A study finds that caffeine reduces the effects of Alzheimer's in a mouse model. It appears that along with cognitive tests, there was a 50% reduction in levels of the beta amyloid protein, hinting towards some form of mechanism.
http://news.bbc.co.uk/2/hi/health/8132122.stm
I have not looked at the original paper (Pebble's area I think) and so I am just being a bit cautious taking information from journalists (even the BBC).
The question that comes to my mind is that we are generally exposed to quite high levels of caffeine on a daily basis. Presumably Alzheimer's patients are exposed like the rest of us and so if this study proves to be positive in humans, I wonder what impact the background levels are already having.
Frankly, I've given up worrying about the health benefits or dangers from particular foods. Each report of a benefit is usually followed by one concerning a risk (e.g. eating more of food X will reduce your cancer risk but increase your stroke risk, or consuming some of drink Y has a positive effect, but more of it is harmful, and so on). So I just eat and drink what I enjoy in moderation, ensuring that lots of veg and fruit is included, and don't bother with any other advice.
There have been only 24 publications on caffine and alzheimer's over the past 20 years, mainly reviews and mechanistic considerations. Arendash appears to be referring to this 3 year old paper. Cannot get at the original at present, so it is possible that the article refers to unpublished data.
My main thought is that if only we were treating mice, drug development would be so much easier. The main problem is that almost everything seems to work on mice. This needs confirmation in a second model, then dose ranging studies, then clinical trials then randomised clinical trials. So for the moment I think the publicity is just a way of increasing the liklihood that his lab will get funding for further research.
Neuroscience. 2006 Nov 3;142(4):941-52. Epub 2006 Aug 28.Links
Caffeine protects Alzheimer's mice against cognitive impairment and reduces brain beta-amyloid production.
Arendash GW, Schleif W, Rezai-Zadeh K, Jackson EK, Zacharia LC, Cracchiolo JR, Shippy D, Tan J.
The Byrd Alzheimer's Center and Research Institute, Tampa, FL 33647, USA. arendash@cas.usf.edu
A recent epidemiological study suggested that higher caffeine intake over decades reduces the risk of Alzheimer's disease (AD). The present study sought to determine any long-term protective effects of dietary caffeine intake in a controlled longitudinal study involving AD transgenic mice. Caffeine (an adenosine receptor antagonist) was added to the drinking water of amyloid precursor protein, Swedish mutation (APPsw) transgenic (Tg) mice between 4 and 9 months of age, with behavioral testing done during the final 6 weeks of treatment. The average daily intake of caffeine per mouse (1.5 mg) was the human equivalent of 500 mg caffeine, the amount typically found in five cups of coffee per day. Across multiple cognitive tasks of spatial learning/reference memory, working memory, and recognition/identification, Tg mice given caffeine performed significantly better than Tg control mice and similar to non-transgenic controls. In both behaviorally-tested and aged Tg mice, long-term caffeine administration resulted in lower hippocampal beta-amyloid (Abeta) levels. Expression of both Presenilin 1 (PS1) and beta-secretase (BACE) was reduced in caffeine-treated Tg mice, indicating decreased Abeta production as a likely mechanism of caffeine's cognitive protection. The ability of caffeine to reduce Abeta production was confirmed in SweAPP N2a neuronal cultures, wherein concentration-dependent decreases in both Abeta1-40 and Abeta1-42 were observed. Although adenosine A(1) or A(2A) receptor densities in cortex or hippocampus were not affected by caffeine treatment, brain adenosine levels in Tg mice were restored back to normal by dietary caffeine and could be involved in the cognitive protection provided by caffeine. Our data demonstrate that moderate daily intake of caffeine may delay or reduce the risk of AD.
I love coffee, freshly ground, strong and milky! I'm busy guzzling my 4th espresso measure so I'm believing the above news - mostly because it makes me happy and happy has all kinds of health benefits. Ok, I know it's unlikely to go unchallenged for long but it's still good enough to give me an extra smile!
Ben Goldacre spoke on the falacy of this position at his recent pub meeting.Originally Posted by Tony Williams
He, roughly (I'm working from drunken memory here), said that there is a broad consensus amongst experts on most foods and drinks and how good/harmful they are. However, every time a new paper is published journalists look for a headline scare story and frequently completely misrepresent the paper. Thus the public are left with the false impression that scientists/doctors are constantly changing their minds, which is far from the truth.
This leads people to ignore very sensible health advice on the grounds that the batty boffins will only change their advice again next year. This leads to preventable ill health and early death.
Although your eating habits do sound quite sensible.
