Smoking pot may stave off Alzheimer’s

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1 in 5 Boomers May Develop Alzheimer's...

18% of All Boomers Expected to Develop Alzheimer's
March 18, 2008 - Aging Population Worries Many Health Experts

About 14 million, or roughly 18 percent, of the USA's 79 million baby boomers can expect to develop Alzheimer's or some other form of dementia in their lifetime, a newly released report shows. Americans are developing Alzheimer's at an accelerating rate, says Stephen McConnell, vice president of public policy for the Alzheimer's Association. Medical advances have allowed people to beat cancer and heart disease. But with longer life comes the added risk of Alzheimer's, a progressive brain disease that causes severe memory loss and confusion.

The oldest baby boomers are turning 62 this year and are by definition entering the risk zone. Age is the single biggest risk factor for the disease: The likelihood of developing Alzheimer's doubles every five years after age 65. "What we're faced with here is the boomer population coming of age," says Gary Small, director of the UCLA Center on Aging. "There are going to be a lot more people at risk."

The report, "2008 Alzheimer's Disease Facts and Figures," states that one out of eight boomers will be diagnosed with Alzheimer's, the most common type of dementia, at some point. If no cure for Alzheimer's is found, the nation will be faced with a half-million new cases of Alzheimer's in 2010 and nearly a million a year by the middle of the century.

The report doesn't minimize the burden on the population today, noting that 5.2 million people now have the disease, which can take more than 10 years to destroy the mind. That figure includes a small group of people struggling with the disease in the prime of life. The report says as many as 500,000 Americans are diagnosed before the age of 65. According to the Alzheimer's Association, 70% of people with Alzheimer's and other dementias live at home, where friends and family members pitch in to help them, often at great cost.

More ABC News: 1 in 5 Boomers May Develop Alzheimer's

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Medication doesn't always help...

Medication 'worsens Alzheimer's'
Tuesday, 1 April 2008 : Anti-psychotic drugs commonly given to Alzheimer's patients often worsens their condition, a study suggests.

Neuroleptics provided no benefit for patients with mild behavioural problems, but were associated with a marked deterioration in verbal skills. The research focused on 165 people with advanced Alzheimer's who were living in nursing homes in four British cities. Up to 60% of Alzheimer's patients in nursing homes are given the drugs to control behaviour such as aggression. The study appears in the journal Public Libary of Science Medicine.

CASE STUDY

Rita Clark's husband was diagnosed with Alzheimer's seven years ago. Rita, from Cleveland, said: "My husband developed a range of side effects while receiving anti-psychotic drugs.
"Since the drugs have been withdrawn, the side effects have gone and he generally seems much better and more settled. "I'm not saying it's the same for everyone, but in my husband's case, withdrawing the drugs has led to a clear improvement in his quality of life."

The researchers, from Kings College London and the Universities of Oxford and Newcastle, found the drugs offered no long-term benefit for most patients with mild symptoms of disturbed behaviour. But just six months of treatment was enough for patients to show a marked deterioration in their verbal fluency. Further preliminary analysis already under way on the data suggests the use of neuroleptics may also increase death rates.

More BBC NEWS | Health | Medication 'worsens Alzheimer's'

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Blood test for earlier diagnosis...

Alzheimer's blood test 'promise'
Sunday, 6 April 2008 - A US company hopes to be the first to market a blood test to detect early signs of Parkinson's and Alzheimer's.

Several teams are working on such a test but Power3 Medical Products says its could be launched in Europe this summer, Chemistry and Industry reports. The diseases can currently only be diagnosed once symptoms develop. UK experts said the test sounded promising for detecting and monitoring the diseases but more work was needed.

The company plans to launch the test in Greece first, before promoting it in the US by the end of the year. It hopes the test could be launched in the UK early next year, if authorities are satisfied with trial results.

Monitoring aid

The test, called NuroPro, measures levels of 59 biomarkers - proteins in the blood. The relative levels of the markers is used to distinguish between Alzheimer's, Parkinson's and another neurodegenerative disease called Lou Gehrig's disease. "A blood test could be particularly useful in monitoring the progression of Parkinson's" - Kieran Breen, Parkinson's Disease Society

More BBC NEWS | Health | Alzheimer's blood test 'promise'

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Parkinson's Disrupts Stem Cell Therapy Transplants
SUNDAY, April 6,`08 -- Dopamine neurons may not work long-term, as disease causes pathologic changes in cells

Current therapies using stem cell transplants in the brains of patients with Parkinson's disease may not work long-term, because the disease is an ongoing process that continually causes damage, new findings suggest. Dopamine cells are sometimes transplanted into the brain of Parkinson's patients in the hope that they can replace those neurons that have degenerated. In theory, this should improve the disease's symptoms, which include tremors, stiffness of the limbs and trunk, slowed movement and impaired balance and coordination.

