Aug 052010
 

The story that is the subject of this blog entry talks about why higher primates do not get Alzheimer’s but human beings do. The confusion is that human beings are so similar to higher primates, scientists cannot figure out why getting Alzheimers would be different for the two species.

As usual the scientists are going on about microscopic this and that. In all stories of this type, Happeh Theory will not argue with the microscopic findings these scientists have made. The scientists probably did find what they say, and there probably is the correlation that the scientists claim to find.

The position of Happeh Theory though is that there is no need for the microscopic approach other than curiosity. There is an easier way to describe why higher primates do not get Alzheimers and human beings do.

The reason human beings get Alzheimer’s and higher primates do not, is because Alzheimers can be thought of as the cost to human beings of having the brain they do. According to Happeh Theory, the bodily changes that make a human being different from a primate, are responsible for the susceptibility of human being’s to Alzheimers.

The explanation can be given in terms of Yin Yang Theory. Higher primates would be considered to be strongly Yin. Human beings are a different combination of Yin and Yang that makes them more Yin and Yang, as opposed to mainly Yin or mainly Yang.

According to Happeh Theory, it is those differences in the Yin and Yang parts of the body that make human being’s susceptible to Alzheimer’s while primates are not susceptible to Alzheimer’s.

Human being’s get Alzheimer’s as they age because the Yin drains out of them as they get older. Since human’s are a combination of Yin and Yang, their Yin is not as strong in the first place.

Because higher primates are strongly Yin, even when they get old they are still strongly Yin, which protects their brain from Alzheimer’s.

The original news story is reprinted below

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Scientists have long noticed a curious phenomenon among primates: Humans get the devastating neurological disorder known as Alzheimer’s disease, but their closest evolutionary cousins don’t.

Even more inexplicable is the fact that chimpanzee and other non-human primate brains do get clogged with the same protein plaques that are believed by many to cause the disease in humans.

The answer to this puzzle could yield valuable insight into how Alzheimer’s develops and progresses, and now researchers report they may have a clue. They report their finding in the latest issue of the journal Neurobiology of Aging.

They found that a “tag” molecule used to track plaque build-up latches easily onto plaques in human brains but not in those of apes and monkeys, suggesting that there is a basic structural difference between the two types of plaque.

Figuring out the difference, they said, could lead to ways to render human amyloid plaques as harmless in human brains as they are in the brains of other primates.

“What this tells us, first of all, is that plaques are structurally distinct in human vs. non-human primates,” said study author Rebecca Rosen, a neuroscience doctoral candidate at the Yerkes National Primate Research Center, at Emory University in Atlanta. “Why that is is a huge question [but] now we have a tool we can use to differentiate the structure [of amyloid plaques] between humans and non-human primates.”

“We can use this [tagging compound] to characterize the toxic nature of the [amyloid plaques] in the human brain in order to understand them better,” she added. “It also confirms the usefulness of the [compound, called Pittsburgh Compound B (PIB)] for diagnosing Alzheimer’s.”

But the true significance when it comes to treating or preventing the disease remains unclear, said another expert.

“This is another finding of unknown significance, but it is a finding,” said Dr. Gary J. Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City. “None of us know why these higher primates don’t get Alzheimer’s disease, but we don’t know why humans get Alzheimer’s disease either. . . Where it leads us, I don’t know.”

Since the amino acid sequence of human amyloid protein is different from that in monkey brains, scientists hypothesized that the structure might be different.

To test this theory, Rosen and her colleagues took PIB, widely used in clinical trials to diagnose Alzheimer’s. PIB binds to amyloid deposits in live human brains, thus “lighting up” the plaques on positron-emission tomography (PET) scans.

They used PIB in brain tissue from nine deceased rhesus monkeys, six deceased squirrel monkeys, three deceased chimpanzees, nine deceased humans with end-stage Alzheimer’s and three deceased older but healthy humans.

“We were able to show that, similar to what has been seen in mouse brains, PIB does not bind with high affinity to plaque in monkey or ape brains,” Rosen said.

Another group of researchers at the Yerkes Center recently reported separately that a test involving infrared eye tracking may help pick up mild cognitive impairment in humans. The condition is sometimes a precursor to Alzheimer’s.

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