Author Topic: Missing Link to Alzheimer's?  (Read 36030 times)

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Richard Myers

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Missing Link to Alzheimer's?
« on: February 16, 2004, 03:57:00 PM »
Italian scientists have discovered what appears to be a new form of Mad Cow disease in cattle. We have been concerned for some time that CJD that is said to be sporadic and not caused by eating diseased animals is in fact transmitted from diseased animals.

Both the human and cattle diseases cause holes to form in the brain. The Italian researchers found that, in addition to the holes, two cows had an accumulation of amyloid plaque in their brains. Amyloid plaques are an indication of Alzheimer's Disease in humans. They have also been found in people with sporadic CJD but had not been found in cattle.

This is the first scientific indication that I have come across that reveals a possible connection between Alzheimer's Disease and infections in animals. This information ought to cause great concern to those who are still eating animal products.

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JimB

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Missing Link to Alzheimer's?
« Reply #1 on: February 17, 2004, 04:48:00 AM »
If you don't have to eat it but simply be exposed to animals, it would interesting to see a study done to see if farmers and/or veternarians have a higher rate of these kinds of diseases.
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Richard Myers

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« Reply #2 on: February 17, 2004, 05:19:00 PM »
Brother Jim, the infectious agent, as I understand does not have to be ingested. My guess is that the amount of infective agent is increased considerably when it is eaten versus a vet who may or may not come in direct contact with infectious material. I don't think there is any question about the infective nature of the prions and that it can infect in many ways that would allow it access to the blood stream.
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Richard Myers

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« Reply #3 on: January 30, 2005, 08:24:00 PM »
Many have wondered how their loved ones developed Ahlzeimers. Like sporadic CJD it just happens or it is the result of aluminum. No, neither of these diseases just happen an no, aluminum cannot be shown to cause it. I have suspected for a long time that both diseases come from eating the flesh or products of animals with spongiform disease.

We now have found "mad cows" with lesions similar to the ones found in Ahlzeimer patients. I believe this is the evidence we needed to begin to discuss a relationship between the two. Sporadic CJD and Ahlzeimers are caused, they don't just happen. I believe we shall soon find out that they are both caused by infections from animals with a spongiform disease.

I have been looking for the evidence of such a connection for some time. Today, I believe I have found it. There are those who have been aware of this for over thirty years. It is sad that the public has not been informed.

Almost thirty years ago the Agricultural Research Council (ARC) at its meeting on October 12, 1976 stated "The USDA concluded that it could 'no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or renderng plants.' (ARC 84/77).The problem is emphasized by the finding that some strains of scrapie produce lesions identical to the ones which characterise the human dementias."

It is very interesting to note that we see here something that ought to interest us all. That the lesions in human dementia (Ahlzeimers) correspond to the lesions produced by scrapie is the "smoking gun" that I believe will be found to explain a cause of Ahlzeimers.

Those who have concern and love for humanity need to take this information to heart. There is no safety in eating the flesh of animals nor in eating any animal product. The government is not to be trusted when it comes to our health. They have other concerns that compete with human and animal health.

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Richard Myers

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Missing Link to Alzheimer's?
« Reply #4 on: April 20, 2006, 09:22:00 PM »
For many years I have suspected that Scrapie and BSE along with other TSEs are the cause of Alzheimer's. When the study found the amyloid plaques in the mad cows that was enough for me to say the evidence is rather significant.

Now, we have a human that manifests the amyloid plaques and he was diagnosed with CJD, the human form of mad cow disease. Yes, many would like to point to another "unknown" cause of the plaques, but the evidence is very suggestive that we have another link to the cause of Alzheimer's.

