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5.4 million people of all ages have Alzheimer’s Disease (AD) in the US, 5.2 million of that 5.4 million are ages 65 and older, according to Alz.org.  This statistic means that 1 in every 8 older American has Alzheimer’s.  Alzheimer’s is the 6th leading cause of death in the US and payment for care of those with AD is estimated to be $200 billion.  The following link goes to a site with lots of information on Alzheimer’s Disease symptoms, diagnosis, statistics, treatment…etc.

http://www.alz.org/downloads/facts_figures_2012.pdf

Recent findings have led experts to consider AD to be Type 3 Diabetes.  The findings have been based on insulin’s effect (or lack thereof) on aging and brain cell death.  Experts have found a correlation between people who have type 2 diabetes and those who develop AD.  In fact, the correlation goes all the way back to weight gain: weight gain (chronic) leads to obesity, which sometimes leads to Type 2 diabetes which now is found to lead to AD.

Experts think that a decrease of insulin in the brain or a decrease in the “potency” of insulin in the brain is what leads to cell death and then to all the effects of AD including memory loss, inability to do simple task or tasks once able to do, time or place confusion and changes in mood and personality.  What they are finding as the cause of AD is a lowering of insulin effect in the brain which causes an enzyme to activate far more often than it should, which leads to hyperphosphorylation of a protein labeled as the τ (tau) protein.  Hyperphosphorylation of tau  leads to the proteins aggregating, which blocks functions of brain cells and causes them to be broken down, leading to lower brain functions. Sorry for the neurochemical jargon.  Basically what all that mumbo-jumbo means is that insulin stops the “bunching up” of tau proteins and keeping the brain cells from breaking down.

One thing we talked about in our group discussions is whether research should be focused on how to prevent AD or to creating a “quick fix” drug with minimal side effects.  And the overall consensus was that prevention was the best route because preventing AD also can help prevent type-2 diabetes.  Also messing with insulin in the body is risky because insulin has other jobs besides blood glucose control and brain cell survival.

Another topic was the ethics of trying to end the aging process and whether or not it is worth all the time and effort and money that would go into it.  Again we had a general consensus that it wasn’t worth all the time and effort because the older you get the more chance you have of developing numerous age-related illnesses and disabilities.  Another aspect is if we slow the aging process, will we age differently in terms of brain vs. body.  What I mean by this is if slowing the aging process works, will it slow body aging, brain aging or both?  Will our brains be “younger” than our bodies, vice versa, and what effect on the individual will this have?

As you can see, there still remains a lot of work in order to understand exactly what AD is and how we can go about preventing or treating it.

Next week is glutamate and its role on opioid addiction.

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