Firstly, genetic findings are only in minor part about prediction. The main hope is in understanding cause so that the disease can be disrupted. APOE4 has been a major contributer to that. Quite frankly the amyloid hypothesis looks right and the next wave of treatments are starting to hit trials now. Are they going to work? That’s why we have trials.

Now, as to this finding. It comes out of a new wave of genetic methodology, the genome wide association study (GWAS). The idea with these is that you can look at the kinds of common genetic variants we all share in large groups of people with disease and large groups without. To do it properly takes tens of thousands of people, as was done here. The problem is that the things you find are common in everybody. The changes here are seen in 22% of people with Alzheimers and 18% of people without. In essence, although the association can be robust (and this one is on the borderline in terms of p-value) the magnitude of effect is pretty small. On a good day these things give you a new potential pathway. Usually, as here, they spend a bomb to reconfirm what you know about mechanism.

Oddly enough, some of the best work in the world on Alzheimers is done in Melbourne by a group led by Colin Masters. Expect big breakthroughs in the next decade or so.

I’ve read that paper, it is one in a long list of papers pointing out the potential for cannabinoids to inhibit the formation of protein tangles. What is not well known is that the two principal cannabinoids, THC and cannabidiol, are such powerful antioxidants that they outperform vitamins C and E. The great advantage is that cannabinoids are fat soluble and very safe.

I love the cheeky title of that paper you cited, I could just see the minions rushing to read the latest paper proclaiming that pot causing Alz!

For those worried about the psychoactive effects, cannabidiol is a good alternative as it targets the CB2 receptor, found mostly on immune cells and microglia. Via this receptor cannabidiol has potent anti-inflammatory properties.

As to the genetic studies, don’t pay much heed to that.

When I first saw the headlines about the linking of marijuana with dementia I heaved a sigh of relief since I wouldn’t know one end of a reefer from the other. But no, it seems that marijuana is good for preventing dementia and I should have been smoking it. So where do you get it?

Knowing that exercise is good for preventing the big A. I’ve conscientiously kept on dancing, in fact done rather more of it in my latter years than in my baptist bound youth.

So whoopee! Let’s go for it and become the wild, cafeeine addicted, joint smoking, beepoppers we should have been way back in the fifties and sixties. Not to forget that flagon of red, either. The older I get the better I feel.

http://icanhascheezburger.files.wordpress.com/2009/08/funny-pictures-cat-eats-flower.jpg

More mundane protective factors are level of education and exercise.

Though personally I’ve had a fairly sober view of genetic science proclamations. Ever since learning one of the first insights in the field was that less than 5% of our DNA was intelligible (at the time) genes, so everything else must be ‘junk’?
As if the natural system lying at the very heart of life was >95% redundant?
Now we know that this ‘junk’ DNA is not junk at all really.
We now have epigenetics, proteomics etc as well, as new fields to try and cover the complexity of the self-regulating, self-reproducing distributed interactive biological system that is DNA and multi-cellular life.
Seems the reality to dream ratio is high in this area, with a vast sea of data making everything more complex to comprehend really.
The ultimate puzzle, ourselves, life.
Anyone who thinks otherwise is kidding as far as I can see.
.
Perhaps it’s time to reconsider an older remedy, with recently proven biological action as a CNS anti-inflammatory and anti-amyloid.
Aside from a long (5,000 yrs+) history of use in nervous afflictions, epidemiological studies amongst now ageing baby boomers suggested there was a dose related protective effect from cannabis use for dementia.
So a few scientists put it to the test in a few ways, and have found it to be a potent inhibitor of the beta-amyloid plaques found in alzheimer’s. Along with numerous other effects directly related to our endo-cannabinoid receptors, which are widely distributed and involved in neurological-immune system communication. MS, motor neurone and many other CNS degenerative conditions are being investigated as well.
“Cannabis alzheimer’s” search at google scholar will turn up >11,000 hits alone these days.
As I’m sure we just about all know from experience, THC does cross the blood brain barrier and get to where it’s needed.
It might be a question, why, how?
To which I could only answer, well it just is, it seems.
.
From one recent paper
A Molecular Link between the Active Component of Marijuana and Alzheimer’s Disease Pathology, Molecular Pharmaceutics, 3 (6), pp 773–777, 2006
.
“Alzheimer’s disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer’s disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients and reduce the health care costs attributable to Alzheimer’s disease. Here, we demonstrate that the active component of marijuana, ?9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid ?-peptide (A?) aggregation, the key pathological marker of Alzheimer’s disease. Computational modeling of the THC?AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer’s disease, THC is a considerably superior inhibitor of A? aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.”