"We report the case of a 28 year old man who had received a cadaverous dura mater graft after a traumatic open skull fracture with tearing of the dura at the age of 5 years. A clinical suspicion of Creutzfeldt-Jakob disease (CJD) was confirmed by a brain biopsy 5 months prior to death and by autopsy, thus warranting the diagnosis of iatrogenic CJD (iCJD) according to WHO criteria. Immunohistochemistry showed widespread cortical depositions of disease associated prion protein (PrPsc) in a synaptic pattern, and western blot analysis identified PrPsc of type 2A according to Parchi et al. Surprisingly, we found Alzheimer-type senile plaques and cerebral amyloid angiopathy in widespread areas of the brain. Plaque-type and vascular amyloid was immunohistochemically identified as deposits of beta-A4 peptide. CERAD criteria for diagnosis of definite Alzheimer’s disease (AD) were met in the absence of neurofibrillar tangles or alpha-synuclein immunoreactive inclusions. There was no family history of AD, CJD, or any other neurological disease, and genetic analysis showed no disease specific mutations of the prion protein, presenilin 1 and 2, or amyloid precursor protein genes. This case represents (a) the iCJD case with the longest incubation time after dural grafting reported so far, (b) the youngest documented patient with concomitant CJD and Alzheimer-type neuropathology to date, (c) the first description of Alzheimer-type changes in iCJD, and (d) the second case of iCJD in Austria. Despite the young patient age, the Alzheimer-type changes may be an incidental finding, possibly related to the childhood trauma." Journal of Neurology, Neurosurgery, and Psychiatry 2006;77:413-416;doi:10.1136/jnnp.2005.070805
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[This message has been edited by Richard Myers (edited 04-20-2006).]

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Michelle

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« Reply #5 on: April 20, 2006, 10:20:00 PM »
So what do we say about vegetarians who get Alzheimers?  Is there a study following this line of reasoning?  Is there an anecdotal evidence of vegans not being susceptible?  Or of vegans who have developed Alzheimers?

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« Reply #6 on: April 21, 2006, 04:04:00 AM »
Hi Michelle:

According to what I have read this morning the link between vegetarians an Alzeimers disease seems to be grounded around low B12.

The statistics states though there is a far more link between Alzeimer's with meat than with vegetarians. Also the link with cholesteral, diabetes and blood pressure problems with meat was even higher of Alzeimer's disease found.

There was also a study that said there was a higher risk of Alzeimer's with those that consumed a high amount of soy products.

No question about it, there is much confusion and no sure answer regarding any of this and the Alzeimer's Association says there have been no conclusive study regarding what really causes Alzeimer in people. They even state there is a genetic factor link to this disease as well.

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Richard Myers

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« Reply #7 on: April 21, 2006, 10:46:00 AM »
Sister Michelle, that is a good question. It is one that we need to consider when trying to pinpoint the causes of such dreaded diseases.

In the case of CJD, the human form of BSE (mad cow)we know that the route of transmission is more than just diet. So, the same would hold true with Alzheimer's. If it is indeed infectious, then it is not just the diet that can infect the person.

It is my understanding that the prions are highly infectious. One of my concerns is that they have gotten into many products that people are not aware of. There are strict vegetarians that have eaten candy made with gelatin. And there are strict vegetarians that have taken vitamins and other supplements in capsuls made with gelatin. Gelatin is a very high risk matertial that was allowed into the U.S. from England when the BSE problem was at its  height.

Since the manufacturing of the products that may contain this infectious prion never reaches temperatures that can inactivate the infectious nature of the material, we can be exposed to many products that may contain them.

A route of transmission that concerns me that I feel is a high risk, especially to children is pet food. We have reached the point in this world's history where we must move beyond not eating infected animal products, but take greater care in coming into contact with them. Cleanliness has never been more important.

Another route of transmission of disease that is becoming more of a problem is our water supply. BSE and other TSEs including Chronic Wasting Disease is a threat to our water supply. Much drinking water comes from surface sources such as rivers and streams. They are all contaminated to various degrees from many infectious materials. But, TSEs is not a subject that I have heard discussed by those responsible for water treatment. It appears to me to be a very serious health threat.

Chronic wasting disease (mad cow disease in deer and elk) is spreading rapidly throughout the U.S. It must be in about half the states now and moving quickly into those not infected. Cattle are infected with BSE and they pose a problem for our water supply, but I see deer and elk as a great risk also. One of the suspected routes of transmission amongst the deer and elk is thought to be urine. While the risk appears to be very low from water supplies, I don't think we can ignore the risk.

As an example, ecoli is another very infectious disease that comes from cattle. Does it pose a risk to our water supply? You bet it does. If you live in Canada or the U.S. and there are cattle in the neighborhood. If your source of water is a well, then you need to get it tested regularly. It is a very deadly disease for humans, especially the elderly and the young.

