Alzheimer Related News Items

News as of 9/10/06

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

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

Sweet Solution For AD? - Certain variants of a simple sugar ameliorate AD-like disease in mice, according to a new study by Canadian researchers. Although the new studies are still in the early stages, the findings could lead to new therapies that prevent or delay the onset of AD. The new studies show that some types of a sugar called cyclohexanehexol —also known as inositol—prevented the accumulation of amyloid β deposits, a hallmark of AD. Scyllo- inositol treatment also improved cognitive abilities in the mice and allowed them to live a normal lifetime. Senior author Peter St George-Hyslop cautioned that the chemicals tested in these studies are not the type of inositol sold commercially as a nutritional supplement. That type - - myo-inositol - -has been shown previously to be ineffective at breaking up amyloid aggregates, he said. In the brain of a person with AD, small proteins called amyloid β aggregate into plaques, and a protein called tau clumps into neurofibrillary tangles. The brain becomes inflamed and neurons atrophy and die. It’s not completely clear what kind of amyloid β peptide (monomers, oligomeric aggregates, or fibrillar aggregates) is responsible for the onset of disease, said St George-Hyslop of the University of Toronto. “Because we were able to show that scyllo-inositol specifically dispersed the high-molecular-weight oligomeric aggregates, this study confirms that the initiating event is the accumulation of oligomeric aggregates of amyloid β peptide,” he said. When the researchers treated transgenic mice with human genes that predispose them to an AD like disease with scyllo-inositol, all of the animals’ disease symptoms improved. Cognitive function was improved, amyloid plaques disappeared, inflammation declined, and the mice lived longer. The scientists found that scyllo-inositol conferred these benefits not only if the mice were treated when they were very young and disease-free, but also if they were treated after the onset of disease. Scyllo-inositol “is an exciting experimental therapy, but until it has actually been tested in humans, it should not be considered the cure for AD,” St George-Hyslop said. “There are many things that are very promising when done in animal models that turn out to either not work in humans or to have unexpected toxicity.” Science Daily 6/12/06 Nature Medicine, 12, 801-808 (01 July 2006)

A Second Dimension To AD Suggested By Study - The genes responsible for an inherited form of AD play a direct role within cells that has largely been overlooked, according to a 9/8/06 report. The findings suggest that there may be an additional dimension to the irreversible neurodegenerative disorder, which potentially suggests a new avenue for the pursuit of therapies, the researchers said. The researchers found that two genes mutated in familial AD known as presenilins may control the balance of calcium within cells by acting as a calcium channel. Calcium is an important signaling molecule, with effects on the nervous system that include functions relevant to learning and memory, the researchers said. The research team also discovered that the mutant forms of presenilin--which have been linked to about 40 percent of familial AD cases--lose the ability to serve this function. Presenilins are primarily known for their role as an enzyme that cleaves amyloid precursor protein (APP) to form amyloid β-peptide, the principal constituent of the plaques that riddle the brains of AD patients. “Clearly it makes sense that presenilin’s role in cleaving APP would affect AD,” said Ilya Bezprozvanny of UT Southwestern Medical Center at Dallas. “But our findings suggest a totally different angle, raising the possibility that presenilin’s effect on the disease may be two-fold.” Bezprozvanny cautioned, however, that further work is required to determine whether or not the genes’ other role in calcium regulation has a causal connection to the symptoms of AD. The findings suggest that drugs that restore normal calcium levels might be useful for treating AD, Bezprozvanny said. Indeed, he added, a drug called memantine, which is already in use against AD, acts on receptors that are a component of the calcium pathway. The development of AD drugs has almost exclusively focused on amyloid plaques,” he said. The current findings begin to suggest the possibility that a combination therapy targeting both amyloid and calcium signaling might be a “best case scenario,” Bezprozvanny speculated. Medical News Today 9/9/06 Cell, 126, 981-993, Sept. 8, 2006

