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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: Curr Opin Genet Dev. 2016 May 25;38:90–96. doi: 10.1016/j.gde.2016.04.006

Figure 4. The MAM hypothesis.

Figure 4

The hypothesis proposes that the functional cause of AD is upregulated ER-mitochondria communication at the MAM. This results in alterations in the indicated functions, as well as an increase in the Aβ42:Aβ40 ratio; the plaques and tangles arise as a downstream result of that perturbation. The increased ER-mitochondrial connectivity is the result of a derangement in specific biochemical pathways brought on by mutations in PS’s and APP (in the case of FAD) or by other causes (in the case of SAD).