A little misunderstanding is creeping into the debate I think. The study was on caffeine, not coffee. I think that the coffee part was journalistic illustrative license. And caffeine, of course, has well known and well studied pharmacological effects. I don't disagree with the skepticism on the health effects of certain foods, but in this case I believe we are talking about caffeine as being the active compound, just like any other drug - the fact it is in certain food stuffs is co-incidental.
(The trap of course is that the "herbal lobby" quote these sorts of studies as evidence for natural remedies and that's a whole different argument. Given the myriad of organic chemicals in the plant kingdom alone, if none of them were pharmacologically active, then I think that would be evidence that there was a god).
I must go through Pebbles critique in more detail (thanks Pebble). The point about mice (or rats come to that) is well taken. It is has almost become a cliche to say that we have cured laboratory rats of cancer. However modern therapies start off in animal models and the models have become more sophisticated in recent times. The mouse model in this particular study was one developed for the study of Alzhheimer's. Having said all that, I agree we should not get too excited until we see human data.
As a bit of an aside, caffeine is used to test for the activity of a certain enzyme in the body (CYP 1A2). It is commonly used in vitro but enzymic and pharmacokinetic studies with caffeine in humans are notoriously difficult to control simply because we are exposed on a daily basis and it's difficult to separate background from the dose being studied. If caffeine does turn out to be active against Alzheimer's (admittedly that's a big if at present) I just wonder what pharmacological action there is from the background levels. All very speculative I accept.
A news item that will be of interest I have left the links on, but still not sure I’d want to know but then again I prefer the unadorned facts to being deluded.
New tests may help spot early-stage Alzheimer's
http://www.newsdaily.com/stories/tre56d11l-us-alzheimers-diagnosis/
CHICAGO, July 14, 2009 (Reuters) — New tests assessing brain changes and body chemistry are showing promise at diagnosing Alzheimer's disease in its earliest stages, aiding the search for new drugs, researchers said on Tuesday.
In one study, Irish researchers found scans measuring brain volume and a combination of memory tests accurately identified nearly 95 percent of people who had progressed from mild cognitive impairment to early Alzheimer's disease.
In another study, U.S. researchers found that a type of brain scan that measures glucose combined with low scores on memory tests was a strong predictor of disease progression.
The findings, presented at an Alzheimer's Association meeting in Vienna, Austria, are some of the first from a five-year, $60 million study aimed at identifying brain changes that signal the advance of Alzheimer's disease.
"The idea is if there could be biological markers identified that tracked what was going on in the brain, this would give you a better idea of whether a drug was having a biological effect," Neil Buckholtz, who heads the U.S. National Institute on Aging's Alzheimer's Disease Neuroimaging Initiative, or ADNI, said in a telephone interview.
NIC5-15 is a natural compound so what do us normal mortals call this natural compound. Ok I’ve looked it up you get it from pine cones with a fresh zesty fragrance. Not only pine freshness but a cure as well very versatile.
New Alzheimer's Disease Treatment Promising
http://www.sciencedaily.com/releases/2009/07/090712145228.htm
Researchers at Mount Sinai School of Medicine have found that a compound called NIC5-15, might be a safe and effective treatment to stabilize cognitive performance in patients with mild to moderate Alzheimer's disease. The two investigators, Giulio Maria Pasinetti, M.D., Ph.D. , and Hillel Grossman, M.D., presented Phase IIA preliminary clinical findings at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease (ICAD) in Vienna on July 12.
NIC5-15's potential to preserve cognitive performance will be further evaluated in a Phase IIB clinical trial. Early evidence suggests that NIC5-15 is a safe and tolerable natural compound that may reduce the progression of Alzheimer's disease-related dementia by preventing the formation of beta-amyloid plaque, a waxy substance that accumulates between brain cells and impacts cognitive function.
"With Alzheimer's disease affecting 5.2 million Americans, another 5 million with early-state disease, and nearly a half million new cases reported annually, treatments like NIC5-15 would make a significant difference in the lives of many Alzheimer's patients," said Dr. Pasinetti, Professor of Psychiatry, Professor of Neuroscience and Professor of Geriatrics and Adult Development, in the Department of Psychiatry at Mount Sinai School of Medicine. "We are hopeful that the follow up clinical study will support this preliminary evidence."
Disclosure: Dr. Pasinetti has a patent pending for the use of NIC5-15 in the treatment of Alzheimer's disease. The patent application was filed on his behalf by the Mount Sinai School of Medicine. Dr. Pasinetti and the School of Medicine could benefit financially from the results of this trial.
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