Alzheimer Related News Items

News as of 4/06/03

For more info on these abstracts write/call Ed Cabic (edcabic@comcast.net or 410-992-7197)

NOTE - e-mail address change to new address as of 2/02

For more AD information, see Alzheimer Information athttp://www.connext.net/~seniors/infoad.htm

Copies of these reports are posted there

This web page was started at the Florence Bain Senior Center in Columbia MD


Top Items

Memantine in Moderate-to-Severe AD - (1) A drug, Memantine, long used in Germany slows down memory loss and physical decline in advanced AD patients, according to a six month study published 4/3/03 in the New England Journal of Medicine of what could be the first effective treatment for late stages of this disease. “It’s a breath of fresh air for caregivers and for patients,” said Dr. Barry Reisberg of New York University School of Medicine, who led the study. Memantine works differently than approved AD drugs by blocking excess amounts of a brain chemical, glutamate, which can lead to nerve cell damage. The most commonly used AD drugs — Aricept, Exelon and Reminyl — prevent the breakdown of another brain chemical. Doctors usually keep AD patients on those drugs as they move into later stages of the disease because they are thought to do some good, said Bill Thies, medical-science director of the Alzheimer's Association. Memantine would give them a welcome option, he said. (2) A second study of memantine used with one of the current AD drugs, Aricept, suggests the combination actually improves memory and thinking skills in advanced patients. That study is being presented 4/3/03 at the American Academy of Neurology’s annual meeting. Dr. Martin R. Farlow of Indiana University School of Medicine, one of the researchers, described the combination study where 403 patients who were already taking one of the AD drugs, Aricept, were given either Memantine or a dummy pill for six months. The patients who got Memantine showed a significant improvement in their memory and thinking, he said . “The best of all worlds is if you can treat an illness with one medication, but often the real world is you find drugs that work in different ways and you are able to gain additional benefits in patients,” said Farlow. “And I think that’s what this study says.” Ivan Gergel, a researcher at Forest Labs, the New York City company that wants to market Memantine in America said the Food and Drug Administration may make a decision on whether to approve Memantine in the United States this fall. If it is approved, Gergel estimated that patients may be able to get the drug by the summer of 2004. By Stephanie Nano, Associated Press Writer 4/2/03 and Shankar Vedantatam Washington Post 4/3/03 The New England Journal of Medicine Vol 348:1333-1341 3/4/03


Gene Therapy May Ease AD in Mice - A form of gene therapy appears to reduce the buildup of harmful amyloid-beta proteins in the brains of mice, a signature feature of the memory-robbing condition AD, according to new research from the Salk Institute for Biological Studies in California . The researchers reduced amyloid-beta in the brains of mice with AD by increasing brain levels of the amyloid-killing substance neprilysin. Neprilysin, a substance naturally found in the brain, alters amyloid-beta proteins in ways that lead to their destruction. To increase levels of neprilysin in the body, the researchers injected the gene that produces neprilysin into one side of the brains of mice with AD. The gene then became incorporated into the mice’s genetic material, causing their own cells to manufacture the protein. One month later, the researchers inspected the animals’ brains, and found that the plaques on the side of the brain injected with the neprilysin gene were 50 percent smaller than those found on the other side. “The size of the plaques is tremendously reduced," study author Dr. Inder M. Verma told Reuters Health. An important aspect of this research is that only one injection was needed to produce such a dramatic change, Verma noted. “You give one injection, and it’s a lifetime treatment,” he said. “A lifetime production of the protein.” He added that he and his colleagues are currently testing a new batch of mice to determine if the treatment can also improve symptoms of AD. Whether adding extra neprilysin might cause unwanted side effects remains unclear, lead author Dr. Robert A. Marr noted. “The effects we can’t anticipate are potentially more serious than those we can,” he said. Marr noted that neprilysin also degrades substances that influence pain, so increases in the protein might also increase our perception of pain. Other proteins in the body besides neprilysin degrade amyloid-beta, Verma added, and future gene therapy techniques that increase levels of these proteins in the brain may achieve similar results to those seen in the current research. By Alison McCook Reuters Health 3/28/03 Journal of Neuroscience 2003;23:1992-1996



