Type III Diabetes - ?

To reach her conclusions, de la Monte examined the brains of 45 deceased elderly Alzheimer's patients and found that among those "in the most advanced stage of Alzheimer's, insulin receptors were nearly 80 percent lower than in a normal brain." In healthy brains, insulin stimulates the enzyme that produces the neurotransmitter acetylcholine, the lack of which is seen as a key marker of Alzheimer's disease. In patients with Alzheimer's, de la Monte believes, the brain gradually becomes resistant to insulin.

Previous animal brain studies by de la Monte and others have supported the hypothesis that insulin resistance may be a root cause of Alzheimer's, although many researchers believe that it will emerge as just one of several possible causes, including genetics. Most Alzheimer's patients are not diabetics and while many appear to have insulin-signaling concerns, not all do.

Like Alzheimer's, diabetes has no cure. According to the American Diabetes Association, there are already nearly 26 million diabetics in the country, a number that is growing. Many diabetics do not develop Alzheimer's, but there is measurable overlap and the rates of both diseases are rising. If fatty foods provoke insulin resistance in our brains, then, as New Scientist magazine put it in a recent cover story about the link between diabetes and Alzheimer's, "we may be unwittingly poisoning our brains every time we chow down on burgers and fries."

In the New Scientist article, SUNY-Albany neuroscientist Ewan McNay said: "The epidemic of Type 2 diabetes, if it continues on its current trajectory, is likely to be followed by an epidemic of dementia. That's going to be a huge challenge to the medical and care systems."
http://www.nextavenue.org/blog/alzheimers-really-type-diabetes

This one is a great example of how one wrong conjecture shapes another.

The issue is whether diabetes results from too much ingestion of sugar, or too much ingestion of fat.  For those who have bought the "too much fat is bad" conjecture, the other issues become confusing.  For example, fat in the blood (triglycerides) is a better correlate for heart disease than is cholesterol, and if you reduce carb consumption (especially sugar/fructose) triglycerides decrease significantly for almost all folks.  But fat intake is the problem, right?  But if you eat more fat, lots of fat - up to 85% of total intake - trigs plummet.  Why?  Most likely because when carb intake goes below the toxic level, the liver can stop making trigs out of sugar (especially fructose), and the body learns how to run on fat (in the presence of high sugars, the body will run on sugar).  In short, when the body is fueled with high fat, moderate protein and the right amount of carbs, the body burns fat, does not make much fat in the liver, and regains insulin sensitivity.  These factors are all measurable - so it makes me scratch my head when I read of professionals in the field who still believe that "high fat ingestion" causes diabetes via obesity.

Burgers and fries may play a role in this, but not because they include fat.  It's the bun, the potatoes, ( especially the giant helpings and free refills of Dr. Pepper and other HFCS laden colas) that crush liver function and pile on with excess blood sugar that brings fat burning to a screeching halt and eventually leaves a person with a big belly, insulin resistant, and with chronically high blood sugars (aka, with metabolic syndrome) - almost begging to get alzheimer's or CVD or cancer (which those with metabolic syndrome and diabetes get at disproportionately high rates).

The fact that you can find cultures eating high carb diets (60% carbs), and who smoke heavily (95% in males), and don't have the diseases of civilization, while you can also find populations that eat sugar and don't smoke who do have the diseases of civilization, indicates that sugar (meaning table sugar or HFCS, both of which are 50% fructose) is likely more toxic than are cigarettes.

I think of the rumored last Japanese soldier on some pacific island who was supposedly still waiting as ordered in defense of the turf for the battle with the Americans - who will be the last medical or scientific professional to believe that fat makes you fat and sick, while sugar/carbs are the innocent bystander?

Diet May Slow Alzheimer's Disease

Mercola on Understanding Alzheimer's
The intro from mercola.com:

"Alzheimer’s disease is the sixth leading cause of death in the U.S. This fatal and progressive condition destroys brain cells, resulting in memory loss and severe thinking and behavioral problems (aggression, delusions, and hallucinations) that interfere with daily life and activities.

"The cause is conventionally believed to be a mystery. While we know that certain diseases, like type 2 diabetes, are definitively connected to the foods you eat, Alzheimer's is generally thought to strike without warning or reason.

"That is, until recently.

"A growing body of research suggests there may be a powerful connection between the foods you eat and your risk of Alzheimer's disease and dementia, via similar pathways that cause type 2 diabetes. Some have even re-named Alzheimer's as "type 3 diabetes.""

It's a good read - 

Remember Your Vitamin D and Fish Oil - Or Forget It All

http://www.sciencedaily.com/releases/2013/02/130205131629.htm#.URJYFe127
The BLUF:
"A team of academic researchers has pinpointed how vitamin D3 and omega-3 fatty acids may enhance the immune system's ability to clear the brain of amyloid plaques, one of the hallmarks of Alzheimer's disease."

Another cut from the article:
"Our new study sheds further light on a possible role for nutritional substances such as vitamin D3 and omega-3 in boosting immunity to help fight Alzheimer's," said study author Dr. Milan Fiala, a researcher at the David Geffen School of Medicine at UCLA.

