Celebrities With Alzheimers: US President Ronald Reagan


Celebrities With Alzheimers: US President Ronald Reagan. Like 30 million mostly elderly people in the world, former United States President Ronald Reagan suffered dementia from Alzheimer’s disease. But now scientists have unlocked — at least in part — how the brain encodes memories, leading to hopes that a cure for the memory and learning loss brought by the neurodegenerative disease may soon be found.

At 69, he was the oldest to enter the White House. But the former film star who became the 40th president of the United States radiated a youthful optimism rooted in the traditional virtues of a departed pre-World War II era.

To a nation wounded by Watergate, Vietnam and the taking of hostages in Iran, former President Ronald Reagan held out the promise that America would “stand tall” again. And, in his first term, he did manage to restore America’s faith in itself and in the presidency.

But late in 1986, halfway through his second term, his government plunged into turmoil when his subordinates sold arms to Iran as ransom for hostages in Lebanon and diverted profits to the rebels fighting the Marxist Sandinistas then governing Nicaragua. The Iran Contra affair had been “characterized by pervasive dishonesty and secrecy,” reported the joint Congressional investigating committee.

Despite that, the Republican president remained tremendously popular, capping his two terms with a new relationship with the Soviet Union under the leadership of Mikhail S. Gorbachev, paved by a nuclear arms agreement with the Soviets that reduced — for the first time — the nuclear arsenals of both countries.

In 1994, Mr. Reagan he again touched the hearts of Americans when he in a handwritten letter that he had Alzheimer’s disease. “I now begin the journey that will lead me into the sunset of my life,” he wrote. “I know that for America there will always be a bright dawn ahead.”

He died in 2004 at age 93, after spending his final years in seclusion, coping with the mental debilitation of Alzheimer’s disease.

Spurred by her husband’s suffering, former first lady Nancy Reagan turned into a strong advocate for embryonic stem-cell research — putting her in conflict with her fellow Republicans. Scientists believe that stem-cell research could lead to treatments for Alzheimer’s and other diseases, but it remains controversial because it involves the destruction of human embryos.

Alzheimer’s: a terrible disease
About 5.4 million Americans — and 30 million people across the world — suffer from Alzheimer’s, a neurodegenerative disease.

Worse, the disease is nearly impossible to diagnose before symptoms develop — physical changes in the brain are difficult to detect before clinical symptoms appear.

Striving to understand the causes of Alzheimer’s, scientists have probed blood samples of patients, animals as varied as fruit flies and fish — and even brain biopsies of patients who died. Still, a drug to cure it or change its course also remains elusive.

But Alzheimer’s is a terrible disease. A progressive brain disorder that often strikes late in life, sufferers slowly but irreversibly lose their memory, language skills and perception of time and space. Eventually, they can’t even take care of themselves.

The disease takes a devastating toll on both patients and those who love and care for them. Sufferers often feel great frustration and fear as they struggle with everyday tasks and slowly lose their independence. Caregivers tend to get burned out; friends and family are hurt to witness how the disease takes their loved one from them bit by bit.

Alzheimer’s is the most common form of dementia, and one of the main effects of dementia is that it damages the brain’s memory and learning function. Thus, understanding how memories are encoded is key to developing new treatments for the disease — and perhaps, even preventing it.

Unlocking the mysteries of memory
But memory encoding in the brain remains mysterious, despite almost a hundred years of research. Scientist know that neuronal synaptic connection strengths are involved in memory, but synaptic components are short-lived — the synaptic membranes involved are constantly degrading and being replaced. Meanwhile, memories last lifetimes, at most. Could it be that synaptic information is encoded and hard-wired at a deeper, finer-grained molecular scale? That’s what scientists suspect.

Now, a team of scientists from the University of Alberta thinks they may have figured out what’s going on, and have published their findings in the March 8 issue of the journal, PLoS Computational Biology.

The new study is lead by Dr. Jack Tuszynski, a University of Alberta physicist, his graduate student Travis Craddock and the University of Arizona’s Prof. Stuart Hameroff.

The researchers say they were inspired by another research paper that described experiments in successfully erasing memories from animals’ brains. That study had concluded that the encoding and erasing of memories could be largely ascribed to a specific protein — calcium-calmodulin dependent kinase complex II, or CaMKII. The protein worked this by strengthening or eliminating neural connections.

Meanwhile, the interiors of the brain’s neurons are occupied by microtubule protein structures — cylindrical hexagonal lattice polymers of the protein tubulin. The tubulins, particularly concentrated in the neurons’ axons and dendrites that are active in the memory process, comprise 15 percent of all brain proteins.

The microtubules and CaMKII that are extremely rich in brain neurons are commonly found in all eucaryotes — or all complex-celled living organisms including animals, plants, fungi and protists. They are also capable of connecting membrane and cytoskeletal levels of information processing.

For its part, Dr. Tuszynski’s team noted that the geometry of the CaMKII molecule was very similar to that of tubulin protein compounds.

Setting out to understand the interaction between CaMKII, tubulin and microtubules, the researchers developed highly accurate computer models based on 3D atomic-resolution structural data for all three protein molecules.

What did they discover?
• The spatial dimensions and geometry of the CaMKII and microtubule molecules allow them to fit together.
• The microtubules and CaMKII molecules attracted one another electrostatically, allowing them to bind.


The researchers surmise that this is the process that happens within the neurons to store memories permanently (at least in some cases) — after they have connected synaptically.

The implications of the team’s findings are tremendous. Decoding and stimulating microtubules could lead to therapies for conditions in which microtubule disruption plays a key role — like Alzheimer’s disease. Or, to treatments for brain injury, in which microtubule activities can repair neurons and synapses.

“This could open up amazing new possibilities of dealing with memory loss problems, interfacing our brains with hybrid devices to augment and ‘refresh’ our memories,” says Dr. Tuszynski. “More importantly, it could lead to new therapeutic and preventive ways of dealing with neurological diseases such as Alzheimer’s and dementia, whose incidence is growing very rapidly these days.”

“Many neuroscience papers conclude by claiming their findings may help understand how the brain works, and treat Alzheimer’s, brain injury and various neurological and psychiatric disorders,” says Dr. Hameroff, the study’s senior author. “This study may actually do that. We may have a glimpse of the brain’s biomolecular code for memory.”

Earlier, in January, researchers from the University of California, San Diego used stem cells to create an “Alzheimer’s-in-a-dish” lab model to simulate what goes wrong in diseased brain cells of people with the disease.

In their study, led by Dr. Larry Goldstein took fibroblasts or skin cells from dead patients, four who had died from Alzheimer’s and two who didn’t have dementia when they were alive. Then, employing newly developed stem-cell technology, Dr. Goldstein and his team created induced pluripotent stem (iPS) cells or iPSCs — as regenerative as embryonic stem cells but not as controversial.

Finally, the team turned the iPCs into neurons that closely replicated those found in living Alzheimer’s patients.

The resulting cells of diseased neurons are in effect “Alzheimer’s-in-a-dish models” that researchers can work on in the lab to study the disease more effectively, with the hope of finding a cure. The findings of Dr. Goldstein’s study were published online in January in the journal Nature.

Scientists say such “disease-in-a-dish” neuron cell models creating from reprogrammed skin cells could also be used to explore to many other neurologic diseases, including Parkinson’s and Lou Gehrig’s disease.

RELATED POSTS:
Dr. Larry Goldstein’s Stem Cell Treatment for Alzheimers
Can Vitamin B12 Prevent Alzheimers?
Electric Shock Therapy for Alzheimers?

Celebrities With Alzheimers: US President Ronald Reagan. Posted 17 April 2012.