What is it about?
Obesity is a risk factor for both cancer and Alzheimers disease. Fat cells produce many biologically active substances, including leptin and adiponectin. Leptin can stimulate cancer and inhibit Alzheimer's disease, while adiponectin has opposing effects. These actions are mediated by several known cell signaling pathways. If the leptin/adiponectin ratio favors leptin, cancer risk would be increased and Alzheimer's disease risk would be decreased. If the ratio favors adiponectin, then the risk pattern would be reversed. Further research is needed to verify this relationship and to determine how to modify the ratio to decrease risk of these two diseases.
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Why is it important?
Obesity is a worldwide problem and is associated with a variety of diseases including cancer and Alzheimer's disease. Both these disorders are difficult to treat, making effective prevention and control strategies extremely important. Determination that cancer and Alzheimer's disease risk could be reduced by manipulating the leptin/adiponectin ratio would be a major advance, and it may be that treatment for active disease could be developed as well.
Perspectives
I am a medical oncologist with many years experience in academic clinical care. During my time in the clinic, I have been puzzled by the rarity of Alzheimer's disease in my cancer patients. Others have also noted this, as well as the opposite relationship-cancer is rare in Alzheimer's patients. To try to explain this "experiment of nature", I read through the literature to see what factors might account for this inverse relationship. Body fat produces hundreds of biologically active compounds, including leptin and adiponectin, and I found that these two "adipokines"have actions that may explain the inverse cancer/Alzheimer's relationship.
Daniel Nixon
Morehouse School of Medicine
Read the Original
This page is a summary of: The Inverse Relationship Between Cancer and Alzheimer's Disease: A Possible Mechanism, Current Alzheimer Research, July 2017, Bentham Science Publishers,
DOI: 10.2174/1567205014666170216152905.
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