Drugs

Drug Triggers Body’s Mechanism To Reverse Aging Effect On Memory Process - A drug made to enhance memory appears to trigger a natural mechanism in the brain that fully reverses age-related memory loss, even after the drug itself has left the body, according to researchers at UC Irvine. Professors Christine Gall and Gary Lynch, were among a group of scientists who conducted studies on rats with a class of drugs known as ampakines. Ampakines were developed in the early 1990s by UC researchers, including Lynch, to treat age-related memory impairment and may be useful for treating a number of central nervous system disorders, such as AD and schizophrenia. In this study, the researchers showed that ampakine drugs continue to reverse the effects of aging on a brain mechanism thought to underlie learning and memory even after they are no longer in the body. They do so by boosting the production of a naturally occurring protein in the brain necessary for long-term memory formation. “This is a significant discovery,” said Gall, professor of anatomy and neurobiology. “Our results indicate the exciting possibility that ampakines could be used to treat learning and memory loss associated with normal aging.” Medical News Today 7/31/06 Journal of Neurophysiology 96: 677-685, 2006

AD: THC Inhibits the Enzyme Acetylcholinesterase - Researchers at The Scripps Research Institute have found that the active ingredient in marijuana, tetrahydrocannabinol or THC, inhibits the formation of amyloid plaque, the primary pathological marker for AD. According to the Scripps Research study, which used both computer modeling and biochemical assays, THC inhibits the enzyme acetylcholinesterase (AchE), which acts as a “molecular chaperone” to accelerate the formation of amyloid plaque in the brains of AD patients. Although experts disagree on whether the presence of beta-amyloid plaques in those areas critical to memory and cognition is a symptom or cause, it remains a significant hallmark of the disease. With its strong inhibitory abilities, the study said, THC “may provide an improved therapeutic for AD” that would treat “both the symptoms and progression” of the disease. “While we are certainly not advocating the use of illegal drugs, these findings offer convincing evidence that THC possesses remarkable inhibitory qualities, especially when compared to AChE inhibitors currently available to patients,” said Kim Janda, at Scripps Research. Medicine New.net 8/9/06 Molecular Pharmaceutics ASAP Article 10.1021/mp060066m S1543-8384(06)00066-9 web date 8/8/06

AD Drugs Fail to Deliver - Though research shows promise, current drugs offer modest benefits at an annual cost of $2.16 billion. Thomas Finucane, a geriatric specialist, tells his AD patients and their relatives not to get their hopes up when he prescribes Pfizer Inc.’s Aricept and similar drugs. “In 10 years we are going to be embarrassed that we were sending billions of dollars to the drug companies for a pill that patients can’t distinguish from a placebo,” said Finucane, a professor of medicine at Johns Hopkins University School of Medicine in Baltimore. AD medicines generated $2.16 billion last year, according to IMS Health Inc. Approved in 1996, Aricept became the world’s top-selling drug for the disease even amid doubts about its effectiveness and that of similar pills. Today, in one of the largest reviews of clinical data on AD drugs, researchers found that all medications in the same class as Aricept, known as cholinester- ase inhibitors, offered the same small improvement in mental functioning. The study by the U.K.-based Cochrane Collaboration analyzed data from 18 clinical trials involving 9,200 patients. Patients taking AD drugs showed an average 2.5-point improvement on a 70-point scale measuring cognitive function and activities of daily living compared with those taking a placebo. The analysis found that 29 percent of patients dropped out of the trials because of side effects, such as nausea, vomiting and diarrhea. “The average benefit is very small. It might escape notice,” said lead researcher Jacqueline Birks, a medical statistician for Cochrane’s dementia and cognitive impairment group at University of Oxford. “Don’t expect miracles.” Doctors have long debated whether the drugs, which also include Novartis AG’s Exelon and Johnson & Johnson’s Razadyne, offer any benefit at all. Finucane says his AD patients and their relatives can’t tell whether there is improvement after taking the pills. John Morris, a professor of neurology at Washington University School of Medicine, says the treatments do help patients. Both say there’s dire need for new medicines. By Angela Zimm and Michelle Fay Cortez Bloomberg News 7/27/06

