Let’s be honest: eating healthy is difficult. It takes time, money, and quite a bit of determination. Still, diet has long term effects on our body and mind.
This last week, we discussed Alzheimer’s disease in class. One of the main physiological causes of Alzheimer’s symptoms is insulin resistance in the brain. In the brain, insulin activates a pathway called PI3-kinase/Akt/mTOR signaling pathway, this affects hunger and feeding behavior as well as memory and cognition.
The risk of developing Alzheimer’s is significantly higher for pre-diabetic people than for people without this condition. Also, obese individuals are over three times more likely to develop Alzheimer’s. The correlation between insulin resistance and Alzheimer’s is high.
However, we must note that insulin resistance is not the only problem happening in the Alzheimer’s brain. Plaques and tangles form in the tissue, other signaling pathways shut down, plasticity decreases, and neurons die. This horrible disease is nothing if not complicated.
The scary thing about Alzheimer’s is that this process of plaque formation and cell death starts ten to twenty years before you notice any symptoms. By the time symptoms show themselves, it is usually too late to do anything. This prospect is of course terrifying. A horrible illness could be manifesting itself in irreversible ways inside us right now.
Now we can approach these facts in a few different ways. We can tell ourselves its inevitable and become resigned to the fact that we may develop Alzheimer’s, or we can do our best to prevent it.
Despite our best efforts, disease can happen. Still, by eating healthy, we can prevent insulin resistance and hinder the development of Alzheimer’s (and plenty of other health problems too).
We don’t need to be perfect, I’m definitely not; but if we remember that a healthy body leads to a healthy mind, we will all be better off.
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The relationship between high glucose levels and Alzheimer’s disease is a bit complicated. First of all insulin resistance is likely the result of the peroxynitrite-mediated nitration of the insulin receptor substrate. This inhibits the activation of the phosphatidyinositol 3-kinase/Akt pathway which is needed for glucose to get into cells outside of the brain.
https://www.ncbi.nlm.nih.gov/pubmed/15240096
More glucose then enters the brain where it is converted to myo-inositol. Myo-inositol is converted into phosphatidylinositol 4,5 biphosphate. This is a substrate for the phosphatidyinositol 3-kinase and for phospholipase C. The former pathway protects the brain; the latter pathway can lead to neurodegeneration.
http://tmedweb.tulane.edu/pharmwiki/doku.php/mood_stabilizers_antimanic
http://cgap.nci.nih.gov/BIOCARTA/Pathways/h_plcPathway.gif (on the right of this chart it should be PIP3; phoshatidylinositol 3,4,5 biphosphate)
http://www.frontiersin.org/files/Articles/131867/fncel-09-00091-HTML/image_m/fncel-09-00091-g003.jpg (ONOO- is peroxynitrite and GSH is glutathione–a critical brain antioxidant).
There are two types receptors whose overactivation can lead to Alzheimer’s disease: receptor tyrosine kinases and g protein-coupled receptors (the first activates phospholipase C gamma; the second phospholipase C beta). Hyperinsulemnia overactivates insulin receptors and too much glucose overactivates platelet derived growth factor receptors both of which are receptor tyrosine kinases. This can lead to the death of neurons.