DOES LIGHT THERAPY HELP ALZHEIMER'S PATIENTS SLEEP?

Many people with Alzheimer's have trouble sleeping, which can leave them exhausted during the day. Fatigue takes a toll on both patients and their caregivers. Indeed, irregular sleeping is a major reason why families move relatives with Alzheimer's into long-term care. Light therapy is a promising treatment under investigation for people with Alzheimer’s who struggle with sleep.

Alzheimer's patients who have trouble sleeping should first be evaluated for underlying sleep disorders and medical conditions that cause sleep trouble. Also, stopping medications that affect sleep or switching to more tolerable drugs may help.

No studies have found that conventional sleep aids, like Ambien (zolpidem) and Sonata (zaleplon), or sedative antidepressant medications like trazodone (Desyrel) effectively treat disturbed sleep in Alzheimer's patients. And supplements that boost levels of melatonin (a hormone that makes people feel tired) have limited effect, perhaps because Alzheimer's patients have fewer melatonin receptors in the brain than people without dementia.

Light therapy - regular exposure to sunlight or special bright lamps that mimic natural light - is another option. Exposure to bright light signals to the brain that it is daytime and helps set the body's circadian rhythms -- regular mental and biological changes that occur over a 24-hour cycle and regulate important functions, like preparing the body for sleep at night.

How well does light therapy work for Alzheimer’s patients? In a three-week study from the University of North Carolina at Chapel Hill, 66 adults with dementia living in long-term care facilities were exposed for varying amounts of time to bright ceiling lights installed in common areas.

Compared with participants who did not spend time under the lights, those who were exposed to light therapy for two and a half hours in the morning slept 16 minutes longer; those who were exposed for about eight and a half hours off and on throughout the day slept 14 minutes longer. The morning group was also able to fall asleep 29 minutes earlier, which is important since Alzheimer's patients often can't fall asleep until late at night.

But not all studies have produced positive results, and there are questions about the appropriate dosage. The amount of light prescribed for other conditions may not be sufficient for older patients with Alzheimer's; eyes transmit less light with age, and visual problems are particularly common in patients with Alzheimer's disease.

While researchers have yet to determine the ultimate benefits of light therapy or how much is needed to have an effect, "It's still reasonable to encourage people with Alzheimer's to stay in well-lit areas during the day," says Peter Rabins, M. D., Director of Geriatric Psychiatry and Neuropsychiatry at Johns Hopkins.

This may be more practical than purchasing specialized equipment, he notes. "The light-therapy boxes used by people with disorders like depression require sitting still in front of a bright lamp, and this can be a challenge for those with Alzheimer's." Spending time outside in the morning may be a convenient way to produce similar effects.

More Tips for Caregivers. The Alzheimer's Association offers these tips for better sleep:

• Maintain regular meal times and sleep schedules.

• Discourage alcohol, caffeine, and nicotine use.

• Encourage daily exercise (but no later than 4 hours before bedtime)

• Don't give Alzheimer's drugs before bedtime.

• Discourage watching TV or staying in bed during wakeful periods.

(Source: John Hopkins Health Alerts, 14 December 2009)

DRUG FOUND TO CREATE NEW CONNECTIONS IN BRAIN, RESTORING AND IMPROVING MEMORY

Scientists at the Blanchette Rockefeller Neurosciences Institute (BRNI) have discovered that a cancer drug – Bryostatin – enhances the formation of new connections in rat brains during memory storage. This drug could potentially increase normal memory capacity in humans as well as repair and restore memory lost from Alzheimer’s disease, stroke and head trauma.

In an article in the December 4 issue of the Proceedings of the National Academy of Sciences (PNAS), BRNI Scientific Director Daniel Alkon, M.D., and Jarin Hongpaisan, Ph.D., describe how the cancer drug Bryostatin stimulates the production of connections between neurons in the same structural way that memory storage does naturally. Bryostatin essentially rewires the brain.

"There have been no effective drugs to promote brain repair,” Dr. Alkon said. “Bryostatin and other BRNI drugs in this class could introduce a whole new era for brain repair. At the same time, we are now closer to understanding what controls the growth of synaptic connections in the adult brain."

The BRNI research shows that a healthy brain normally undergoes some ‘rewiring’ when it stores memories. Bryostatin enhances this rewiring in normal healthy brains and also creates new connections in brains that have been ravaged by Alzheimer’s disease, stroke or head trauma.

Alkon and Hongpaisan used high-powered electron microscopes to directly visualize these synaptic connections between neurons. They also used molecular markers to label these connections to confirm the synaptogenesis induced by memory and Bryostatin.

“Diseases like Alzheimer’s actually destroy synapses in the human brain. There is still no recognized cure,” said Dr. Alkon. “In our animal studies with Bryostatin, damaged brains repaired synaptic connections of cells that were ruined from disease, giving the brain more capacity for memory. If this result is applicable to humans, this could be life-changing for Alzheimer’s patients.”