Researchers at Mount Sinai School of Medicine in New York City and Rush University Medical Center in Chicago studied brain tissue from a patient who had received a dopamine transplant 14 years earlier and found that the transplanted cells developed changes characteristic of Parkinson's disease (PD) and did not appear to function normally. The patient had improved initially after the transplant but then deteriorated, noted the study, published in the April issue of Nature Medicine.

"While, on the one hand, these results may sound disappointing, this information is crucially important if we are to develop better therapies for PD. The more knowledge we gain about the nature of the disease, the better our chances to find the cause of why cells degenerate and to develop a treatment that can protect them," Dr. C. Warren Olanow, director of the Robert and John M. Bendheim Parkinson's Disease Center at Mount Sinai School of Medicine, said in a prepared statement. "These findings also do not mean that transplant strategies such as stem cells cannot be made to work -- our findings just represent another obstacle that will have to be overcome."

According to researchers, these new findings counter the theory that a single event, like an infection, causes the initial damage to cells and triggers their gradual degeneration over time. Since the newly implanted cells in the Parkinson's patient also became damaged, they suggest that the disease process is ongoing.

Parkinson's Disrupts Stem Cell Therapy Transplants

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Check that cholesterol...

Midlife Cholesterol Tied to Alzheimer’s
April 18, 2008 -- Heart disease is the most well known complication of high cholesterol, motivating many to cut the fat, exercise and take cholesterol-lowering drugs. But results of a new study showing high cholesterol in your 40s is a risk factor for another troubling disease could prompt more people to fight the fat.

Alzheimer’s disease -- the most common cause of dementia, which affects memory, attention, language and problem solving -- has been linked to high cholesterol in one’s midlife. Researchers say in a recent study, people with total cholesterol levels between 249 and 500 milligrams were one-and-a-half times more likely to develop Alzheimer’s disease than those people with cholesterol levels of less than 198 milligrams.

“High mid-life cholesterol increased the risk of Alzheimer’s disease regardless of midlife diabetes, high blood pressure, obesity, smoking and late-life stroke,” study author Alina Solomon, M.D., with the University of Kuopio in Finland, was quoted as saying. “Our findings show it would be best for both physicians and patients to attack high cholesterol levels in their 40s to reduce the risk of dementia.”

To keep cholesterol under control, the American Heart Association recommends eating foods low in cholesterol and saturated fat and free of trans fats. They also say maintaining a healthy weight and being physically active will help control cholesterol levels.

Ivanhoe's Medical Breakthroughs - Midlife Cholesterol Tied to Alzheimer’s

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Alzheimer gender differences...

Alzheimer's Risk And Gender: Stroke In Men And Depression In Women Are Factors
Thursday, May 01, 2008 - The risks of developing Alzheimer’s disease differ between the sexes, with stroke in men, and depression in women, critical factors, according to research published in the Journal of Neurology Neurosurgery and Psychiatry.

French researchers based their findings on almost 7000 people over the age of 65, drawn from the general population in three French cities. None had dementia, but around four out of 10 were deemed to have mildly impaired mental agility (mild cognitive impairment) at the start of the study. Their progress was assessed two and four years later. In all, just over 6.5% of those deemed to be cognitively impaired developed dementia over the next four years. In just over half, no change was seen. Just over one in three reverted to normal levels of cognitive agility.

Progression from mild cognitive impairment to dementia was more likely among those who were depressed and who were taking anticholinergic drugs, which influence chemical signalling in the brain. A variation in the ApoE gene, a known risk factor for dementia, was also more common among those whose mild cognitive impairment progressed but risk factors also differed between the sexes, the results showed.

Men with mild cognitive impairment were more likely to be overweight, diabetic, and to have had a stroke. Men who had had a stroke were almost three times as likely to progress. Women with mild cognitive impairment were more likely to be in poorer general health, disabled, suffering from insomnia and to have a poor support network.

Women unable to perform routine daily tasks, which would allow them to live without assistance, were 3.5 times as likely to progress. And those who were depressed were twice as likely to do so. Stroke was not a risk factor for women, despite a similar rate of occurrence in both sexes.

Source

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Alzheimer's families ask Senate for more research...

Senators Hear From Alzheimer's Patients
May 14, 2008 - Patients and Caregivers Ask for Greater Research Commitment

Chuck Jackson has early-onset Alzheimer's disease. So does his older brother and three of his cousins. Jackson, an Alzheimer's patient from Albany, Ore., said 17 of his relatives have lost their battle with Alzheimer's, most before the age of 65. In 1967, at the age of 13, he became a caregiver for his mother.

