Figure 3 | Scientific Reports

Figure 3

From: A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer

Figure 3

Potential scenario of the molecular pathways driving inverse and direct co-morbidities between AD and LC, and AD and GBM, respectively. (a) Potential molecular processes involved in the direct co-morbidity between AD and GBM. Proteasome inhibition could drive mitochondrial dysfunction, dampening oxidative phosphorylation and the TCA cycle. ROS are generated as a consequence of decreased rates of oxidative phosphorylation and glutathione levels. ROS generation activates the innate immune system, driving tumorigenesis by establishing a chronic inflammatory state through autocrine and paracrine loops. Synaptic transmission is decreased due to low levels of mitochondrial energy generation. (b) Potential molecular processes involved in the inverse co-morbidity between AD and LC. In this case, proteasome activity is enhanced, accompanied by increased levels of oxidative phosphorylation, TCA cycle and glutathione. As a consequence, lower levels of ROS are generated and so, redox sensitive transcription factors like FOXO are not activated, favoring the G1/S phase transition.

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