into shared pathologogical mechanisms of distinctly different neurological and psychiatric disorders such as depression, psychosis and cognitive decline / dementia.
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