The Dollars and Sense of Alzheimer’s

June 19, 2015

By Medical Discovery News

As people age, they begin to worry about developing dementia and its most common cause, Alzheimer’s. Alzheimer’s is a neurodegenerative disease that can affect your cognitive abilities, the ability to function in daily life, and orientation. If that’s not devastating enough, those with Alzheimer’s only live four to eight years on average after diagnosis.

In America, Alzheimer’s is the 6th leading cause of death. Today 5.1 million of those 65 or older are living with this disease, a number that is only expected to grow as the population ages – by 2050 it is projected to affect 13.5 million of those 65 or older. The few drugs readily available only moderate the symptoms, as there is no way to cure, slow, or prevent Alzheimer’s.

Recently, the Alzheimer’s Association published a report called “Changing the Trajectory of Alzheimer’s Disease: How a Treatment by 2025 Saves Lives and Dollars.” It focuses on the costs associated with a theoretical treatment that could delay the onset of Alzheimer’s for five years. If such a thing were discovered, it could have a huge impact on people’s lives and their financial.

Since Alzheimer’s is a disease of older Americans, treatments for it are mostly funded by Medicaid and Medicare. Currently, Medicare covers 80 percent of the total costs of Alzheimer’s care in America, which equates to $153 billion. By 2050, the total costs of caring for those with Alzheimer’s is expected to rise to $1.1 trillion, with Medicare allocating one-third of all its expenses to treating it.

Within the Alzheimer’s population, a higher proportion will be in severe stages of the disease by 2050, as opposed to early or moderate stages. In the early stage of the disease, people can continue everyday functions and may appear symptom-free. They do have deficits in their abilities to think and learn, but the financial impact and burden on family members are low. In the moderate stage, memory lapses, inability to express thoughts, and confusion become apparent. Finally, in the severe stage, people have trouble taking care of themselves and require extensive daily care. In 2050, almost half of those affected will be in the severe stage.

The Alzheimer’s Assocation presents a case for funding biomedical research now, before the human and economic costs can be realized. For the sake of argument, they describe a hypothetical new treatment that would delay the onset of Alzheimer’s symptoms by five years. If such a thing were available by 2025, it would save $220 billion in its first five years. By 2050, 6 million fewer people would be affected by Alzheimer’s, saving families $90 billion in healthcare costs and the federal government $367 billion. Even if such research costs $2 billion a year starting today, a way to delay Alzheimer’s by just five years would pay for itself within three years.

Research from very basic studies on the brain to translational research leading to new therapeutics and early diagnostics are desperately needed. There are many promising studies that suggest a delay in the progression or even cure for Alzheimer’s are possible.

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The Tau of Dementia

Dec. 27, 2013

By Medical Discovery News

The Tau of Dementia

All it takes is the instantaneous crash of an oncoming car. The heavy blow of a linebacker’s tackle. The explosion of a roadside bomb in Afghanistan. All these instances and more can cause traumatic brain injury (TBI). It used to be considered a one-time event, but its long-lasting impairments make it more of a chronic disease.

Sadly, there are no cures for TBI and each person experiences them in their own way. Just as each person is different, no two brain injuries are exactly alike. This makes it a very challenging condition to study and to treat. 

A silent injury, the damage of TBI is not outwardly visible, unlike a broken arm or an amputated leg. Some people have been accused of faking a brain injury, and some denied medical assistance because their injury is undetectable. Others think they are fine, but their reaction times are slower and they may have trouble with memory, focus, attention, and motor skills. Even a mild concussion can produce these effects. 

What’s more, someone with TBI is at a greater risk of developing dementia. Autopsies of the brains of athletes who had multiple concussions prove this connection. Their brains revealed that they had chronic traumatic encephalopathy (CTE), which has symptoms similar to Alzheimer’s disease. There isn’t a way to detect CTE and dementia other than through an autopsy, so it is difficult to know who has it for sure.

In the lab, CTE is recognizable through the detection of a protein called tau in certain areas of the brain. The presence of tau can impair normal cellular processes and result in trouble thinking or remembering. It seems like an easy fix – remove the tau and repair the dysfunctional brain cells. Unfortunately, it’s not that simple. Tau plays an important role in stabilizing the structure of brain cells, so removing all the tau from the brain would cause damage and dysfunction.

