The Disease That Robs Us of Ourselves

 

Alzheimer's graphicOne day, you try to read a book, but can’t understand the words. Later, you get lost in your own neighborhood. Eventually, you won’t recognize those you love. Your body is still there… but you’re gone.

Alzheimer’s Disease was first identified in 1906 by German scientist Alois Alzheimer. Today, the World Health Organization estimates some 18 million people suffer from the cognitive disease; this number is expected to rise to 34 million by 2025. It will have a huge impact on our society.

For those at risk, or already suffering, or caring for a sufferer, here is help and advice for preventing, delaying, and coping with Alzheimer’s, as well as information about treatments available, now and in the future.

How do you know if it’s Alzheimer’s?

Anyone can struggle, at times, to remember the title of an old movie, or the name of an acquaintance, or why they went to the fridge. But the first symptoms of Alzheimer’s Disease are more dramatic than occasional memory lapses.

People with incipient Alzheimer’s are unable to do what they’ve always done, like paying bills or counting out money for a purchase. A study published last year [2011] in the Journal of the American Medical Association calls such difficulties “the canary in the coal mine of impending dementia.” The sense of smell often diminishes before the disease is apparent. Or its onset can make people suddenly suspicious of those they have always trusted.

If you or someone you care for has such symptoms, go to your doctor for an evaluation. Usually he will test memory, using a standard cognitive test. Questions vary, but the patient might be asked to count backward from 100 by sevens, for example, or to spell common words backwards. If these tasks prove too difficult, the doctor will probably refer the patient for further tests, including a brain scan.

Although not yet widely used, spinal fluid testing is considered one of the most accurate indicators of the disease. It measures levels of the proteins involved in Alzheimer’s and, when combined with a brain scan, offers an 85 to 90 percent accurate diagnosis, says Kaj Blennow, MD, Professor in Clinical Neurochemistry at Sweden’s Sahlgren- ska University Hospital.

Treating the symptoms

If Alzheimer’s disease is diagnosed, there are several drugs that treat the symptoms, including Aricept, Exelon, and Mentamine.

These drugs may improve memory and reasoning symptoms temporarily, say several experts, but they might not work for everyone. According to Professor Blennow, “the long term outcome is not well known” and the disease will probably “catch up” in the end. “They don’t do anything to slow disease progression,” says Kurt Brunden, Ph.D., who is in charge of neurodegenerative disease drug research at the University of Pennsylvania.

Your doctor may recommend an exercise program. A few studies suggest that exercise might help slow progression of the illness, even after symptoms appear.

He might also suggest certain vitamins and other supplements. One recent study showed that when those with mild cognitive impairment took high doses of Vitamins B 12 and B 6, the vitamins “slowed the rate of shrinkage of the brain … and also slowed their cognitive decline over two years,” according to researcher A. David Smith, at the University of Oxford.

A new medical drink, Souvenaid (made up of essential nutrients including omega 3 fatty acids), is currently in clinical trials and expected to be available soon by prescription in Europe and the US. After 24 weeks, people with mild Alzheimer’s who drank Souvenaid scored better on memory tests than those who drank a placebo. Says Philip Scheltens, MD, director of the Alzheimer Center at the VU University Medical Center in Amsterdam, “The combination of essential nutrients is better than each of them alone.”

Research failures may lead to success

Scientists often learn as much from their failures as their successes. Over the past couple of decades, most Alzheimer’s drug development has focused on trying to clear plaques of the protein amyloid from the brains of people with the disease. And most or all of those drugs, according to Dr. Wendy Noble, of King’s College, London, have failed. “We certainly haven’t heard of any good ones yet.”

The notable failure of one such vaccine was to point scientists in a new direction. In 2002 the vaccine’s clinical trial was stopped after several patients died from side effects.

More than four years later, there were no significant cognitive improvements in those participants who, over time, died from the disease. But autopsies revealed that two such patients had virtually no plaques in their brains. So although the vaccine had worked to eliminate plaques, something else had continued destroying their brains.

The something else appeared to be another protein, called tau, which tangled up inside brain cells. Despite the absence of amyloid plaques, “The tau pathology remained,” says Dr. Noble.

Scientists came to a startling conclusion: once tau tangles reach a certain point, the cell-killing process “can go on without [plaques],” says John Hardy, a professor of Neuroscience at UCL Institute of Neurology in London.

So, in order for a plaque-targeting strategy to have any chance of success, some scientists believe treatment must start at a very early stage. That means when the damage is only detectable on a brain scan, but the person appears to be functioning normally. By the time Alzheimer’s telltale confusion is apparent, the window for stopping its progression with drugs that remove plaques has probably closed.

How Alzheimer’s might be treated in the future

Thanks to the just-announced findings on how Alzheimer’s spreads, more pharmaceutical companies are likely to turn their attention to drugs that target the development of tau tangles. But only a few are actually in the pipeline, and assuming one proves safe and effective, it will take several years for it to enter the market. Here’s what Reader’s Digest has learned about drugs in this family.  

