27 April 2011

The Role of CD40 in Neuroinflammation

After going over the different factors that can lead to Alzheimer's Disease, I was interested in learning more about the role CD40 plays. The study, by Laporte et al, that I found looks at a transgenic mouse model that have an over-expressing tau phosphorylation, which leads to amyloid plaques and deposits. The study argues, if one genetically disrupts CD40, this will decrease cdk5 levels in mice, which will reduce tau phosphorylation. This is important, because this study alludes to that tau hyperphosphorylation is directly correlated with neuroinflammation, and that the dysregulation of cdk5 will lead to hyperphosphorylation of tau. The results of this study, looking to see if one disrupts CD40 will this decrease amyloid deposits, showed that by disrupting CD40 there is a relative loss of tau phosphorylation. So the study concludes by stating that, CD40 does not act directly on amyloid deposits, however there are inflammatory pathways, such as CD40, that have a direct effect on the phosphorylation of tau.
I thought this was a really good study and good article. It was very easy to understand what they were trying to do, and what their results were. Figure 3, which showed amyloid deposits in dystrophic neurites, was an excellent figure, it showed exactly what was going on, and pointed out where the amyloid deposits were. Overall, this was a good paper, I would be interested to see what you all thought of it.


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