Blood Product Shows Promise in Treating AD - A blood product normally used to treat immune disorders and a type of leukemia may also slow or stop mental decline in people with AD, researchers reported 7/18/06 at an AD conference in Madrid. The product is called IVIg (pronounced EYE-vig), for intravenous immunoglobulin, also known as gamma globulin. Made from pooled blood plasma, it is a thick soup of antibodies, the proteins made by the immune system to get rid of unwanted substances. It has been used for 30 years for other diseases and is dripped into a vein like a transfusion. But the findings in AD are based on an experiment involving only eight patients with no comparison group and need to be verified by larger studies, scientists said. “This is not ready for widespread use,” said Dr. Norman R. Relkin, director of the Memory Disorders Program at NewYork-Presbyterian/Weill Cornell Medical Center. Although the findings were preliminary, Dr. Relkin said, some doctors were already giving IVIg infusions to people with mild cognitive impairment, a mental decline that is often an early form of AD. IVIg is in short supply and can cost up to $10,000 a month, depending on the dose, and since it is not approved for AD, patients will probably have to pay for it out of their own pockets. The leading theory of AD is that the disease is caused by deposits of a protein called amyloid that build up in the brain, disrupt nerve function and ultimately kill brain cells. IVIg contains antibodies that stick to amyloid and may help clear it out of the brain. IVIg may also have anti-inflammatory properties that help patients with AD. By Denise Grady New York Times 7/19/06

New Results Published on Pharmexa’s PADRE Epitope in AD Vaccine - A group of scientists from the Institute of Molecular Medicine at Huntington Beach (California) and the Institute of Brain Aging and Dementia at the University of California has published new pre-clinical data on an experimental AD vaccine incorporating Pharmexa’s proprietary PADRE epitope. The prototype vaccine, a combination of a fragment of the Abeta peptide and Pharmexa’s PADRE epitope, gave rise to high anti-Abeta antibody titers in vaccinated mice. No unwanted cellular immune responses were detected, and there were no signs of side effects in the brains of the animals. These independent data therefore confirm Pharmexa’s hypotheses that a safe and effective AD vaccine may be developed using dominant helper cell epitopes such as PADRE that will alleviate the side effects observed with earlier Abeta vaccines. The results also once again confirm the versatility of the PADRE epitope across a broad range of applications. The Abeta peptide is believed to have a central role in the onset and progression of AD. Pharmexa, in collaboration with H. Lundbeck, as well as other pharmaceutical and biotech companies, has therefore been targeting the Abeta peptide for a therapeutic AD vaccine. WebWire 8/25/06 The results were published in Vaccine, vol. 24, issue 13, 2275-2282, 20 March 2006

Irish Study on AD Drug - A new partnership comprising the Roskamp Institute, a Florida-based Neuroscience Center, and the Trinity College Institute of Neuroscience (TCIN) will conduct a clinical study to determine if the drug Nilvadipine might be useful in the treatment of AD.

Research carried out by the Roskamp Institute over the past 10 years, suggests that some medications have the potential to increase the removal of the amyloid protein from the brain into the blood, which is believed to be beneficial in developing a potential treatment for AD. The purpose of the new study is to establish whether Nilvadipine alters the level of amyloid in the blood. The drug is currently used to treat blood pressure and is available in Ireland on prescription for this condition. The research will involve 150 mild to moderate AD patients who must be referred by their hospital physician or GP. A key element of the study is the formation of a new group of specialist doctors in the areas of geriatrics and old age psychiatry in Dublin hospitals, called the Dublin Ageing Research Network. These doctors will participate in a new partnership to promote clinical research studies in ageing in Dublin, of which the Nilvadipine research is the first study. By Niall Hunter - Editor Irish Health 8/9/06