Jackson joined several other Alzheimer's patients and caregivers on Capitol Hill Wednesday to ask lawmakers to increase their commitment to researching the disease. Alzheimer's affects as many as 4.5 million Americans, according to the National Institute on Aging. It is a disease in which a protein called A-beta becomes excessive in the brain, cutting off communication between nerve cells, eventually resulting in memory loss.

Among those testifying today before the Senate Special Committee on Aging is former Speaker of the House Newt Gingrich and former Supreme Court Justice Sandra Day O'Connor. O'Connor retired from the court in 2006 to care for her husband, who has Alzheimer's.

"It's so painful for someone you care about to see them disappear, in effect, before your eyes in every way, both mentally and physically. Very depressing," O'Connor told ABC News' Jan Crawford Greenburg in an exclusive interview before the hearing.

More ABC News: Senators Hear From Alzheimer's Patients

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Hope for early Alzheimer's sufferers...

Promising drug fights Alzheimer's in three ways
Wed., June. 11, 2008 WASHINGTON - Medication aims to stop 'plaque' from developing in brain, researchers say

A type of drug that may offer promise in treating Alzheimer's disease works in three ways to fight the formation of "plaques" in the brain that are a hallmark of the ailment, scientists said on Wednesday. The researchers looked at a kind of drug called a gamma-secretase modulator, or GSM, now being tested to see if it slows Alzheimer's disease progression. One GSM drug now being tested in people with Alzheimer's is Myriad Genetics's Flurizan, also called tarenflurbil.

A series of lab experiments showed these drugs inhibit production of long pieces of amyloid beta protein in the brain, block them from forming clumps, and boost production of shorter pieces that can make the longer ones less likely to stick together, the researchers said. "In fact, you're sort of getting three bangs for the buck," Dr. Todd Golde of the Mayo Clinic in Jacksonville, Florida, one of the researchers whose findings appear in the journal Nature, said in a telephone interview.

These abnormal clumps in the brain, called amyloid plaques, are considered a major feature of the disease, along with tangled bundles of fibers known as neurofibrillary tangles. Results from a Flurizan study involving 1,600 people with Alzheimer's are expected this summer, Golde said. Alzheimer's disease is incurable and is the most common form of dementia among older people. It affects the regions of the brain involving thought, memory and language. An estimated 5.2 million people in the United States have Alzheimer's, according to the Alzheimer's Association, and 26 million globally — a number projected to grow to 106 million by 2050.

Amyloid beta protein seems to be harmful only when it sticks together and accumulates in the brain, the researchers said. This type of drug actually sticks to the amyloid beta protein, preventing it from clumping, they said. Myriad Genetics did not fund this study but has funded other work by Golde. A number of other companies, including Elan and Wyeth, are developing drugs that also aim to fight beta amyloid plaques, but are not GSM drugs like the Myriad Genetics's Flurizan.

Promising drug fights Alzheimer's in three ways - Alzheimer's Disease - MSNBC.com

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Surprising discovery in Alzheimer's research...

New Clue to the Cause of Alzheimer's
Sunday, Jun. 22, 2008 (WASHINGTON) — Researchers have uncovered a new clue to the cause of Alzheimer's disease.

The brains of people with the memory-robbing form of dementia are cluttered with a plaque made up of beta-amyloid, a sticky protein. But there long has been a question whether this is a cause of the disease or a side effect. Also involved are tangles of a protein called tau; some scientists suspect this is the cause. Now, researchers have caused Alzheimer's symptoms in rats by injecting them with one particular form of beta-amyloid. Injections with other forms of beta-amyloid did not cause illness, which may explain why some people have beta-amyloid plaque in their brains but do not show disease symptoms.

The findings by a team led by Dr. Ganesh M. Shankar and Dr. Dennis J. Selkoe of Harvard Medical School were reported in Sunday's online edition of the journal Nature Medicine. The researchers used extracts from the brains of people who donated their bodies to medicine. Forms of soluble beta-amyloid containing different numbers of molecules, as well as insoluble cores of the brain plaque, were injected into the brains of rats. There was no detectable effect from the insoluble plaque or the soluble one-molecule or three-molecule forms, the researchers found. But the two-molecule form of soluble beta-amyloid produced characteristics of Alzheimer's in the rats, they reported.