Ecoli is easily treated in the water, but not so prions that are infectious. I takes higher amounts of chemicals to inactivate the infectious nature and these levels are too high for the safe drinking water. It is a bridge that soon we shall have to deal with as the epidemic of TSEs continues to grow.

If we believe that Jesus is soon to return, and I do, then we can expect to see much pestilence. When we love the Lord and give our hearts to Him, He gives us wisdom and power. The wisdom is the light He has given in these matters regarding the infectious nature of animal products. The power is given to walk in that light in spite of our depraved appetites.

We ought not to fear when we have done all that we can do. We have this promise: "I will say of the LORD, He is my refuge and my fortress: my God; in him will I trust. Surely he shall deliver thee from the snare of the fowler, and from the noisome pestilence.  He shall cover thee with his feathers, and under his wings shalt thou trust: his truth shall be thy shield and buckler.  Thou shalt not be afraid for the terror by night; nor for the arrow that flieth by day;  Nor for the pestilence that walketh in darkness; nor for the destruction that wasteth at noonday. A thousand shall fall at thy side, and ten thousand at thy right hand; but it shall not come nigh thee."

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Curt

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Missing Link to Alzheimer's?
« Reply #8 on: May 06, 2006, 01:58:00 PM »

Alzheimer's Theory Set for Drug Test (Diabetes Link)
May 3, 2006

WASHINGTON (AP) -- A provocative new theory suggests that one root cause of Alzheimer's disease is linked to diabetes -- a theory about to be tested in thousands of Alzheimer's patients given the diabetes drug Avandia in hopes of slowing brain decay.

It's a scary scenario: Alzheimer's already is expected to skyrocket as the population grays, rising from 4.5 million sufferers today to a staggering 14 million by 2050. If the new theory is right, the nation's current obesity-fueled epidemic of Type 2 diabetes could worsen that toll.

But proponents see potential good news: If diabetic-like changes in the way brain cells use sugar to generate energy truly trigger Alzheimer's in at least some patients, then maybe doctors could intervene early and slow down that degeneration.

A preliminary experiment involving 511 Alzheimer's patients found signals that Avandia might help -- albeit in people who lack a gene that spurs more aggressive Alzheimer's.

Those results, combined with other evidence that the diabetes pathway is important, have Avandia maker GlaxoSmithKline poised to open three Phase III clinical trials this summer to test whether the diabetes drug, also called rosiglitazone, might protect certain patients' brains.

Diabetes has long been listed a risk factor for Alzheimer's later in life because it damages blood vessels that supply the brain.

The Avandia research suggests a more insidious connection: that Alzheimer's can be silently triggered when brain cells can't properly use their main fuel, sugar -- just as Type 2 diabetes is triggered when insulin gradually loses its ability to process sugar body-wide.

"When they're in an insulin-resistant state, it does not just affect the body, it affects the brain as well," explains Suzanne Craft of the Veterans Affairs Puget Sound Health Care System, who led the initial research.

There are 18 million Type 2 diabetics, considered to have two to five times a non-diabetic's risk of developing Alzheimer's -- if they live long enough, into the 60s and 70s when Alzheimer's typically strikes, Craft says. Type 2 diabetes often leads to heart disease or other ailments that kill before then.

Avandia, and the competing drug Actos, treat Type 2 diabetes by resensitizing the body to insulin.

Don't use Avandia for Alzheimer's until that question is settled, cautions Glaxo's Allen Roses, a highly regarded Alzheimer's researcher who, before joining the pharmaceutical company, discovered the brain disease's main genetic link.

He published the diabetes hypothesis in the medical journal Alzheimer's & Dementia last week.

If it pans out, "one thing we can do is, possibly, slow down the onset of the disease showing up," Roses says. But for now, "it's a hopeful experiment that's in progress."

Yet it's generating intense interest.

"This is an exciting new approach," Yadong Huang of the University of California, San Francisco, wrote in an accompanying review of Roses' hypothesis, which is backed by genetics research from Huang's own lab.

"I don't think this is hype for rosiglitazone," adds Dr. Sam Gandy, director of the Farber Institute for Neurosciences at Philadelphia's Thomas Jefferson University and an Alzheimer's Association spokesman. "This does dovetail with some existing knowledge."

No one knows what causes Alzheimer's creeping brain degeneration. Today's drugs only temporarily help symptoms. Now, researchers are hunting new ones that target the disease's hallmark, a sticky gunk called beta-amyloid that clogs up, and probably kills, neurons.

