Alzheimer’s Disease (AD) is the most common form of dementia in the US, affecting approximately 5.4 million Americans. One in eight people over the age of 65 have AD, or nearly half (45%) of people over 85 years old (1). As the baby-boomers move ever-closer toward their golden years, these numbers are expected to increase drastically in the years to come. Health care costs for AD are expected to soar from an estimated 200 Billion in 2012 to 1.1 Trillion dollars annually by 2050 (1). As a country on the brink of bankruptcy largely due to our staggeringly high health care costs, this is a road we simply can not afford to go down. 
If you asked people off the street what disease they feared most, I’m sure many people would say Alzheimer’s. The thought of losing our marbles some day, losing your memories and your personality that makes you you, is literally terrifying. But we’re not going to get anywhere by crossing our fingers and hoping we don’t get it. So let’s talk about Alzheimer’s Disease and, more importantly, what we can do to protect ourselves from getting it.

So what causes Alzheimer’s Disease? Most people will tell you that it’s the Beta-amyloid plaques and neurofibrillary tangles that are the causative agent behind AD. While these are indeed part of the AD pathogenesis, they are a most likely a result of the disease process, not a cause. As such, our question can be rephrased to ask “why would our brain lay down beta-amyloid plaques and neurofibrillary tangles?” The short answer is that there is no official answer yet, but there is a large body of research pointing toward one mechanism: Inflammation.

Everybody utters the phrase “I’m getting too old for this” at some point in their life. But while we all talk about the act of getting old, nobody ever talks about what happens to the body as we age. Aging is generally accompanied by an increase in oxidative stress (aka inflammation), which is most likely due to waning antioxidant defenses (2). Unfortunately, the part of the cell that is most vulnerable to oxidative stress is the mitochondria- the organelle in charge of making the cell’s ATP (energy source). Mitochondrial dysfunction and damage has been implicated to play an important, possibly causative role in AD pathology (3). Without an adequate source of fuel, the cell can not repair itself and maintain function, and eventually will die. It is now believed that beta-amyloid (BA) plaque is actually an anti-oxidant, and my in fact be the cell’s last futile attempt to quench the inflammation that is killing it from the inside-out (4). There has also been evidence to show that BA is an anti-microbial peptide, and may be a by-product of immune activation in the brain (5).
Before you know it you have a vicious cycle of inflammation that eventually takes out enough neurons that you experience symptoms. Only after symptoms appear will your doctor be able to make the diagnosis of AD, Parkinson’s, ALS, etc… However, by this point there is often so much damage to the involved structures that it’s too late to make any substantial changes. That’s not to say that these patients can’t benefit from the treatments I am sharing with you, but they are not a cure. With few exceptions, neurons do not regenerate. More importantly, the rate at which you are losing neurons every day far out-paces your brain’s ability to make new neurons. Therefore, it is MUCH easier and FAR more effective to prevent diseases of this nature, rather than trying to fix it once the disease has set in.


Stay tuned for Part 2: Prevention soon!

Nikki

References:
(2)  Galasko, Douglas. Biomarkers of oxidative damage and inflammation in Alzheimer’s disease. Biomark med. 2010 February: 4 (1): 27-36
(3) Bonda, David. Mitochondrial dynamics in Alzheimer’s disease opportunities for future treatment strategies. Drugs aging 2010 March 1; 27 (3): 181-192.
(4) Mondragon-Rodriguez, Siddhartha. Causes versus effects: the increasing complexities of Alzheimer’s disease pathogenesis. Expert rev neurother 2010 May: 10 (5): 683-691
(5) Soscia, Stephanie. The Alzheimer’s disease-associated amyloid B-protein is an antimicrobial peptide. 2010; PLoS ONE 5(3): e9505

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