Too much tau is not good either. Then, individual units of tau protein accumulate and form structures of their own such as neurofibrillary tangles. These interfere with cells’ ability to communicate with each other. Aggregate tau can be toxic as well and is suspected to perpetuate the cell death processes that occur in the hours and weeks after an initial injury.

Researchers with the Sealy Center for Vaccine Development at UTMB have developed an antibody that detects this toxic form of tau protein without interrupting the processes of normal tau proteins. Using this antibody, they were able to find toxic tau tangles in animal brains after TBI. 

Next, they plan to use a similar antibody to inactivate the tau tangles with the hope of preventing further damage. This antibody appears to improve learning and memory in rodents with Alzheimer’s disease. In the future, it might be used as a therapeutic vaccine for many neurodegenerative disorders.  Right now though, researchers are working to ensure this therapy is safe and effective in animals before moving on to clinical trials with people.

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Staving Off Dementia

Nov. 8, 2013

By Medical Discovery News

“When I was younger, I could remember anything, whether it had happened or not; but my faculties are decaying now and soon I shall be so I cannot remember any but the things that never happened.”

While American novelist Mark Twain can invariably add his iconic sense of humor to any situation, it is no laughing matter when patients lose their memories and cognitive function to dementia. And for their family members, there is hardly anything harder than caring for a loved one who can no longer remember them or any shared experiences. But lowering a person’s risk of dementia may be as simple as changing their lifestyle.

The incidence of dementia increases with age. As the average age of Americans increase, the number of people with dementia also increases. In 2010, more than 30 million people worldwide had dementia, and this figure is estimated to more than triple by 2050.

Despite the many medical advances over the past 20 years, there are no effective pharmacological therapies for dementia yet. Some drugs are being evaluated and still others are in development, but it could be some time before there is a truly successful treatment for this disease. 

However, studies have uncovered risk factors that can lead to dementia, such as low physical and mental activity, obesity, hypertension, and hyperlipidemia. The good news is that all these risk factors can be controlled by changes in a person’s lifestyle and behavior.

A group of scientists at the Karolinska Institute in Stockholm examined the effects of lifestyle modification on dementia risks. One of the strongest correlations to reducing the risk of dementia is increasing physical activity. Changing from a sedentary lifestyle to one with at least moderate physical activity will also improve cognitive performance. Both aerobic exercise and strength training may delay of the onset of dementia. 

For those with nutritional deficiencies, taking vitamin supplements did help prevent dementia onset, but those with normal levels did not affect their dementia risk by taking supplements. 

Computer games have become a popular way to enhance mental abilities in older people. There are some positive effects of gaming on cognitive performance, but these effects decline with age.  A recent study showed that improvements in language skills and reasoning abilities lasted for a full year after computerized training. While encouraging, more clinical trials are needed to establish the benefits of these activities on cognitive functions and the delay of dementia.

For now, the best advice to delay or prevent dementia is to engage in physical exercise and maintain a healthy weight and nutrition.

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Astronauts with Alzheimer’s

July 19,2013

By Medical Discovery News

“That’s one small step for a man, one giant leap for mankind.” Since Neil Armstrong uttered those iconic words as he stepped onto the moon for the first time in 1969, researchers have learned that the high levels of radiation an astronaut is exposed to while traveling in space can harm them long after they have returned to Earth. As scientists debate the likelihood of a manned mission to Mars, the issue of long-term exposure poses a significant obstacle, especially now that it has been linked with Alzheimer’s disease.

The radiation in space is more complex than that on Earth, because it includes galactic cosmic radiation and solar particles normally blocked by Earth’s atmosphere. In addition, the Earth’s magnetic field traps some of the radiation from the sun in belts, which space shuttles fly through on their way to outer space. The longer the trip, the greater the exposure, so within a 750-day roundtrip to Mars an astronaut would be exposed to four times the acceptable lifetime radiation limit for a human.

The average person is exposed to 3 millisieverts (mSv) of radiation each year, from radon that naturally exists in the air, small radioactive particles in water and soil, rays from the sun, and medical tests (a chest X-rays delivers about .02 mSv). But if a person were exposed to 50mSv, their blood would start to change. Exposure to 1,000 mSv causes hemorrhage, vomiting, hair loss, and even death within two weeks, such when an accident occurs at a nuclear energy facility like Chernobyl or Fukushima. Exposure to 20,000 mSv can cause death in minutes, as with a nuclear bomb. 