The new theory: The metabolism of neurons' internal power factors, called mitochondria, go awry so that those cells don't use enough sugar. That eventually leads to impaired brain cell function, including the buildup of that gunky beta-amyloid. It also means that neurons in youth and middle age don't sprout enough communication connections, providing less "cognitive reserve" once their neurons start dying off.

Among the evidence Roses cites:

   * Decades before dementia symptoms begin, PET scans of people who carry an Alzheimer's-linked gene show their brain cells underuse sugar.
   * Mice engineered to develop Alzheimer's-like disease experience the metabolism changes before beta-amyloid plaques appear -- and insulin-sensitizing drugs enhance their brains' sugar use.
   * Researchers who tracked 140,000 diabetic veterans found those who received insulin-resensitizing drugs were less likely to be diagnosed with Alzheimer's years later.

Then there's that preliminary Avandia study. Alzheimer's patients showed modest improvement in cognitive function -- unless they carried the Alzheimer's-linked gene called ApoE4 that spurs more aggressive disease. The new studies will try to prove if that benefit was real.

Copyright 2006 The Associated Press. All rights reserved.
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stephen

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Missing Link to Alzheimer's?
« Reply #9 on: May 10, 2006, 09:46:00 PM »
It is thought that the same spongiform bacteria is responsible for the increase in Lou Gherig's Disease also.  That spongiform bacteria is called Mad Cow in cattle.  It is called Chronic Wasting Disease in Deer.  It is also found in swine, sheep, goats.  It goes by a different name in each species.  There have been deaths caused by this bacteria in humans but under a different name.  A dentist told me of one death last year here in Michigan.  Two physician friends told me of two cases last summer in northern Michigan.  I don't remember the name it was diagnosed by.  But one thing for sure, the US Beef Industry is a powerful lobby and the people are not going to be informed too much.  At the same time people are dying and more is known about the links between this disease and the likes of alzheimers and LGD, etc., our government is very interested in opening foreign markets more to US Beef.  Don't expect much warning of food borne plagues from government agencies!

Another interesting link is that the further you go from the equator, the higher the incidence of Multiple Sclerosis and Lupus.  Also, the further you go from the equator the more the normal diet includes animal protein.  Those who live at the equator or closer to it eat mainly fruit, vegetables, and nuts.

Further, a study has been underway for close to fifty years on MS patients.  According to Doctor Skank, an MS researcher who has now left his practice to another doctor, all of the MS patients he treated with medications and drugs were either dead or wheel chair bound within ten years.  95% of the patients who followed a special diet, no medications, had no progression of the disease in fourty years!  That 'special diet' was a vegan diet.  No animal protein.  No casein, no whey either.  (Casein and whey are dairy products)  

I have heard of a possible link between the Bovine Growth Hormone and the increase in diabetes, too.  It seems the BGH acts upon the natural insulin in humans.  This hormone was given to dairy cattle to promote higher milk production.  Strangly, at the same time they were promoting the use of BGH, the government was paying farmers to cull their dairy herds, slaughter the cattle because of a milk glut!  Does that make any sense??

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Richard Myers

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Missing Link to Alzheimer's?
« Reply #10 on: June 06, 2006, 08:07:00 PM »
It is being reported that the USDA is saying that the U.S. mad cows had atypical BSE. Well, how about that! Seems to me that there may be two smoking guns.

For those who still don't mind eating animal products, I am sure you are following this closely, at least for your children's and grandchildren's sake.

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Richard Myers

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« Reply #11 on: June 06, 2006, 08:09:00 PM »
Oh, btw, don't expect to find this on the front page of today's newspaper or on your television network news. I don't think it will be there for some reason.
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Richard Myers

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« Reply #12 on: June 06, 2006, 08:47:00 PM »
Some are calling this BSE in the US a "new strain". It has a longer incubation time than the mad cow disease in England. 2+2 ummm. You mean that it would take longer to manifest the disease? ummmm. Like instead of getting CJD or maybe Alzheimers at 25 to 35 you would come down at say age 60 or 70?

Very interesting!