In previous BRNI studies, Bryostatin was found to markedly increase survival of mice with human Alzheimer's genes, decrease the production of the toxic Alzheimer's protein called A Beta, and increase the production of the healthy proteins from human cells.

Bryostatin also shows the ability to accelerate the production of synapses when paired with learning exercises. According to Dr. Alkon, this could eventually lead to new treatment therapies for children with compromised memory activity.

In 2004, BRNI received patent protection for the use of Bryostatin - originally developed as a cancer drug - to treat Alzheimer's disease. BRNI is preparing now for the first clinical trials of Bryostatin for the treatment of neurological disorders. Clinical trials will test whether Bryostatin’s promising preclinical results generalize to humans.

Source: http://www.alzheimersweekly.com/Research/drug-found-to-create-new-connections-in-brain-restoring-and-improving-memory-a226.html

(From The Malaysia National Alzheimer's Caregivers Online Network - NACON)

TROUBLE WITH DAILY ACTIVITIES COULD POINT TO ALZHEIMER'S RISK

Problems carrying out daily chores or enjoying hobbies could predict which people with "mild cognitive impairment" will progress more quickly to Alzheimer's dementia, U.S. researchers report.

According to the Alzheimer's Association, mild cognitive impairment (MCI) is "a condition in which a person has problems with memory, language, or another mental function severe enough to be noticeable to other people and to show up on tests, but not serious enough to interfere with daily life." This type of mental state is considered a risk factor for dementia.

In fact, some studies have found that about 10 percent to 15 percent of those with MCI will progress to dementia each year, according to background information in the new study.

Reporting in the September issue of the Archives of Neurology, the researchers sought to determine if there were telltale signs within MCI that might spot those people who would progress more rapidly to full-blown dementia. To do so, they collected data on 111 people with mild cognitive impairment, then evaluated these individuals using brain scans and cognition tests.

Over the next two years of follow-up, 28 people did go on to develop dementia.

"On their own, the tests did not predict which patients went on to develop dementia," said lead researcher Sarah Tomaszewski Farias, an Associate Professor of Neurology at the University of California, Davis.

"However, level of daily function was a key predictor," Farias said.

"So, if an older adult is starting to display problems in daily life, such as problems shopping independently, problems managing their own finances, problems performing household chores, and problems maintaining their hobbies, they are more likely to develop a dementia within several years," she said.

Farias cautioned that the study involved people visiting a clinic because they were already having memory and other problems, so the implications could be different among the general population of older adults.

"If you look at individuals in the community, you see a much slower progression to dementia in those with some mild cognitive impairment," she said. "The time to develop dementia once someone has mild cognitive impairment is probably slower in the general population of older adults than we had previously thought."

Still, any kind of early warning is helpful, and Farias believes health-care providers should ask patients and those who know them well - a spouse or adult child - about how they are doing in their daily lives.

"It is important to keep in mind that sometimes individuals themselves lack awareness of some of these problems. So it is important, if at all possible, to get feedback from individuals who are familiar with how the older adult is functioning in their daily life," she added.

"If there is evidence or suspicion that an older adult has some mild cognitive or memory problems, and it is starting to interfere with their ability to do daily activities, there is a higher likelihood this individual is developing a dementia and they should be closely monitored," Farias said.

Greg M. Cole, a Neuroscientist at the Greater Los Angeles VA Healthcare System and Associate Director of the Alzheimer's Center at UCLA David Geffen School of Medicine, said it is crucial to be able to identify people with early Alzheimer's disease, "if we want to test methods of preventing it."

"This study illustrates the difficulties in early diagnosis of Alzheimer's disease in aging people with mild problems with memory and cognition," Cole said.

"In my view, because memory and cognitive performance vary widely in our population no matter what age, the best indications of ongoing decline are going to be seen against past individual performance rather than some cross-sectional 'normalized' standard," he said.

Dr. Ronald C. Petersen, Director of the Alzheimer's Disease Research Center at the Mayo Clinic in Rochester, Minn., agreed that, despite the lack of effective treatments, spotting Alzheimer's disease early remains important.

"If people in the family start to recognize a change in memory/learning patterns, that might be sufficient to identify someone who could develop Alzheimer's disease," Peterson said. "Don't wait until the person is having trouble driving, is having trouble paying their bills or having trouble functioning in the community - that's dementia," he said. "This study tells us that we can identify important symptoms earlier and it may be worthwhile doing so."

Source: HealthDay, September 17, 2009

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INFECTIONS MAY SPEED ALZHEIMER'S MEMORY LOSS

A split-view image showing PET scans of a normal brain (L) and a brain with Alzheimer's disease. Reuters/National Institute on Aging/Handout

Catching a cold or the flu could speed memory loss in people with Alzheimer's disease, researchers reported.

