Alzheimer Related News Items

                                 News as of 6/04/06 (NOTE - new email address)

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Sick Mice Show Dramatic Improvment When Given Immune Cells from Normal Mice -

Researchers have found evidence that weakened or suppressed immune responses may be responsible for AD and that boosting the immune system of AD mice with cells from normal mice causes dramatic improvement in learning and memory. This new research is based on a 2002 report by Professor Douglas Ethell at the University of California Riverside (UCR) that found that beta-amyloid, a protein, increases the amount of the immune suppressor, Fas ligand, and that prolonged suppression of immune responses to that protein is implicated in AD. Ethell wondered if boosting immune responses to beta-amyloid could improve learning and memory in mice that develop AD. He teamed up with Professor Gary Arendash at the University of South Florida who had previously shown that vaccinating mice with beta-amyloid caused temporary improvements in AD mice. However, clinical trials with beta-amyloid vaccinations had been halted due to brain inflammation in some patients. In this study, however, Ethell and Arendash tried a different approach. They injected the AD mice with just the immune cells from normal mice that had been vaccinated with beta-amyloid. The researchers found that with just one injection the mice did significantly better on memory tests and that the improvements lasted one to two months after receiving the cells, which was the longest time-point they tested. Findings from this study may shift the search for an AD cure away from beta-amyloid injections. Instead, the research suggests that a subtle shift in immune responses to the protein may be all that is required for the development of an effective therapy for AD. “We believe these findings show that resetting the responsiveness of specific immune cells to beta-amyloid can provide an effective therapeutic approach to treating AD,” Ethell said. “Translating this research into the clinic may involve isolating immune cells from a compatible donor, expanding them in the lab and delivering them to an AD patient. As we learn more about these cells, it may be possible to isolate them from the AD patient’s own blood, reactivate them in the lab and then return those cells to the patient.” PR 05/31/06

Caregivers May Contribute to AD Symptoms - Symptoms like hallucinations, wandering and paranoia inAD patients are more likely to occur if their caregivers are younger, less educated, more heavily burdened or more depressed, a new study shows. While these symptoms, known collectively as neuropsychiatric symptoms, are due to the AD process, Dr. Kaycee M. Sink told Reuters Health, environmental factors, caregiver behaviors and caregiving styles may exacerbate them. “These dementia-related behaviors are probably the number one reason that people get put into a nursing home,” she added. Sink, of Wake Forest University School of Medicine in Winston-Salem, North Carolina, and her colleagues surveyed the caregivers of 5,788 community-dwelling AD patients in eight US cities, asking them whether the patient had any of twelve different neuropsychiatric symptoms. On average, caregivers reported patients had about 4 or 5 of these symptoms. Using statistical techniques the researchers found that certain caregiver characteristics made neuropsychiatric symptoms more likely in patients. The strongest effects were seen for burden, depression and age. The youngest caregivers reported 1.5 more neuropsychiatric symptoms in the patient, on average, than the oldest. Older caregivers are more likely to be the patient’s spouse, rather than a son or daughter or a young hired caregiver, meaning they are familiar with his or her pre-AD habits and preferences and better able to adjust the patient’s environment appropriately, Sink said in an interview. Also, more educated caregivers may have better coping skills for dealing with stress, and may also understand dementia better than less educated individuals, she added. The findings show that efforts to help caregivers won’t work if they are “one size fits all,” because younger, less educated caregivers may have very different needs for support and information compared to older, more highly educated caregivers, she said. Caregivers of AD patients need to know, she added, that medication can do little for neuropsychiatric symptoms, but that behavioral and environmental approaches can help. When the burden of caring becomes overwhelming, “Caregivers need to know that they should ask for help, ask for support,” Sink concluded, “and get educated as to what some of the behaviors represent and behavioral or environmental ways to deal with them.” By Anne Harding Reuters Health 5/17/06 Journal of the American Geriatrics Society, 54(5):796-803 (May 2006)

Team-based Approach Best for AD - For adults with AD and their caregivers, a collaborative team approach to care leads to significant improvements in behavioral and psychological symptoms of dementia and markedly alleviates caregiver stress, the findings of a new study indicate. However, it does not appear to slow the rate of memory decline or need for nursing home placement. The current guidelines for AD care emphasize “a full package of care ranging from drugs to education to support for the family caregiver and integration of community resources with medical resources,” study leader Dr. Christopher M. Callahan explained. But “many primary care physicians question the utility and practicality of these recommendations.” “We found that patients and their caregivers do benefit from the current treatment guidelines,” said Callahan, director of the Indiana University Center for Aging in Indianapolis. “This benefit,” he added, “is primarily seen in helping the patient and family cope with the behavioral disturbances that are a hallmark of AD. This includes problems like insomnia, depression, agitation, and aggression. Treating these symptoms is important because they distress both the patient and the caregiver and may lead to caregiver burnout or over-medication.” By Megan Rauscher Reuters Health 5/9/06 Journal of the American Medical Association 2006;295:2148-2157