Genes & Genetic Issues

Long Island Scientist Part of Break in AD Research on Tangles of Tau Protein - A scientist at Cold Spring Harbor Laboratories was part of an international team of researchers that has identified what might be a way to slow the effects of AD. Cordula Schulz was part of the discovery of what appears to be a natural protective mechanism against the effects of AD and other neurodegenerative diseases. The hope is that, if they are correct, it will be possible to use drugs to enhance that mechanism and alleviate AD pathology. In their studies with mice, flies, and human brain tissue, they discovered that the enzyme puromycin-sensitive aminopeptidase (PSA) takes apart abnormal tangles of the protein known as tau. It is these tangles that are blamed for declines in patients with neurodegenerative diseases. Brain cells that become tangled ultimately die. The group reportedly noted that PSA gene expression in patients with neurodegenerative diseases is greater in the cerebellum portion of the brain than in the cortex, which is known to be less resistant to such diseases. In the study, mice were engineered to have a mutant form of human tau that causes neurodegeneration. DNA microarrays – or “gene chips” – were then used to identify genes that were more active in some brain regions than others. Among the thousands of genes examined, the PSA gene stood out as being more active in the resistant cerebellum. Studies with the fruit fly Drosophila revealed that loss of PSA gene function speeded up neurodegeneration. Test tube studies also showed that PSA directly acts on tau tangles to dismantle them for degradation by the cell. Next, the PSA gene activity of samples of both cortex and cerebellum brain tissues from both healthy patients and patients with neurodegenerative diseases were analyzed. In both types of samples, the group reported, PSA levels in the cerebellum were five times greater than those in the cortex. The group wrote: “Data derived from in vivo studies with animal models and a cell-free system suggest that PSA may play a pivotal role in protection from tau-induced neurodegeneration, most likely by direct cleavage of tau.” The Northender 9/6/06 Neuron, 51, 549-560, 07 Sept. 2006

TNF-alpha Polymorphisms Tied to AD Risk - Variations in the tumor necrosis factor (TNF) alpha promoter region appear to be associated with the risk of late-onset AD, researchers report8/25/06. “We studied the genetic variations of subjects from a community-based population; and our data suggest that the genetic modulation of a prominent inflammation mediator, TNF-alpha, is related to AD risk,” senior investigator Dr. Lee-Way Jin, University of California-Davis, told Reuters Health. Dr. Jin and associates conducted a case-control study involving 265 elderly white subjects who met criteria for probable or definite AD. They were compared with 347 controls. Genotyping results indicated that the TNF-alpha-863 A allele was associated with reduced odds of developing AD. This allele was seen in 16.9% of controls and 12.6% of cases. The researchers note that the TNF-alpha-863 A allele is associated with 31% lower transcriptional activity and significantly lower serum TNF-alpha levels than normal. The team looked at haplotypes based on transcriptional activity, and after adjusting for factors including age and the presence of the APOE epsilon 4 genotype, they found increasing odds of AD with increasing transcriptional activity. These results suggest that strategies designed to reduce TNF-alpha protein production or activity might offer a treatment for AD, Dr. Jin concludes. Reuters Health 8/25 Archives of Neurology 2006; 63:1165-1169

“Sticky” Mice Lead to Discovery of New Cause of Neurodegenerative Disease - When a faulty protein wreaks havoc in cells and causes disease, researchers are usually quick to point the finger at a wayward gene. Now scientists are learning that some neurodegenerative diseases can develop even though a gene is perfectly normal. The diseases can be caused when the genetic instructions contained in the gene are not executed properly, leading to a lethal buildup of malformed proteins in brain cells. The new studies by Howard Hughes Medical Institute (HHMI) investigator Susan L. Ackerman and colleagues at The Jackson Laboratory point to a novel mechanism behind the buildup of the toxic sludge that accumulates in neurons. Researchers have long known that neurodegenerative disorders can be caused by the gradual yet persistent accumulation of misfolded proteins in neurons that eventually triggers cell death. But this new mechanism points to errors in executing the genetic instructions, which are distinct from known causes of neurodegenerative diseases, such as AD and Huntington’s diseases. The researchers made their discovery by studying mice with a mutation called sticky (sti). Although named for the sticky appearance of their fur, the mice harbor much more serious problems beneath their unkempt coats: poor muscle control, or ataxia, due to death of Purkinje cells in a region of the brain called the cerebellum. No one knew why Purkinje cells were dying in sticky mutant mice. To find out, Ackerman and her colleagues searched for the gene that was disrupted by the sti mutation. They were surprised to find a subtle defect in a gene that codes for part of the cell’s protein synthesis machinery — an enzyme called alanyl tRNA synthetase. This enzyme is responsible for loading, or “charging” the amino acid alanine onto transfer RNAs (tRNAs). Transfer RNAs transport individual amino acids to the cell’s protein synthesis machinery, where they are added to the growing stringlike protein molecules being manufactured there. Ackerman said that when the team began its studies, the team did not expect that such a fundamental defect in protein synthesis could be behind the neurodegeneration they had observed in sticky mice. “So, a major question to be explored in human populations is whether the subtle loss of translational fidelity from such a defect could lead to various human diseases - particularly those that involve the accumulation of misfolded proteins,” she said. Howard Hughes Medical Institute 8/13/06 Nature 443, 50-55 (7 Sept. 2006).

