Inflammatory mechanisms in neurodegeneration and Alzheimer's disease: The role of the complement system
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Mesenchymal stem cell-mediated immunomodulation in cell therapy of neurodegenerative diseases
2018, Cellular ImmunologyCitation Excerpt :This interaction has been shown to stimulate microglial phagocytosis [10]. In a genetically modified animal model that C3 was inhibited, Aβ accumulation and neuronal degeneration were enhanced compared with the control group [11]. Similarly, elevated mRNA levels of complement components have been found in affected brain regions in animal models of PD [12].
Age-Related Macular Degeneration-Associated Genes in Alzheimer Disease
2015, American Journal of Geriatric PsychiatryCitation Excerpt :It was suggested that C3 had a protective role against AD, perhaps by mediating opsonization and facilitating phagocytosis of amyloid centrally or peripherally. Complement may prevent β-amyloid build-up or reduce hippocampal excitotoxicity.37 If apoptosis contributes to AD then complement activity may facilitate clearance of cellular fragments.
Immunity and Alzheimer's disease: Immunological perspectives on the development of novel therapies
2013, Drug Discovery TodayCitation Excerpt :Moreover, production of C5a results in activation of mitogen-activated protein kinase (MAPK) [24]. Animals genetically deficient for C5 were found to be more susceptible to excitotoxins [25]. Furthermore, mice expressing soluble Crry (a rodent Creg with inhibitory activities on complements similar to CD46 and CD55) had a significant increase in Aβ accumulation and neuronal degeneration [26].
Inhibition of complement alternative pathway suppresses experimental autoimmune anterior uveitis by modulating T cell responses
2011, Journal of Biological Chemistry