Oh, and there is another difference with the American mad cows. It was originally detected through active surveillance of live animals rather than during inspection of a suspect fallen animal. ummm. Maybe slaughtering live cows that don't look sick may be a problem? I guess Japan thinks so since they won't take our beef and they test every single cow they slaughter to see if it has BSE.

For those who have been given great light, it seems to shining ever brighter. We ought to walk in it even as He walked.

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Richard Myers

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« Reply #13 on: June 08, 2006, 04:45:00 PM »
There is a chinese scientist who has made a very important discovery. He discovered a similar pattern of amino acids in the prion protein and the amyloid precursor protein: a reductive amino acid followed by three non-reductive amino acids. He says "This suggests a common molecular mechanism underlying the initiation stages of sporadic Alzheimer's disease and both sporadic and genetic prion diseases..." Don't you just really see the lie in "sporadic"? It just happens!

Now, it seems that the evidence is building. And, if Alzheimer's is indeed caused by eating infected animal products, then we have a world-wide problem regarding the use of animal products as food. Don't suppose that God's messenger is being confirmed?

When we accept what God has said and use it for the foundation of our studies, we shall be given wisdom that surpasses that of those in the world who reject God and His Word. Does this surprise anyone?

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Richard Myers

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Missing Link to Alzheimer's?
« Reply #14 on: June 03, 2007, 09:27:00 AM »
We are at the leading edge of science regarding the health of humans. While infectious disease is rampant in the world, few understand the relationship to the injesting of animal products. It is so very sad that God's church has not warned the world, but instead has followed their ways in suggesting a diet composed of animal products is necessary.

Here is another little glimpse into the truth and where we are headed:

At a recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.

In other words the evidence is building that "sporadic" is not sporadic, but rather infectious from coming in contact with animals, most likely the eating of animals that have a spongiform disease. This more than likely will prove to be the source of Alzheimer's also.

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Mimi

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« Reply #15 on: June 04, 2007, 05:48:00 PM »
This is big!
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Curt

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« Reply #16 on: June 08, 2007, 06:46:00 PM »
The scientific community is still baffled about the possible cause of Alzheimers. Today's report points towards a particular Genetic abnormality common in Anzheimer patients which hwas isolated by a computer program on several gene samples.

It is my personal opinion that sometimes the genetic relationships is a case of mapping the result rather than the cause.

Here is today's medical report.

******************************************  
Scientists Find Gene Link to Alzheimer's
June 8, 2007

PHOENIX (AP) -- A team of Arizona researchers think they've found a gene that could help better predict a person's risk of developing Alzheimer's disease.

The gene -- called GAB2 -- seems to affect the odds that some people will get the progressive neurological disease that afflicts about 5 million Americans, according to the research team led by the Translational Genomics Research Institute and Banner Alzheimer's Institute.

"This is a major breakthrough in Alzheimer's genetic research that will have an impact on the clinical treatment of the disease," said Dr. Dietrich Stephan, director of TGen's neurogenomics division.

Researchers here believe the study marks a new milestone for genetic research of Alzheimer's disease because it used a high-powered computer chip to measure more than a half-million genetic variations, the most robust such study to date.

Alzheimer's triggers memory lapses, clouds the thought process and leads to confusion and death in older adults.

About 78,000 Arizonans suffered from Alzheimer's in 2000, a number expected to jump to 130,000 by 2025, according to Banner Alzheimer's Institute.

Researchers worldwide are not sure what causes the disease. They do know that sufferers' brains are harmed by plaques and tangles that block signals and ultimately cause cells to shrink and die.

TGen's Stephan began investigating the possibility of conducting an ambitious study of the disease three years ago.

He sought funding from the Kronos Science Laboratory in Phoenix, which provided most of the money for the $5 million project.

In turn, Kronos secured the intellectual property rights from the Arizona study and is seeking patent protection for the GAB2 gene and its role in the onset of Alzheimer's.

The study is the latest to draw national attention for the gene investigators at TGen, which launched here five years ago as part of a push to build Arizona's research prowess.

Other significant studies conducted by TGen and collaborators in Arizona include genetic tests relating to pancreatic cancer and amyotrophic lateral sclerosis, also known as Lou Gehrig's disease.

