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In conclusion, the reason why the ApoE 4 allele increases the risk of developing AD is not because it interacts with amyloid or tau but because of the physiological roles it plays in being less effective in supporting insulin signaling and energy utilization by neurons and in activating the inflammation response more than the other two alleles

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Furthermore, these potent biological elements are highly expressed and secreted in the diabetic context, supporting the inflammation theory that emphasizes the pivotal roles of inflammatory responses in the pathophysiology of diabetes mellitus and its associated complications [28], [36]