It’s 16 years since the last genetic identification of Alzheimer’s factors. This is potentially huge, as at least 1 in 4 cases of Alzheimers are known to have a strong genetic component, and it has long been suspected that other gene clusters are very important factors in the development of the disease.
The most exciting part – two of the three genes found appear to be crucial in cleaning up the protein deposits that form a type of plaque in the brain which interferes with neuronal function in cases of Alzheimer’s Disease. i.e. it could be possible to devise a form of gene therapy for people currently showing signs and symptoms of Alzheimer’s.
But even before such therapies can be developed, people who know/believe that they have a genetic predisposition to Alzheimer’s can look to other strategies to manage their risk –
Carrying mutated genes that are linked to Alzheimer’s may not ultimately result in Alzheimer’s disease. According to Dr. Colin T Campbell, a distinguished nutrition professor at Cornell University, genetics may only play a small role in the development of diseases such as Alzheimer’s and cancer. Environmental factors have the major effect on the outcome.
As a matter of fact, many studies have suggested that following a healthy diet and lifestyle, the risk for Alzheimer’s disease can be substantially reduced.
One study recently reported by foodconsumer.org found that high intake of meat, butter, high-fat dairy products, eggs, and refined sugar are more likely found in Alzheimer’s patients than healthy people.
The study was conducted by Polish scientists and reported in the April 6, 2009 issue of International Journal of Environmental Research and Public Health.
Previous studies also found that lack of dietary omega3 fatty acids and presence of high sugar levels and high cholesterol levels in the blood may increase risk of Alzheimer’s disease.
The article quoted above goes on to mention other research into dietary supplements that have demonstrated some benefits in vitro in inhibiting the aggregation of amyloid proteins into plaque formations, but that research seems to be still in the early stages; very promising nonetheless.
Other factors identified in Alzheimer’s:
- high levels of language skill in one’s twenties seems to have a protective effect against the disease (Snowdon et al 1996, Iacono et al 2009) – summary at Wired.
- an antibody has been identified in populations that do not display Alzheimer’s signs/symptoms that may lead to an immunological avenue for treatment (Relkin et al, 2008)
- daily caffeine also appears to have a measurably beneficial effect on brain function over time
As a sideline, it’s interesting how reports of this discovery identify the researchers depending on the presumed readership. The most general description mentions 80 researchers from all over the world, AFP describes a coordinated “gene trawl” taking place in seven countries. Other reports mention “British and French”, “European” or just “UK” researchers. Ain’t parochialism grand?
As someone who has had a lot of relatives with Alzheimer’s, I find this news to be very exciting. I hope that researchers can come up a preventative drug before it’s too late for me!
As someone who has had a lot of relatives with Alzheimer’s, I find this news to be very exciting. I hope that researchers can come up a preventative drug before it’s too late for me!
“I saw the future, and yea, my vision did contain an excruciatingly predictable Alzheimer’s joke in the first comment on the thread.”
I’m good at prophecy. I should turn professional.
On the serious side, this is very encouraging. The multiple strands of research into this serious form of dementia-causing disease alluded to here will hopefully continue to come together. Everyone is behind this one.
The cause may have been inflammation and cholesterol breakdown. These new genes gives Alzheimer hope.
Everyone is behind this one.
That would have been more predictable on a thread about haemorrhoids.
Oh, Helen.
I bet you’re the low-brow type that would laugh at the menu outside that Parramatta Korean restaurant. The one that says bibimbap is “…a dish served in a heated bowel, which makes it sizzle at the bottom.” Typical.
However, my grandparents were fine upstanding people, but loved toilet humour. So I suppose we should all take care not to be upstanding at the wrong time!
That spambot comment @3 was pretty perceptive though. They’re getting good, aren’t they? But why do they think anyone here would want a boat engine heater?
I should probably go and edit the spambot’s l9ink to point to an appropriate LOLcat. Any suggestions?
Good luck to them.
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.
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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.
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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
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“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, Δ9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) 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 Aβ aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.”
These genetic link stories are generally way, way, over-hyped.
More mundane protective factors are level of education and exercise.
I don’t want to be pessimistic but this sounds like another over-hyped ‘breakthrough’. We’ve known about the ApoE4 gene for more than a decade and that hasn’t really brought gene therapy treatment for Alzheimer’s much closer. And some Alzheimer’s researchers are saying these new genes aren’t really as closely associated with the disease as ApoE4.
Gene therapy sounds like a great idea but at the moment it’s only slightly more feasible than cold fusion engine power. It might work on a short term basis for some rare diseases caused by a single gene defect. But as we’ve learned, Alzheimers is linked to several gene abnormalities. It’s going to be a long time before we have the capability to deliver therapeutic DNA for multiple gene defects into the CNS so that it ’sticks’ and remedies the defect in billions of cells.
The gene might be useful as a marker of risk, like the BRCA genes in breast cancer.
As for the link with fatty foods – well, again, with a study based on 74 people, I won’t be giving up sausages just yet.
As a layperson I’m a bit bemused by the idea of avoiding fatty foods, b/c I understand (I think) that myelin is a fatty substance. But I’m just, as I say, a layperson.
TT:
http://icanhascheezburger.files.wordpress.com/2009/08/funny-pictures-cat-eats-flower.jpg
Reading all this stuff on how to avoid Alzheimers is very exciting. As an addictive personality in the now vulnerable age group I managed to give up junk food and instead obsess about getting enough fresh fruit and vegetables though I still hadn’t got off the cheese. So it’s been wonderful to discover that red wine is a plus and I still enjoy a double brie as long as I’m careful to have a glass of good red at the same time. I recently read that coffee is also a plus so I make sure I have not one, but certainly two, and sometimes three a day as recommended by the experts! That really gives me a lift.
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.
Quoll,
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.
Any research that provides additional insight into Alzheimer’s is critical to finding a cure. It is also important for patients and families affected by diseases such as Alzheimer’s to consider participating in clinical studies. One such study is the ICARA (Bapi) Study (www.icarastudy.com), whose goal is to explore if an investigational drug, called Bapineuzumab, can help slow the progression of Alzheimer’s Disease. Clinical studies that test new treatments are the best chance we have for fighting this disease. Current therapies for Alzheimer’s treat the symptoms associated with it, not the disease itself.
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.
Right, just saw this. Time for boring clinical genetic wonkery…
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.