Testing

New Study Provides Further Evidence that The MCI Screen Accurately Detects Mild Cognitive Impairment - A recent study, the Hancock County Aging Study, found 23% of patients in a primary care population had cognitive impairment. However, two-thirds of those who were diagnosed as impaired had no outward symptoms or functional decline. The MCI Screen developed by Medical Care Corporation enabled the diagnosis of pre-sympto-matic patients and identified impaired patients much more accurately than assessments that have historically been used by clinicians. The recent findings were presented 7/17/06 at the 10th International Conference on AD and Related Disorders, presented by the National Alzheimer’s Association held in Madrid, Spain. Mild Cognitive Impairment is the first clinical stage of AD and often lasts approximately seven years before progressing to mild AD. Currently, up to 95% of AD patients are diagnosed when the disease has progressed to the moderate stage. Diagnosing and treating AD in the mild cognitive impairment stage will have a tremendous impact on patients, caregivers and the health system. PR 7/31/06

New AD Urine Test Will Help Early Diagnosis - The world’s first non-surgical diagnostic test for AD is to be unveiled in Edinburgh in September 2006. Nymox, a Canadian company, is poised to market the urine-based test - which is designed for physicians to administer - in the UK but concern has been raised it could be a precursor to the development of a DIY dementia test. The test uses a urine sample to measure the level of a brain protein called neural thread protein (NTP) known to be elevated in patients suffering from AD. The AlzheimAlert test is described by its designers as the only painless urine test available to assist a physician in diagnosis. A spokesman for Nymox said: “An accurate clinical diagnosis of AD is crucial for patients and their families. It enables them to make informed social, legal and medical decisions and allows treating physicians to take advantage of new improvements in drug treatment and care.” By Brian Donnelly The Hearld (Scotland) 8/28/06

In-home Sensors Spot Dementia Signs In Elderly - An Oregon Health & Science University study shows motion and door sensors placed in elders’ homes can help track activity patterns thought to relate to memory changes that are early signs of dementia. The study results, presented near the end of July 2006, at the 10th International Conference on AD and Related Disorders in Madrid, show that continuous, unobtrusive monitoring of in-home activity may be a reliable way of assessing changes in motor behaviors that may occur along with changes in memory. “To see a trend over time, you need multiple measures - good days and bad days - and it often takes years to see that trend in a clinic setting,” said Tamara Hayes, Ph.D., assistant professor of biomedical engineering at OHSU’s OGI School of Science & Engineering, and the study’s lead author. She noted that most clinic visits by elders are spaced over months or even years, and their memory and motor skills performances are evaluated in a small number of tests completed in a limited amount of time. “In contrast, we’re looking continuously at elders’ activity in their own homes,” Hayes said. “Since we’re measuring a person’s activity many times over a short period, we can understand their normal variability and identify trends. If there’s a change over a period, you can see it quickly.” Medical News Today 7/31/06