Testing

Visual Test Could Help Diagnose Dementia - A visual test based on images of faces and scenes could help doctors diagnose patients suffering from AD or other types of dementia, researchers said on 5/9/06. After giving patients groups of photos of scenes and faces and asking them to identify “the odd one out,” the scientists found AD patients have difficulty choosing the odd scene while sufferers with semantic dementia (SD), a disorder of language, had problems with faces. Dr. Kim Graham, of the Medical Research Council Cognition and Brain Sciences Unit in Cambridge, England who headed the team, said an image test could be used along with standard memory evaluations to identify dementia patients. “While further research is needed, facial and spatial tests such as ours could help in differentiating between the various forms of dementia,” Graham said. The findings support earlier research that suggested different areas in the medial temporal lobe of the brain could be responsible for various aspects of memory and perception. Knowing which type of dementia patients suffer from is useful because the prognosis, types of problems they may encounter as the disease progresses and treatment can vary. “Having an accurate diagnostic label is important for the individual and their family in terms of how they can plan for the future and for the clinicians in terms of decisions they will hopefully eventually be able to take in regards to drugs,” Graham added in an interview. By Patricia Reaney Reuters Health 5/10/06 Journal of Neuroscience, May 10, 2006, 26(19):5198-5203

Researchers Map Links Between Size of Hippocampus and Progression to AD Dementia -

UCLA researchers sought to test the theory that the hippocampus -- the area of the brain that processes memory -- is smaller in patients with mild cognitive impairment who develop into AD dementia, and that it is larger in patients with mild cognitive impairment who experience cognitive stability or improvement. Using novel 3-D mapping techniques to analyze MRI (magnetic resonance imaging) data from 20 patients with mild cognitive impairment, they found that the patients with the smaller hippocampus did, in fact, face an increased risk of developing dementia. The technique helps physicians detect subtle anatomical differences and can be applied to any disease affecting the hippocampus such as other forms of dementia, epilepsy, hippocampal sclerosis, etc. Tools such as this for predicting cognitive decline hold great promise for patient counseling, advanced planning and therapeutic decision-making. PR 5/8/06 Archives of Neurology 2006;63:693-699

Prevention

Elderly Level Of Physical Fitness An AD Predictor - A new study, carried out in Seattle by the Group Health Cooperative, has found that elderly people who enjoy a good level of physical fitness and performance are much less likely to develop AD or other declines in mental ability. The researchers said that testing how an elderly person walks, his/her strength of grip, and his/her level of balance when standing still can be a simple way of predicting AD risk. Study leader, Dr. Eric Larson, monitored 2,288 people over 65 every two years over a six year period from 1994 to 2000. By the end of this six year period 319 people had dementia, of which 221 had AD. Dr. Larson said that he and the researchers had expected just to detect gradual, slight signs of cognitive decline. They had not expected to discover that physical changes often preceded declines in thinking. They noticed that the first signs of impending dementia seemed to be difficulties with balance and simple walking. They also found that a weaker hand grip was a later indication of impending dementia. Previous reports have indicated that those who do regular exercise in old age have a lower probability of developing dementia/AD. The researchers in this study suggest that elderly people may put off the arrival of dementia or AD by taking regular exercise. The study suggests that there is a close link between the mind and the body in old age, said Dr. Larson. He suggests that physical and men-t-al performance go hand in hand and that what one can do to improve one will also help the other. Medical News Today 6/23/06 Archives of Internal Medicine 2006;166:1115-1120

Study: Plasmalogen Substance Could Prevent AD - AD could be prevented by plasmalogen, contained in seafood such as the sea squirt, a team of researchers at Tohoku University has discovered. The effect was proved in animal experiments, and a company set up by the head of the group plans to study its effect on humans. AD causes severe memory loss and is thought to be caused by the death of nerve cells in the brain. The team led by Prof. Teruo Miyazawa, who specializes in food chemistry at the Graduate School of Agricultural Science at the university, experimented with cell cultures and discovered that plasmalogen prevents the death of nerve cells. It had already been known that plasmalogen in the brains of those with AD decreases by about 30 percent, but its function had not been clarified. Miyazawa fed plasmalogen to rats with AD and had them search a maze for food. The experiment showed that the rats’ declining memory, ability and learning could be prevented. Miyazawa discovered plasmalogen in sea squirt, oyster and sea urchin. Knight-Ridder 5/3/06

