The Adaptive Immune System Restrains Alzheimer 's Disease Pathogenesis By Modulating Microglial Function

The Adaptive Immune System Restrains Alzheimer 's Disease Pathogenesis By Modulating Microglial Function

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Review and analysis of “The adaptive immune system restrains Alzheimer’s disease pathogenesis by modulating microglial function”. This article presents eight important findings, these will be mentioned and discussed together the data that support them. First, immunocompromised Alzheimer’s disease (AD) mice model, showed aggressive development of AD-neuropathology. In figure 1, is shown that the accumulation of Aβ soluble and insoluble is elevated in the immunocompromised AD mice compared with the “normal” AD mice model. Image analysis was executed and it was concluded that there was an increase of Aβ plaques in the dentate gyrus confirming their findings. Second, increase in pathology is not driven by altered Aβ production, but likely via impaired clearance. As discussed by the authors the development of the pathology isn’t due to accelerated production of Aβ. It was concluded this after the results they obtain performing protein quantification and qPCR analysis. In Figure S2, from the supporting information; neither the protein levels of APP and/or PS1 were elevated in comparison with the “normal” AD mice also qPCR confirms the findings with no alteration in APP or PSEN1 expression. Validating their conclusion that the pathology is due to lack of clearance. Third, microglial function and changes in both adaptive and innate immunity are implicated in AB clearance. This finding is supported by figure 2C where gene ontology was performed, this data showed different pathways involving adaptive and or innate immunity, antigen presentation and Ig binding were significantly altered. Figure 3 also supports this finding, where it was presented that the number of microglia was increased in immunocompromised AD mice in comparison to the wil...

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... (math) that confirms or deny the “association”. And in order to improve the advances of AD research the same set of experiment should be preform to understand the effects of immune system with the other major protein associated with AD development Tau. Lastly science is always moving forward to which I would recommend the following repeat Gammagard’s work in this mice model, re-visit how IgG levels become elevated normal AD mice brains. Also investigate what is the role of the choroid plexus in regulating the influx of IgG into the brain. And the role of microglial Fc receptors or decreased in the clearance of IgG’s from the brain. Also I would like to understand why there was a higher presence of IgG in the brain only in the “normal” AD mice model.  The next and final thing would be to continue the research in in the role of the immune system in the develop of AD.

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