Prevention

Juices May Reduce AD Risk - In a large epidemiological study, researchers found that people who drank three or more servings of fruit and vegetable juices per week had a 76 percent lower risk of developing AD than those who drank juice less than once per week. The study was conducted by Qi Dai, M.D., Ph.D., assistant professor of Medicine at the Vanderbilt University Medical Center and colleagues. For the current study, called the Kame Project, the researchers identified 1,836 dementia-free subjects in the Seattle population and collected information on their dietary consumption of fruit and vegetable juices. They then assessed cognitive function every two years for up to 10 years. After controlling for possible confounding factors like smoking, education, physical activity and fat intake, the researchers found that those who reported drinking juices three or more times per week were 76 percent less likely to develop signs of AD than those who drank less than one serving per week. The benefit appeared particularly enhanced in subjects who carry the apolipoprotein E-4 allele, a genetic marker linked to late-onset AD - the most common form of the disease, which typically occurs after the age of 65. The next step, said Dai, is to test the subjects’ blood samples to see if elevated levels of polyphenols are related to the reduced risk of cognitive decline and AD. This would provide further evidence of the role of juice polyphenols in AD risk. It also may point to the types of juice that would be most beneficial. PR 8/31 American Journal of Medicine 119, (9), 751-759, Sept. 2006

Other Items

Boosting a Newly Discovered Enzyme Helps Mice Regain Normal Cognitive Function -

Researchers at Columbia University Medical Center have successfully restored normal memory and synaptic function in mice suffering from AD. They have identified an enzyme that is required for normal cognition but that is impaired in a mouse model of AD. They discovered that mice regained the ability to form new memories when the enzyme’s function was elevated. The research suggests that boosting the function of this enzyme, known as ubiquitin C-terminal hydrolase L1 (Uch-L1), may provide a promising strategy for battling AD, and perhaps reversing its effects. The researchers discovered that the enzyme Uch-L1 is part of a molecular network that controls a memory molecule called CREB, which is inhibited by amyloid beta proteins in people with AD. By increasing Uch-L1 levels in mice that had AD, they were able to improve the animals’ ability to create new memories. “Because the amyloid beta proteins that cause AD may play a normal, important physiological role in the body, we can’t destroy them as a therapy,” explained Ottavio Arancio, M.D., Ph.D., Assistant Professor of Pathology at Columbia University Medical Center and co-principal investigator of the study with Michael Shelanski, MD, Ph.D., Chairman of the Department of Pathology at the Columbia University College of Physicians and Surgeons. “What makes this newly discovered enzyme exciting as a potentially effective therapy is that it restores memory without destroying amyloid beta proteins.” Innovations Report 8/28/06 Cell, 126, 775-788, 25 August 2006

Link Between Diabetes and AD Deepens - Several new studies suggest that diabetes increases the risk of AD, adding to a store of evidence that links the disorders. The studies involve only Type 2 diabetes, the most common kind, which is usually related to obesity. The connection raises an ominous prospect: that increases in diabetes, a major concern in the United States and worldwide, may worsen the rising toll from AD. The findings also add dementia to the cloud of threats that already hang over people with diabetes, including heart disease, strokes, kidney failure, blindness and amputations. But some of the studies also hint that measures to prevent or control diabetes may lower the dementia risk, and that certain diabetes drugs should be tested to find whether they can help AD patients, even those without diabetes. Current treatments for AD can provide only a modest improvement in symptoms and cannot stop the progression of the disease. The new findings were presented 7/16/06 by the AD Association at a six-day conference in Madrid attended by 5,000 researchers from around the world. Not everyone with diabetes gets AD, and not all AD patients are diabetic. But in the past decade, several large studies have found that compared with healthy people of the same age and sex, those with Type 2 diabetes are twice as likely to develop AD. The reason is not known, but researchers initially suspected that cardiovascular problems caused by diabetes might contribute to dementia by blocking blood flow to the brain or causing strokes. More recently, though, scientists have begun to think that the diseases are connected in other ways as well. In both, destructive deposits of amyloid, a type of protein, build up: in the brain in AD, in the pancreas in Type 2 diabetes. By Denise Grady NY Times 7/17/06