NASA believes that a 3 percent increase of chance of death due to radiation exposure during a space mission is an acceptable risk for astronauts. This increases the astronaut’s lifetime risk of death from cancer to 23 percent, almost a one in four chance. Now a study reveals an additional risk for astronauts exposed to radiation in space: Alzheimer’s disease.

Scientists at the University of Rochester and Harvard University exposed mice to doses of radioactive iron at levels comparable to those expected on a trip to Mars. Six months after the radiation exposure, the mice showed mental impairments including issues with memory. Furthermore, male mice had accumulated the beta-amyloid protein that is associated with the start of Alzheimer’s, suggesting a more rapid progression in male mice.

Obviously mice are different than humans and space explorers would be exposed to more than one type of radiation, so this model may not exactly mimic what would happen to humans traveling to Mars. However, in addition to the increased risk of cancer and death, space explorers must now consider the increased chance for and more rapid development of dementia. New technology to provide radiation shielding for astronauts could minimize the amount of radiation they are exposed to.  

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An Early Start to Alzheimer’s

April 12, 2013

By Medical Discovery News

More and more data suggest that treatment for Alzheimer’s disease may be more effective if started early, even before symptoms appear. In addition, recent clinical trials of treatments for mild to moderate Alzheimer’s have failed, suggesting that waiting to treat the disease until these stages may be too late, and once the degenerative process has started it cannot be stopped. But since Alzheimer’s has no identifiable markers in its early stages, how would doctors know when and whom to treat?


Alzheimer’s is a form of dementia that causes an irreversible loss in brain function and gradually gets worse over time, affecting memory, thinking, and behavior. Buildup of insoluble proteins in the brain causes amyloid plaques or neurofibrillary tangles, two hallmarks of the disease along with a loss in connections between electrically active nerve cells called neurons. There is no definite diagnosis, other than autopsy.

A recent study of an extended family of 5,000 people from Colombia who inherited a form of Alzheimer’s revealed that the disease begins much earlier, and the deterioration of the brain occurs in more ways than previously thought. Affected family members had mild problems thinking and remembering at an average age of 45 and dementia at 53. However, researchers also noticed changes in affected family members at younger ages, before the first signs of plaques in the brain.

The study compared twenty 18- to 26-year-old family members who carried a mutation called presenilin1 E280A and were very likely to develop early onset Alzheimer’s with 24 non-carriers. Both groups underwent a variety of tests including MRIs, memory tests, cognitive tests, blood tests, and cerebral spinal fluid sampling. The groups did not differ significantly in their dementia ratings or psychological scores. However, carriers had fewer neurons in several regions of the brain that are affected by Alzheimer’s. Carriers also had higher levels of the amyloid protein that causes plaques in their cerebral spinal fluid. 

Previous studies of Alzheimer’s patients showed they have lower levels of amyloid than normal, which had been attributed to amyloid accumulating in the brain. Based on this information, scientists thought Alzheimer’s was explained by the progressive buildup of amyloid in plaques that causes brain cells to die, leading to symptoms of Alzheimer’s. This new study suggests that there are early changes in the brain even before amyloid plaques. 

This challenges what we know about when and how Alzheimer’s develops. Inherited, early onset Alzheimer’s may be caused by the body producing too much amyloid, while late onset Alzheimer’s may be the result of the body’s inability to clear amyloid from the brain. Researchers are now focusing on family members ages seven to 17 to determine if they can detect any brain differences even earlier.

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Scanning for Alzheimer’s

By Medical Discovery News

Sept. 15, 2012

Alzheimer's affects 5.4 million Americans

At first it seems to be occasional forgetfulness, followed by jokes of Mom having another “senior” moment. Then her lapses start to get serious. A teapot left on the stove starts a fire. The family doctor suspects she has dementia, which a neurologist confirms, but when asked if it’s Alzheimer’s Disease, doctors can only guess. Today, the only method available to confirm someone had Alzheimer’s is through an autopsy.

Having the ability to diagnose Alzheimer’s while someone is alive can help rule out other possible conditions such as a drug’s side effects or depression, which can cause similar early symptoms.   Patients could then begin therapies to manage the disease and allow families to make necessary accommodations.