In a study of patients with mild to severe Alzheimer's disease, they found that people who suffered acute or chronic infections, or even bumps and bruises from a fall, were much more likely to have high blood levels of a protein involved in inflammation and also experienced faster memory loss than people who did not have infections and who had low levels of this protein.

It's possible that finding a way to reduce inflammation in the body "could be beneficial for people with Alzheimer's disease," study chief Dr. Clive Holmes, from the University of Southampton, UK, said in a prepared statement. Over about 6 months, Holmes and colleagues measured the cognitive abilities and blood levels the inflammatory protein TNF-alpha of 222 people with Alzheimer's disease. They also interviewed each subject's main caregiver several times during the study. During follow up, roughly half of the study subjects experienced a sudden infection or injury that led to inflammation, and a spike in TNF-alpha levels. These people, the researchers found, experienced memory loss that was at twice the rate of those who did not have infections or injuries. People who had high levels of TNF-alpha in their blood at the beginning of the study, a sign of chronic, ongoing inflammation, had memory loss at four times the rate of those with low levels of the protein at the start of the study. By contrast, subjects with low levels of TNF-alpha throughout the study showed no decline in brain function, the report indicates. "One might guess that people with a more rapid rate of cognitive decline are more susceptible to infections or injury, but we found no evidence to suggest that people with more severe dementia were more likely to have infections or injuries at the beginning of the study," Holmes noted in a prepared statement.

Source: Neurology, September 8, 2009.

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NEW ALZHEIMER'S GENE LINK DISCOVERED

Scientists working in seven countries announced they had uncovered variants of three genes which play a role in Alzheimer's, a discovery that should throw open many new avenues for tackling this tragic, mind-killing disease.

The biggest cause of dementia, Alzheimer's has a strong heritability -- nearly one in four cases are believed to have a genetic cause -- but precisely which genes are to blame and how their fiendish mechanism works remain elusive.

So far, three culprit genes have been found in "familial" Alzheimer's, a rare, early-onset form in which the disease shows up before the age of 60. This type accounts for less than three percent of all cases.

Of the far more common "sporadic" type, where there is no readily identifiable family history of the disease, just a single gene, APOE4, has come to light -- and it was spotted way back in 1993.

But hopes are now rising that a few of the many knowledge gaps may now be filled.

In two papers published in the journal Nature Genetics, a team based in Britain and the other in France report that a trawl through the DNA of 36,000 individuals has added three new genes, whose tell-tale variants showed up among people with Alzheimer's.

That finding could be useful in the search for a diagnostic tool, helping people with a heightened susceptibility to Alzheimer's make lifestyle decisions, even if a cure for the disorder remains beyond the far horizon.

Farther afield, it could help tease out a pharmaceutical weapon to interfere with the action of the faulty genes.

In Alzheimer's, clumps of protein called amyloid plaques and tau tangles proliferate in the brain, especially the cortex and hippocampus, destroying brain cells and their connections.

A progressive, degenerative disease, it causes forgetfulness and confusion, disturbs thinking, emotions and behaviour, eventually leading to death.

The role of the three newly-identified genes remains unknown.

Two of them, called CLU and CR1, may be involved in the elimination of amyloid plaques, so faulty variants may allow the toxic compound to build up, the scientists believe.

The other, called PICALM, controls brain chemicals that are important at synapses -- the connection between neurons -- and is involved in the transport of molecules into and inside nerve cells, thus helping to form memories and other brain functions.

"These findings are a leap forward for dementia research," Rebecca Wood, chief executive of the Alzheimer's Research Trust, a British charity that funded research encompassing universities in Britain, Belgium, Germany, Greece, Ireland and the United States.

"At a time when we are yet to find ways of halting this devastating condition, this development is likely to spark off numerous ideas, collaborations and more in the race for a cure."

The other paper was authored by a team from France's National Institutional of Health and Medical Research (Inserm).

The team "has about 10 other genes that may be possible targets" but further work is needed to confirm this, lead researcher Philippe Amouyel, of the Institut Pasteur in Lille, told AFP.

There is no cure at present for Alzheimer's, although some researchers are confident that a first generation of drugs that will slow or block the spread of the disease is not far away.

Present drugs have only a temporary effect. They inhibit an enzyme that reduces acetylcholine, a vital chemical used in communication between brain cells.

A breakthrough is urgently needed.

Alzheimer's primarily surfaces among people beyond their mid-60s, thus as the world's population ages, case numbers will surge, badly straining hospital systems.

According to an estimate published by the journal The Lancet in December 2005, the number of people with dementia will more than triple by 2040, reaching 81 million. China and South Asia will see the biggest increases.

Source: AFP, September 7, 2009

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