UCLA Scientist Awarded $7.9 Million for National Study on AD; Team Aims to Unravel How Sticky Proteins Disrupt Brain Function - David B. Teplow, Ph.D., (Tarzana) professor of neurology at the David Geffen School of Medicine at UCLA, was awarded a $7.9-million grant from the National Institute on Aging to lead a national effort to uncover how brain proteins stick together abnormally to cause AD. The multidisciplinary project will team experts at Boston University, Massachusetts Institute of Technology, UC Santa Barbara and UCLA. “Our consortium aims to illuminate -- at the most fundamental cellular and biological levels -- how the abnormal folding of proteins produces neurological disorders, and to translate our discoveries into effective treatments for AD and other aging diseases,” explained Teplow, principal investigator and director of the UCLA Biopolymer Laboratory. “We knew that no single approach could answer the question of how abnormal protein folding produces disease,” he added. “A multidisciplinary program integrating the efforts of neurologists, physicists, chemists and biologists will create a synergy and potential for new therapies that five individual efforts could not.” In AD, amyloid proteins clump together to form sticky plaques in the brain, interfering with cells’ ability to communicate and eventually causing their death. This disruption results in the progressive memory loss and inability to think that typifies the disorder. Teplow’s team suspects that structural changes to the amyloid proteins make them poisonous and lead to AD. The researchers hope to unravel how the proteins form these toxins, and translate their findings into the design and testing of new drugs for AD and other devastating neurological disorders caused by abnormal protein folding, including Huntington’s, Parkinson’s and prion diseases, such as Creutzfeldt-Jakob disease. PR 8/28/06

AD, Drinking Not Linked, Study Says - Drinking alcohol in moderate amounts can help the heart. But can the benefits of alcohol be extended to other body organs, such as the brain? Alcohol is commonly believed to be harmful to the brain, as seen by slurred speech, stumbling and other drunken behaviors. But it is not clear whether acute alcohol consumption damages the brain. “There is little proof of permanent neurological effects” from mild to moderate alcohol consumption, said John Morris, neurology professor at Washington University in St. Louis. He defines moderate drinking as one to two drinks every day or two. Morris and his colleagues studied whether moderate drinking influenced AD. The results were presented in July 2006. The researchers tracked the mental abilities and drinking habits of people with dementia and their nondemented counterparts for up to 24 years. They found no difference in drinking patterns between the two groups. The results also showed that alcohol’s effects on dementia are neither beneficial nor detrimental. “Daily alcohol use had no influence on the development of AD or the rate at which the disease progresses,” Monique Williams, a professor and clinician at Washington University, wrote in an e-mail from Madrid, Spain, where she presented the findings at a recent conference. But alcohols lack of effect on mental abilities does not mean that alcohol is healthy. “The findings should not serve as encouragement to drink alcohol,” Williams cautioned. Risks associated with alcohol use in the elderly include injuries from falling, slower metabolism of alcohol and interaction of alcohol with medications. Austin American-Statesman 9/28/06

Multi-tasking Adversely Affects Brain’s Learning - Multi-tasking affects the brain’s learning systems, and as a result, we do not learn as well when we are distracted, UCLA psychologists reported 7/25/06. “Multi-tasking adversely affects how you learn,” said Russell Poldrack, UCLA associate professor of psychology and co-author of the study. “Even if you learn while multi- tasking, that learning is less flexible and more specialized, so you cannot retrieve the information as easily. Our study shows that to the degree you can learn while multi-tasking, you will use different brain systems. The best thing you can do to improve your memory is to pay attention to the things you want to remember,” Poldrack added. “Our data support that. When distractions force you to pay less attention to what you are doing, you don’t learn as well as if you had paid full attention.” The researchers used functional magnetic resonance imaging (fMRI) to examine brain activity and function, a technique that uses magnetic fields to spot active brain areas by telltale increases in blood oxygen. “Our results suggest that learning facts and concepts will be worse if you learn them while you’re distracted,” Poldrack said. The researchers noted that they are not saying never to multi-task, just don’t multi-task while you are trying to learn something new that you hope to remember. Listening to music can energize people and increase alertness. Listening to music while performing certain tasks, such as exercising, can be helpful. But tasks that distract you while you try to learn something new are likely to adversely affect your learning, Poldrack said. “Concentrate while you’re studying,” he said. Medical New Today 7/29/06 Proceedings of the National Academy of Sciences, 8/1/06, 103, no. 32, 11778-11783 

D:\AD18\adn0906.htm