The brains of Alzheimer's patients accumulate beta-amyloid plaque. For a long time, there's been a controversy over whether the plaque is a cause or a side effect. This is tremendously important, because it will direct treatment research for a horrendous disease.
Well, now it looks like we may have resolved the chicken and egg problem:
Now, researchers have caused Alzheimer's symptoms in rats by injecting them with one particular form of beta-amyloid. Injections with other forms of beta-amyloid did not cause illness, which may explain why some people have beta-amyloid plaque in their brains but do not show disease symptoms.
I think a lot of researchers are barking up the wrong tree by not looking for a pathogenicly induced model for Alzheimers, so I'm glad that these folks have made some advances in that area.
Interestingly, Alzheimers responds somewhat to minocycline. Minocycline is a broad spectrum antibiotic capable of targeting cell wall deficient (tuburculosis-like) bacteria and penetrating the blood-brain barrier. Cell wall deficient bacteria are very small and tremendously difficult to culture. Normal bacterial cultures won't grow them. You need a blood agar culture and several months for the slow-growing bugs, and even then you can fail. So they're often ignored. Standard agar culture only grows about 1% of all bacteria, acutally, and is not an exhaustive test of anything.
That minocycline has this possitive effect suggests one of two things;
1. Some kind of cell-wall-deficient pathogen is involved in the process.
2. A prion is involved. Tetracycline class antibiotics are known for their ability to reduce inflammation. Their mechanism for reducing inflammation is still debated. However inflammation is proving to be a significant factor in prion pathogenesis and infectivity. (Though there's some evidence that repeated prion exposure over time can also lead to prion infection in the absence of some other pathogen causing the inflammation.) Further, simply blocking the body's inflammation response doesn't seem to delay alzheimers.
"Cell wall deficient bacteria are very small and tremendously difficult to culture."
This should read "Some cell wall deficient bacteria are very small..."
Some may be relatively large.
Elan pharmacueticals (ELN) is currently rising in the markets because of the phase II results of a drug that targets beta-amyloid plaque removal. Full phase II results should be available in July. The company went to phase III early because of the drugs anticipated success. Elan & Wyeth are co-developing this drug; other drugs are in development as well (by them and other companies).
It may be that many people will have drugs that can significantly help slow/combat the disease in a couple/few years.
Further evidence that animal testing is evil.
And oddly enough, smoking seems to ward off the evil Alzheimer's. Six of one, half a dozen of the other.
Smoking wards off Alzheimers?
Certainly can't argue the fact that lung cancer and emphysema significantly reduces the chances of living long enough to go senile.
It seems that both Alzheimers and Heart attacks have a similar genesis. Both involve a build-up of bacteria where they shouldn't be. Both diseases could be contributed to by a progressive weakening of the immune system with age and a subsequent progressive invasion by pathogens that find their ingress in lungs, gums and a compromised gut lining. If this is so then strategies that strengthen the immune system might help. Certain strains of probiotics, notably L. acidophilus LAFTI strain L10 and Bifidobacterium lactis LAFTI strain B94 have shown an ability to optimise production of gamma interferon if taken is sufficient quantities. This plus a range of vitamins might offer at least a partial answer.