Other Items

Free Radical Molecules May Help Drive Brain Illnesses - Researchers believe they’ve found a link between the cellular stress caused by free radical molecules and the accumulation of misfolded proteins that may cause neurodegenerative conditions such as AD and Parkinson’s disease. A team at the Burnham Institute for Medical Research in La Jolla, Calif., found that overproduction of oxidizing free radicals, specifically nitric oxide (NO), causes inhibition of Protein Disulphide Isomerase (PDI) -- a “chaperone” protein that’s necessary for proper protein folding in times of cellular stress. Inhibition of PDI reduces its neuroprotective benefits for nerve cells, the researchers explained in the May 25 issue of Nature. The researchers said this is the first study documenting a direct link between NO free radicals and protein misfolding, which is believed to be a common pathway in the development of nearly all neurodegenerative diseases. The finding may help lead to the development of new treatments for these diseases. “Our data demonstrate a previously unrecognized relationship between NO and protein misfolding in degenerative disorders, showing that PDI can be a target of NO in cellular models of Parkinson’s disease and human neurodegenerative disease,” senior author Dr. Stuart A. Lipton, director of the Del E. Webb Center for Neurosciences and Aging at the Burnham Institute, said in a prepared statement. HealthDay News 05/25/06 Nature 441, 513-517 (5/25/06)

Heart Failure Linked to Dementia Risk - The results of a new study suggest that there is an association between heart failure and an increased risk of dementia or AD in the elderly. Several previous studies have linked heart failure with mental impairment, “but to our knowledge, no investigations have explored the relationship between heart failure and the risk of dementia,” Dr. Chengxuan Qiu, of the Karolinska Institute, Stockholm, and colleagues found. The risk of dementia due to heart failure was lower in patients who were on drugs to reduce high blood pressure, decreasing the risk to 38 percent. Conversely, the risk of dementia in heart failure patients increased as diastolic blood pressure (the bottom number in the blood pressure measurement) dropped below 70 mm Hg, raising the risk by more than three-fold. The authors suggest that it may be worth looking at possible biological pathways linking heart failure to dementia, specifically to AD. The markedly impaired cerebral circulation that results from chronic heart failure, for example, may play a role in the neurodegenerative process, especially in the elderly population. Poor blood circulation in the brain could further promote neurodegeneration by depriving the brain of oxygen, Dr. Qiu’s group notes. The authors note that blood pressure-lowering drugs may partially counteract the negative effects of heart failure in the brain by improving blood flow and by preventing the formation of obstructions. Reuters Health 5/11/06 Archives of Internal Medicine,2006;166:1003-1008

Different Forms Of Amyloid Beta In AD Harm Neurons In Different Ways - Researchers at UC Irvine have shown that different forms of amyloid beta lead to neural damage in different ways, leading to an increasingly complex view of amyloid toxicity in the AD brain. The finding could modify the way therapeutic approaches for the treatment of AD are designed. The researchers studied the effects of different forms of the amyloid beta peptide on human brain cells. Amyloid beta accumulation is one of two hallmarks of AD and is considered a major target for researchers looking into therapies for the treatment of the disease. After death, most amyloid beta found in the brains of AD patients is in fibrillar form -- long, insoluble fibers bound together in deposits called senile plaques; however, there are also soluble forms of amyloid beta, or oligomers, that may decisively contribute to neural degeneration. The experiments conducted at UCI showed that the soluble forms of amyloid beta are much more toxic and lead to neuronal death in as little as 12 hours. The fibrillar form, meanwhile, does not actually kill the neurons, but slowly, over a period of 10 or more days, renders them useless. Not known is whether the soluble amyloid beta in the AD brain eventually turns into the fibrillar kind, or whether the two are completely different. “These findings are quite significant because, although both fibrils and oligomers may contribute to dementia, they do so in very different ways over different time spans,” said Jorge Busciglio, an assistant professor of neurobiology and behavior. “This complexity of the amyloid beta species will require more sophisticated therapeutic approaches. For example, it might be dangerous to create compounds that target fibrillar amyloid and try to break them up, because if the fibers dissolve into the soluble form, that could actually speed up cell death and the onset of dementia rather than treat it.” Researchers now will have to determine why the soluble form of beta amyloid is so much more toxic. One theory is it binds to neuronal connections, or gateways into the cell, and gives soluble amyloid beta easier, quicker access into the neuron. The UCI research also showed that the soluble form quickly impairs the function of mitochondria, the cells’ energy generators. Brain cells consume more energy than any other cell in the body. If that energy source dies, the cells die as well. Medical News Today 5/31/06 Journal of Neuroscience, May 31, 2006,26(22):6011-6018

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