Drugs

Painkillers May Dissolve AD Plaque - Painkillers routinely used by millions of Americans may dissolve abnormal plaque deposits in the brain that are linked to AD, a study out 3/13/03 suggests. The test-tube study adds new evidence to the theory that non-steroidal anti-inflammatory drugs such as ibuprofen and aspirin may prevent this brain disease, which causes memory loss. Jorge Barrio, a researcher at the University of California-Los Angeles, and his colleagues knew previous studies suggested that anti-inflammatory drugs protected people from developing AD. But those studies just showed a statistical link between such protection and the drugs. The team mixed a chemical marker FDDNP that highlights plaque with diseased human brain tissue. They then added naproxen or ibuprofen, painkillers often used to treat arthritis pain. Using a microscope that detects the chemical marker, the researchers found the drugs melted away some of the plaque. That finding suggests that people who take such drugs regularly may get some protection against AD, Barrio says. Still, Bill Thies of the Alzheimer’s Association in Chicago cautions against jumping to conclusions about these drugs.” “'This is a test-tube study,” he says. The findings need to be confirmed with human studies, he says. The UCLA team plans to give the same drugs to people with early-stage AD and then use a newly developed brain scan to see if the drugs dissolve some of the plaque. But such studies will take years. Kathleen Fackelmann USA TODAY 3/13/03 Neuroscience 117;3 31March 2003, pp723-730


Vaccination Delays ‘Mad Cow’-Like Symptoms in Mice - Vaccination may one day be able to slow the onset of symptoms in fatal brain-wasting illnesses like "mad cow" disease, new research in mice suggests. Such conditions, known as prion diseases, are marked by the build-up of abnormal prion proteins in the brain. Prion diseases include mad cow disease -- or bovine spongiform encephalopathy (BSE -- scrapie in sheep, and similar conditions that affect game animals such as deer and elk. Creutzfeldt-Jakob disease (CJD) is a rare human prion disease, and a type of CJD -- called new variant CJD -- is believed to have arisen in humans through the consumption of BSE-tainted beef. Researchers hope that vaccines against these rare prion diseases will also turn out to have value in treating common disorders involving abnormal protein accumulation in the brain, such as AD. In the new study, researchers at New York University investigated two immunization approaches in mice with prion disease: passive immunization, in which mice received weekly prion antibody injections immediately following and for one month after exposure to the scrapie prion; and active immunization, in which an oral vaccine was given prior to scrapie exposure. With passive immunization, they found, the incubation period from scrapie exposure to the first signs of symptoms was significantly prolonged. The active immunization studies are still ongoing, Dr. Marcin Sadowski reported here at the annual meeting of the American Academy of Neurology Sadowski and his colleagues hope that immunization may act against prion-based diseases by delaying the onset of symptoms. “These findings show that the immune system is an important therapeutic target for the prion disease,” he said. He added that these findings may yield useful information for other neurodegenerative illnesses, such as AD, that are characterized by abnormal protein build-up in the brain. By Paula Moyer Reuters Health 4/1/03



Caregivers

Experimental Robots May Offer Aid at Bedsides - Its bedside manner has kinks to work out, but an experimental robot may one day help the U.S. health care industry cope with burgeoning ranks of the elderly and ill. For now the robots operate primarily as a form of mobile video telephone allowing patients and doctors to communicate. But eventually, they may help the health care industry serve millions by wheeling patients to dinner, or even taking temperatures and drawing blood. “This technology enables health care professionals to care for people in remote locations at a fraction of the time it would normally take,” said Loren Shook, chief executive of Silverado Senior Living, an operator of assisted living facilities for people with AD. Silverado’s Calabasas, Calif., care center is the site for a clinical trial of a robot made by InTouch Health Inc. that is designed to allow real-time, one-on-one communication between doctors and patients, health care management and staff or between patients and their families. The mobile robot, called the Companion, is fitted with a camera that films the patient while the caregiver’s face appears on the robot’s television screen-like head. Controlled from an off-site console, the robot uses software and a broadband wireless Internet connection to allow the patient and caregiver to see, hear and talk to each other. “The goal is to extend the reach of health care ... A nursing shortage and cuts in government reimbursement are straining the system and its going to get worse,” said Yulun Wang, chief executive of InTouch and founder of Computer Motion Inc., which makes robotic systems used in surgery. The technology is still at an early stage, Wang said. “First there is communication, but the second thing would be manipulation. Eventually the robot could be designed to do things like push a wheelchair or even be used in private homes,” he said. The robots have not received Food and Drug Administration approval to perform medical tasks yet. But the company believes they ultimately will and sees the risk of mistakes or malfunction as low. For now, InTouch Health plans to lease Companion robots to institutions caring for the elderly, probably at around $2,500 to $3,000 per month. “It is a breakthrough event when people with dementia can tolerate another form of engaging them in life,” Shook said. Reuters 3/6/03