Copyright 2007 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

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Richard Myers

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« Reply #17 on: June 08, 2007, 09:43:00 PM »
I think that genetics plays a part in the ease with which disease may find a foothold. But, it is an excuse to a large degree for poor lifestyle. Drink alcohol and you will suffer. Some more than others. The solution is not to use stem cells, but to refuse to drink.
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Curt

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« Reply #18 on: June 12, 2007, 06:20:00 AM »
New research out today shows that treating the Heart related symptoms can assist in controlling the degeneration caused by Alzeimhers. So, even a non-drug approach to controlling high blood pressure and cholesterol can help.

*********************************
   
Heart Disease Treatments May Slow Alzheimer's
June 11, 2007

(USA TODAY) -- Treatment of cardiovascular risk factors such as high blood pressure might slow the progression of Alzheimer's, the incurable brain disease that causes memory loss and confusion in millions of people.

That's the conclusion from a study presented Sunday at the second Alzheimer's Association International Conference on the Prevention of Dementia in Washington, D.C. The findings add to growing evidence suggesting that reducing the risk of heart disease might also shield the brain from a disease that will skyrocket in the coming decades.

If nothing is done to stop the explosion of cases, Alzheimer's worldwide will quadruple from 26.6 million to more than 100 million by 2050, according to a second study presented at the meeting by Ron Brookmeyer, a researcher at the Johns Hopkins Bloomberg School of Public Health.

Previous research had suggested that treatment of high cholesterol and high blood pressure might help prevent Alzheimer's in healthy people. A study at the meeting now suggests that such treatment might actually slow the progression of established disease.

Yan Deschaintre of the Memory Center in Lille, France, studied 891 dementia patients, including people with Alzheimer's. His team gave patients a test that measures thinking ability at the start of the study and then again four years later. The team noted whether patients got treatment during that four-year period for high blood pressure, high blood cholesterol or diabetes.

Patients who received treatment did better on the final thinking and memory test than the people who got no care.

Some doctors don't bother to treat high blood pressure or other cardiovascular risk factors in such cases because they think the treatment won't make much difference for a patient who's declining rapidly, Deschaintre says. But the new findings suggest even standard care for heart risk factors, like reducing high blood cholesterol with a drug, might help an Alzheimer's patient think a little more clearly, Deschaintre says.

A third study, also presented at the meeting, suggests that optimism and the ability to establish and carry out goals might be traits that help keep the aging brain in shape. Simon Forstmeier and colleagues at the University of Zurich in Switzerland studied 120 people ages 60 to 95. He found that seniors with a can-do attitude did better on memory and thinking tests given at the time of the study.

Forstmeier says people can be trained to be more optimistic, to regulate emotion, and to formulate and achieve goals -- all traits that might help build a brain resistant to Alzheimer's.

"We don't know if we'll be able to fully prevent Alzheimer's," Brookmeyer says. But he and other experts are urging people to take steps now that might reduce their risk: "Even a small delay in the disease will have a big impact."

Copyright 2007 USA TODAY, a division of Gannett Co. Inc.

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Richard Myers

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« Reply #19 on: September 13, 2007, 09:35:00 PM »
Here we go, another little piece of the puzzle.  

"Amid growing evidence that the same abnormal clumping of proteins in Alzheimer's disease also contributes to type-2 diabetes, scientists in New York are reporting discovery of a potent new compound that reduces formation of those so-called amyloid plaques.

The report cites evidence correlating increases in amyloid formation in the pancreas with increases in severity and rate of progression of type-2 diabetes, which affects almost 20 million Americans and is rapidly rising worldwide.

Deposits of the abnormal protein damage and destroy insulin-producing "islet" cells in the pancreas. Researchers have been seeking potential new medicines that block formation of an abnormal, misfolded protein called islet amyloid polypeptide (IAPP), which may play a key role in the cell destruction."

Ever hear of a "misfolded protein"? That is what a prion is. Prions are what cause Mad Cow Disease in cows, sheep, deer, cats, and humans.  Now we that amyloid plaques are being related to "misfolded proteins".  Don't we just love mysteries as they unfold! We were warned to avoid animal products for this very reason.  

I don't know about diabetes and misfolded proteins, but I surely would like to think that we can prevent Alzheimer's by eating a strict vegetarian diet.  BTW....we have cured diabetics (type 2) with a strict vegetarian diet and exercise program.

Jesus receives His reward when we reflect His character, the fruits of the Spirit......We deny Jesus His reward when we do not.