March 16, 2009 - When the brazen James Watson had his genome sequenced, he declined to find out whether he carried a gene variant that would increase his risk for Alzheimer's disease. Ditto for Steven Pinker. There are virtually no treatment or prevention options for those who have or are at risk for Alzheimer's. Nor do scientists fully understand what causes it, though for years, opposing camps have duked it out over hypotheses that have focused largely on brain abnormalities called plaques and others called tangles, neither of which has so far proved a good therapeutic target.

Now some experts are proposing an avant-garde way of approaching the disease: as a form of diabetes. Some even dub it "type 3 diabetes" or "diabetes of the brain." The idea is that memory loss and cognitive deterioration in at least some Alzheimer's patients may be caused by low insulin or insulin resistance in the brain, much as lack of production or poor response to insulin in the body is central to the pathologies of type 1 and type 2 diabetes. Effective Alzheimer's treatments, then, might aim to boost brain insulin levels or decrease resistance while addressing destructive factors like inflammation and oxidative stress. If the theory holds up, as early research suggests, it could be a boon to a field scarred by disappointments and dead ends.

Alzheimer's researchers have been bitterly divided over what initially causes the disease and where to look for treatments. For years, the dominant view was that plaques -- sticky deposits of a protein called beta-amyloid -- were the central culprits, destroying neurons and causing cognitive decline. More recently, some researchers in the amyloid camp have begun to focus on toxic, soluble forms of the protein, rather than the plaques themselves, as the real instigator.

At the same time, another faction has emphasized abnormal modifications of a protein called tau that results in so-called tangles, which also turn up in brains ravaged by Alzheimer's. But neither the plaques nor the tangles seem to account fully for the onset of the disease. Plaques often appear in the brains of elderly people without Alzheimer's, and some evidence suggests that tangles form later in the disease's progression, rather than triggering it. Nor has either abnormality yet proven to be a fruitful target for new drugs. Meanwhile, the pitched battles have done damage to the field. It's been "one army against another," a prominent researcher told me. "You see them fighting at meetings," she says, and you think, "Oh, shut up. Try to come up with something that fits both." --

Follow Up

And then there's this from a friend, subsequent to the posting of the above article.

"Thanks for this valuable and precious tidbit of information. I recently read a study that used high doses of b3 (niacinamide form) on a population of rats with Alzheimer's and they had complete reversal of symptoms.

Check this out and draw your own conclusion:

Niacin and niacinamide also have different applications. It its niacinamide form, it is useful in arthritis and early-onset type I diabetes; niacin is an effective reducer of high cholesterol levels.

Niacinamide was first linked to preventing the development of diabetes in experimental animals in the 1950s, a finding confirmed in the 1980s which led to further clinical studies. Niacinamide enhances insulin secretion and increases insulin sensitivity. Evidence points to niacinamide supplements being very effective in preventing type I diabetes from progressing in some patients if given soon enough at the onset of diabetes. It does so primarily by helping restore beta cells." --