Those rats had impaired memory function, especially for newly learned behaviors. Studies were also done on mice and when their brains were inspected, the density brain cells were reduced by 47 percent. The beta-amyloid seemed to affect synapses, the connections between cells that are essential for communication between them. The research, for the first time, showed the effect of a particular type of beta-amyloid in the brain, said Dr. Marcelle Morrison-Bogorad, director of the division of neuroscience at the National Institute on Aging, which helped fund the research. It was surprising that only one of the three types had an effect, she said in a telephone interview.

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Alzheimer's research setback...

Hopes Dashed for Alzheimer's Drug
July 2, 2008 - Researchers Abandon Flurizan; Doctors Hold Out Hope for Effective Approach

Many Alzheimer's researchers deny that the failure of a promising remedy for the degenerative disease requires a return to the drawing board, saying the setback is not a death knell for drugs designed to target a protein in the brain considered the trigger for the disease. Still, doctors are disappointed that the treatment fell short of expectations -- especially when its makers spent $60 million on it during the past year alone. On June 30, Myriad Genetics Inc. announced that its drug Flurizan didn't improve cognitive function or performance of daily activities for people who have Alzheimer's disease. A recent clinical trial tested the drug for 18 months in patients with a mild form of the condition.

"We are disappointed that Flurizan failed to achieve significance in this study, and we will now discontinue development of this compound," Myriad's CEO Peter Meldrum said in a statement. Flurizan targeted one type of protein in the brain called beta amyloid. Researchers believe that the protein forms clumps that clog the connections between brain cells, which may contribute to the symptoms of Alzheimer's, which include progressive memory loss. It was hoped that Flurizan would decrease the production of beta amyloid and slow the progression of the disease.

However, many scientists say they were not surprised by the findings. In fact, they say they even expected the outcome after seeing the underwhelming results of an earlier trial of the drug. "The bottom line is that Flurizan was a nonstarter from the very beginning," says Rudy Tanzi, professor of neurology at Harvard Medical School in Boston. Tanzi is also the co-founder and shareholder of two companies that develop Alzheimer's treatments.

More ABC News: Hopes Dashed for Alzheimer's Drug

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Bad vaccine or plaque not connected to Alzheimer's?...

Vaccine failure deepens Alzheimer's mystery
Thurs., July. 17, 2008 - Experimental shot stopped plaque, but not dementia, researchers say

Some doctors have long suspected that if the plaque that builds up in the brains of patients with Alzheimer's disease could be removed, they could be saved. But a new vaccine that did just that suggests the theory is wrong. British researchers gave 64 patients with moderate Alzheimer's disease an experimental vaccine designed to eliminate plaque from their brains. Some patients were followed for up to six years. Autopsies on seven patients who died of Alzheimer's during the study showed that nearly all of the sticky beta-amyloid protein thought to be dangerous had been removed. But all patients still had severe dementia.

"It may be that these toxic plaques trigger the neurodegeneration, but don't have an ongoing role," said Clive Holmes of the University of Southampton, lead author, in a press statement. The study was published Friday in the medical journal, The Lancet. The study was paid for by the Alzheimer's Research Trust, a British charity. Alzheimer's disease is the most common cause of dementia and affects about 25 million people worldwide.

Other experts said that the study's findings pointed to a major gap in our understanding of the disease. Doctors have never been sure whether the brain plaques are the cause of Alzheimer's disease or just a side effect. "We still don't have enough understanding of what we should target," said Dr. Bengt Winblad, director of the Alzheimer's Centre at Sweden's Karolinska Institute. Winblad was not connected to the study.

Brain tangles may play a role

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Allergy Drug Turned Alzheimer's Therapy
July 17, 2008 - Preliminary clinical results showed first-time gains in dementia treatment.

A pill once used as an antihistamine in Russia has shown a slight but unique promise for treating Alzheimer's disease and is now on a fast track to drug studies in the United States. The drug, called Dimebon, appeared to slow memory loss in patients with mild to moderate Alzheimer's disease. But, unlike current Alzheimer's therapies, Dimebon also slightly improved memory. In another first, Dimebon's effect continued for more than a year, while current Alzheimer's treatments are known to peak at three or six months and then begin to lose their effects.

Yet the results from the study of 155 patients in Russia have left many Alzheimer's experts only cautiously optimistic until larger, longer studies are completed under the Food and Drug Administration.

"The Alzheimer's community has been here before with other drugs only to be disappointed," said Dr. Lon S. Schneider, professor of psychiatry and behavioral sciences at the University of Southern California Keck School of Medicine in Los Angeles. Schneider noted the same Dimebon results that appear in this week's medical journal, Lancet, also were released to scientists a year ago. "There's not much to do except wait for the Phase III trial to be completed," Schneider said.

False Hopes or Future Promise?