**5. Conclusion**

In this chapter, we described several concurrent mechanisms of AD pathogenesis, including the effects of systemic inflammation, metabolic dysfunction, and the gut microbiome. Since there seems to be no cure for AD and current established and experimental therapies are suboptimal at best, we suggest that more research should focus on minimizing peripheral inflammation and maintaining an anti-inflammatory complement of microbiota as early as possible. Targeting these two entities appears to positively affect the plethora of mechanisms implicated in AD (i.e. Aβ aggregation, tau hyperphosphorylation, microglial and complement activation, and BBB breakdown). There is reason to believe that AD arises from a manifestation of multiple hits within and outside of the central nervous system. A multi-system strategy will thus be most efficacious for prevention and treatment.