Epithilone D is much like the chemotherapy agent Taxol and was originally developed to fight cancer, says the University of Pennsylvania’s Brunden. Unlike Taxol, Epithilone D can enter the brain—essential if it’s to work against brain cell tangles. In tests on mice, Brunden’s team found that Epithilone D does exactly that, and “improves the memory loss.” According to unconfirmed reports, Bristol-Myers Squibb may be testing Epithilone D on small numbers of Alzheimer’s patients.

Noscira, a Spanish biopharmaceutical company, is currently testing its tau tangle-targeting drug Tideglusib on 308 Alzheimer’s patients at 55 hospitals in five European countries.  And Canadian company Allon’s drug Davunetide, also aimed at tau tangles, has shown promise in small studies of people with mild cognitive impairment.

Scientists are looking at Alzheimer’s from a number of perspectives, and abnormal brain proteins aren’t the only focus. They may yet discover that other factors contribute to memory loss. One such factor may be insulin, which is essential for the brain to function. Says Brunden: “It keeps neurons healthier.” People with Alzheimer’s, like those with diabetes, have lower than normal levels of insulin. Researchers in Japan, for example, found that diabetes can double your chances of getting Alzheimer’s.

This has led some researchers to try squirting insulin deep into the noses of volunteers, so that it enters the brain. In a small study in people with mild to moderate Alzheimer’s, the insulin appeared to slow the brain’s decline.

Recent research on epilepsy suggests another new direction. In February [2012], UCLA neuroscientists reported that, by stimulating electrodes implanted in the brains of patients with epilepsy, they were able to enhance memory and learning. One day such devices might be implanted in the brains of people in the early stages of Alzheimer’s, to be switched on “when they are trying to learn important information.”

Another study showed that nicotine patches increased attention span among people with mild cognitive impairment, and a nicotine-based drug is in preliminary stages of research.

Month after month, new information adds pieces to the solution of the Alzheimer’s puzzle.

There is hope.

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This article originally appeared in Reader’s Digest international editions.

Discovered: how dementia spreads

On February 2 [2012], scientists at two US universities, Columbia and Harvard, reported findings that could change the course of how we treat Alzheimer’s disease. They proved that it spreads through the brain almost like an infection: from the first brain cell affected to the one next one to it and to the next. It damages each connected cell along a predictable path, eventually destroying a person’s ability to think and remember.

Researchers have long known that the worse the symptoms, the more brain area affected. But most of the research had focused on amyloid beta protein plaques. Because they form between brain cells, scientists believed that they interfere with signals from one cell to the next. These plaques sometimes appear decades before symptoms do.

There is another protein, however, called tau, which tangles up inside cells. This is the protein that eventually kills cells. And these tau tangles seemed to show up at about the time that Alzheimer’s symptoms begin.

Still, scientists couldn’t prove how Alzheimer's actually advanced. Then the Columbia and Harvard scientists implanted abnormal human abnormal tau cells in genetically engineered mice. They watched as the tangled tau replicated, traveling from one connected cell to the next.

In nature, mice can’t produce human tau any more than they can produce human arms and legs, so the only way the tau could have spread into previously unaffected cells was from the introduced cells.

Researchers still don’t know the relationship between the plaques and tangles, but they have theories. “Perhaps the [plaque] part is like the trigger that sets off the disease and the [tangle] part is the executioner that kills the cell,” says Columbia researcher Karen Duff, Ph.D., one of those involved in the breakthrough mouse studies.

What makes these findings so important? If scientists understand how the disease progresses, they’ll know what kinds of drugs might stop it in its tracks. Such drugs should one day be able to “trap the disease when it’s in that early stage,” says Duff.

What can you do to prevent or delay dementia?

Recent research has shown “how to boost the brain’s own protective systems,” says Columbia's Karen Duff. Most of the brain-boosters involve simple lifestyle changes, some of which might be effective even after symptoms appear.

Interestingly, most of the ways scientists have identified to prevent or delay Alzheimer's—including these lifestyle brain-boosters—also reduce inflammation, thought by many to set off the cell damage that leads to the disease. For example, exercise is known to be anti-inflammatory and older adults who exercise regularly are at lower risk for cognitive decline, according to several studies.

Here's how to boost your brain's protective systems:

A diet rich in fish, fruit, nuts, and green leafy vegetables reduces chronic inflammation according to numerous studies. It also lowers Alzheimer’s risk, says a study of 2,000 adults published in April last year [2011] in Archives of Neurology.

People who regularly take non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin are also less likely to get Alzheimer's.

Coffee, as well as moderate wine consumption, seems to protect the brain, say several studies, although heavy alcohol use has the opposite effect.

The highly educated, and those who use two languages on a regular basis, tend to have lower rates of dementia. While education can neither prevent the formation of abnormal proteins, nor stop inflammation, Kaj Blennow, MD, Professor in Clinical Neurochemistry at Sweden's Sahlgren's University, says that the brains of the well educated might have enough connections to re-route around damaged areas.