Prevention

‘Silent’ Strokes Common and Linked to Dementia - People who experience so-called silent strokes face more than twice the risk of developing dementia as those who have not had strokes that strike without symptoms, according to new study findings released 3/26/03 by Erasmus Medical Center in Rotterdam, the Netherlands. The results suggest that people who take steps to prevent strokes might also help ward off dementia, including AD, said study author Dr. Monique M.B. Breteler. “Anything that helps to keep your (blood) vessels healthy -- blood pressure control, healthy diet, adequate physical exercise, etc. -- may help to not only reduce the risk of (heart attack) and stroke but possibly also dementia,” Breteler told Reuters Health. Silent strokes, as with full-blown strokes, result when blood vessels in the brain become blocked or rupture. However, patients experiencing silent strokes do not have severe headaches, dizziness, difficulty speaking, paralysis or other classic stroke symptoms. Doctors do not routinely screen patients for silent strokes, which can be detected with an expensive MRI brain scan. There is increasing evidence that blood-vessel damage may contribute to the development of AD, the researchers noted, though precisely how is unclear. Results from the new study showed that people who had evidence of silent strokes on their initial MRI scans had more than double the risk of developing dementia during the study period as those who had not had silent strokes. By Jacqueline Stenson Reuters Health 3/26/03 The New England Journal of Medicine 2003;348:1215-1222, 1277-1278


Moderate Drinking Cuts Risk of Dementia - Elderly people who drink moderately are less likely to suffer dementia than teetotalers, though seniors who drink too much add to their risk, researchers said on 3/18/03. Seeking to explain their findings, the researchers said consuming moderate amounts of alcohol prevents hardening of the arteries that leads to damaging strokes, lessens the risk of brain lesions and helps blood vessels to function. Better blood flow generally lessens the risks of vascular-related dementia, usually caused by strokes. The study of 373 dementia patients older than 65 and a like number of control subjects revealed that the lowest rates of dementia were among subjects who drank between one and six alcoholic drinks a week, who had half the risk of teetotalers. People who abstained from alcohol and those who consumed between seven and 13 drinks a week were at about equal risk of developing dementia, while those who drank more than 13 drinks a week had a significant 22 percent higher risk. But study author Kenneth Mukamal of Beth Israel Deaconess Medical Center in Boston issued a cautionary note about drawing conclusions. “Given the observational nature of our study, we cannot recommend that older adults begin drinking moderately on the basis of these findings alone. Older adults should discuss their alcohol use with their physicians and make appropriate decisions based on these discussions.” Reuters 3/18/03 Journal of the American Medical Society 2003;289:1343



Other Items

US Life Expectancy Hits Record 77.2 Years - Americans are living longer than ever as deaths linked to major illnesses continue to decline, according to a preliminary report released 3/14/03 by the Centers for Disease Control and Prevention. The latest numbers show life expectancy increased 0.3 years, reaching a “record” 77.2 years in 2001, up from 77 in 2000. Life expectancy increased for men and women as well as blacks and whites, according to the report. The largest decline among leading killers was for influenza and pneumonia, where deaths went down 7%. Deaths from heart disease declined nearly 4%, cancer deaths dropped 2% and stroke deaths fell nearly 5%. But deaths from kidney disease, hypertension and AD increased. The 8 leading causes of deaths remain the same as in past years: Heart disease, which killed nearly 700,000, Cancer 550,000, Stroke 164,000, Chronic lung disease 124,000, Accidents 97,700, Diabetes 71,000, Influenza and pneumonia 62,000, and AD 53,600. By Jesse J. Logan Reuters Health 3/14/03 and By Maggie Fox, Reuters Health and Science Correspondent 3/14/03 Copy of 45 page report in pdf at http://www.cdc.gov/nchs/data/nvsr/nvsr51/nvsr51_05.pdf

 

Scientists Develop First Artificial Brain Section - Scientists have developed the first artificial region of the brain--a silicon chip that mimics an area that controls memory, mood and awareness. Devised by researchers at the University of Southern California in Los Angeles, the chip is designed to carry on the functions of the region known as the hippocampus and could one day be used to help people with brain damage. It will first be tested on tissue from rats’ brains, and then on live animals. “If all goes well, it will then be tested in a way to help people who have suffered brain damage due to stroke, epilepsy or AD,” reports New Scientist magazine 3/15/03. Theodore Berger and his team developed the artificial hippocampus as a test case to see if it could be done. It has taken them nearly 10 years. First they devised a mathematical model of how the hippocampus performs under all conditions. The next step involved building the model into a silicon chip and then interfacing the chip with the brain in laboratory studies. “No one understands how the hippocampus encodes information. So the team simply copied its behavior,” according to the magazine. If the initial brain tissue tests are successful, Berger and his colleagues plan to begin trials in live rats within six months and then in monkeys. “If you lose your hippocampus you only lose the ability to store new memories,” Berger told the magazine. He added that if the chip, which will sit on the outside of the skull, helps someone with a damaged hippocampus regain the ability to store new memories it will be proof that it works. Reuters 3/12/03 New Scientist March 15, 2003, pg 4


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