"For the study, scientists drew blood samples from both Alzheimer's patients and healthy controls, then isolated critical immune cells called macrophages from the blood. Macrophages are responsible for gobbling up amyloid-beta and other waste products in the brain and body."

Every advance in this research is good, but the first step in Alzheimer's defense is to avoid carbing yourself to death.  When your insulin degrading enzyme isn't busy working on insulin, it also gobbles of beta amyloid.  When your proteins aren't gummed up with excess glucose, they don't get wrapped in the amyloid plaques as speedily.  In other words, if you don't make your body into a glucose dumping ground, things work like they should.  

Leptin, Low Carb, and Alzheimer's

Abstract 

Accumulation of amyloid-β (Aβ) is a key event mediating the cognitive deficits in Alzheimer's disease (AD) as Aβ promotes synaptic dysfunction and triggers neuronal death. Recent evidence has linked the hormone leptin to AD as leptin levels are markedly attenuated in AD patients. Leptin is also a potential cognitive enhancer as it facilitates the cellular events underlying hippocampal learning and memory. Here we show that leptin prevents the detrimental effects of Aβ_1–42 on hippocampal long-term potentiation. Moreover leptin inhibits Aβ_1–42-driven facilitation of long-term depression and internalization of the 2-amino-3-(5-methyl-3-oxo-1,2- oxazol-4-yl) propanoic acid (AMPA) receptor subunit, GluR1, via activation of PI3-kinase. Leptin also protects cortical neurons from Aβ_1–42-induced cell death by a signal transducer and activator of transcription-3 (STAT-3)-dependent mechanism. Furthermore, leptin inhibits Aβ_1–42-mediated upregulation of endophilin I and phosphorylated tau in vitro, whereas cortical levels of endophilin I and phosphorylated tau are enhanced in leptin-insensitive Zucker fa/fa rats. Thus leptin benefits the functional characteristics and viability of neurons that degenerate in AD. These novel findings establish that the leptin system is an important therapeutic target in neurodegenerative conditions.

http://www.neurobiologyofaging.org/article/S0197-4580(12)00425-3/abstract

I doubt the author's conclusion will lead anywhere.  It is well established that high levels of triglycerides  prevent leptin from crossing the blood brain barrier.  My conjecture - and admittedly this is way over my head but a plausible conjecture none the less - is that this is one of the ways that high carb diets negatively impact development of "AD".
First, high carb diets drive high triglyceride levels, and with subsequent development of insulin resistance, high insulin levels.  The high trigs mean that less leptin will interact in the brain, perhaps creating the effects described above which drive amyloid-B accumulation at faster rates.
High insulin levels means that the body's scavenger system for amyloid-B, insulin degrading enzyme, is busy with insulin and never has time to attend to amyloid-B.
Third, fasting results in the body finding and using as much protein in the body as possible, and there's some evidence that this "protein scavenging" reduces build of of AGEs (a protein damaged by glycation) and other "junk" proteins that wind up in the plaques associated with AD.
Lastly, high blood sugar levels drives higher levels of advanced glycation end products, which are also accelerants in the plaques that characterize AD.

The example of the diabetics is telling - they get AD at higher rates than everyone else.  It would be interesting to know - can AD develop in a person who maintains normal to low blood glucose across their entire lifespan?  Or, the same question stated differently:  has a person ever been diagnosed with AD who maintained optimal blood sugar levels across a lifetime (or most of a lifetime)?

Exercise/Alzheimer's Link

...when the scientists examined the results for people with the e4 gene variant. Most of those who carried the APOE-e4 gene displayed much larger accumulations of amyloid plaques than those without it.
Unless they exercised. The carriers of the gene who reported walking or jogging for at least 30 minutes five times a week had plaque accumulation similar to that of volunteers who were e4-negative. In essence, the APOE-e4 gene carriers mitigated their inherited risk for developing Alzheimer’s by working out. Or, as the study authors wrote, a “physically active lifestyle may allow e4 carriers to experience brain amyloid levels equivalent to e4-negative individuals.”
http://well.blogs.nytimes.com/2012/01/18/how-exercise-may-keep-alzheimers-at-bay/

This explanation squares well with the carbohydrate hypothesis of disease.  In short, excess chronic intake of glucose leaves too much sugar in the blood stream at abnormally long durations, which creates more glycated proteins, and keeps insulin degrading enzymes busy with too much insulin.  When IDEs are not working on insulin, they help to scavenge the bits of material that become amyloid plaques in Alzheimer's patients. 

So the study shows a correlation between regular exercisers and reduced incidence of Alzheimer's in those with the genetic predisposition.  The walking is likely to either be the result of someone that does not eat too much carbohydrate, or if they do, they are disciplined about other health efforts (IE, eat too many carbs because the health authorities told them to do so, and they comply with a large number of elements of a healthy lifestyle).  Or, it could just be that the consistent walking helps to regulate blood glucose levels even in those that over-carb themselves.

If this article hits close to home, have a look, it is a good read.