A test recently approved by the Food and Drug Administration combined with clinical symptoms can get doctors pretty close to a diagnosis. The test uses a weakly radioactive fluorescent dye called Amyvid that latches on to amyloid plaques in the brain. Amyloid plaques are protein fragments that normally break down, but in people with dementia they accumulate into hard insoluble plaques. It’s unclear whether amyloid plaques cause Alzheimer’s, but their presence is indicative of the disease. Once Amyvid binds to the plaque, a positron emission tomography or PET scan reveals the location and amount of protein clusters in the brain.

While a clear scan is a relief, patients with a positive scan don’t necessarily have Alzheimer’s. Twenty to 30 percent of people over 65 have some plaque and may never develop dementia. But the test is significant to Alzheimer’s research since it will allow scientists to identify and track people with dementia, expanding their knowledge about the causes of Alzheimer’s and its progression. Scientists can also monitor how the disease develops under experimental therapeutics.

Finding effective treatments for Alzheimer’s will become increasingly important as America’s population ages. It is the No. 1 cause of dementia, affecting 5.4 million people. That number is expected to double in the coming years. By 2050, the cost to treat people with Alzheimer’s is projected to soar to $1.1 trillion.

Currently, there is no cure for Alzheimer’s. Some drugs appear to slow its progression, but the benefit is disappointingly small. Most of what can be done is manage symptoms. While scientists don’t yet fully understand what causes Alzheimer’s, it’s clear the illness develops under a complex series of events in the brain over a long period of time. The causes likely include some mix of genetic, environmental, and lifestyle factors.

Typical symptoms of Alzheimer’s include difficulties performing routine tasks and learning new information, getting lost on familiar routes, language problems, and personality changes. Eventually the memory declines to the point where family members aren’t recognized, language is lost, and basic functions such as eating and dressing require help.

This is only one of many studies into understanding Alzheimer’s that could lead to promising diagnostics and treatments.

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An Update on Mad King George

By Medical Discovery News

June 23, 2012

King George III

Before the planet Uranus was given its present-day name, it was called Georgium Sidus, after King George III of Great Britain. Not only was King George a patron of the sciences, under his rule slavery was abolished in England and the country’s Industrial Revolution began. Despite these significant contributions, he’s most remembered for losing America, and for being the Mad King.

A 1994 movie, “The Madness of King George,” depicted the court intrigue surrounding the King’s illness and his son’s maneuvering to become regent and rule the kingdom. In the film, the cause of the King’s mental state is suggested as intermittent porphyria, which has been an accepted diagnosis among many scientists.

Now a new study disputes this claim. TJ Peters and A Beveridge reevaluated King George’s medical records and believe Ida Macalpine and Richard Hunter based the porphyria diagnosis on an incomplete review of historical records. They are a mother and son, both psychiatrists, who studied health accounts of the King in the 1960s and theorized he had acute or variegate porphyria.

Porphyria disorders are a rare hereditary disease, which is the inability to make a key component of the oxygen-carrying molecule called heme.  People with porphyria are missing enzymes that produce heme molecules, which creates the build-up of a precursor biochemical called porphyrins. This can result in abdominal pain, muscle weakness, nervous system deficits, and personality changes. The disease lasts a lifetime and acute attacks and symptoms can appear and disappear over many years.

Those who believe porphyria caused King George’s mental problems point to the drugs and treatments he was given as being partially responsible. Many of those medications contained arsenic, a poison that scientists found in high levels when they tested the King’s hair.

But Peters and Beveridge believe neither medication nor porphyria are to blame. They believe the King’s mania was more likely symptomatic of a recurring bipolar disorder. The researchers examined medical records along with journals from his caretakers and were able to document four bouts of mental illness. His psychiatrists, called “mad doctors” at the time, treated King George and documented these episodes of psychosis. The first happened when he was 50, and then he spent the last ten years of his life suffering chronic mania and dementia.

The researchers further speculate King George’s other health problems may have contributed to his mental decline. At 70 he was blind from cataracts and thought to be increasingly deaf. The isolating effect of these lost senses may have contributed to his eventual chronic mania.  Records also show the king’s favorite daughter, Amelia, died when he was 70. By the end of that year he was declared permanently insane and lived in seclusion at Windsor Castle until his death at 81 years old.

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