Having a thick middle, high blood pressure and other risk factors for heart disease may increase your risk of Alzheimer’s disease and other forms of dementia as well, a new study reports.

The findings come from France, where researchers studied more than 7,000 men and women ages 65 and older living in three French cities. Those who had a constellation of symptoms called “metabolic syndrome” – including hypertension, a large waistline, high levels of a type of blood fat called triglycerides, low levels of “good” HDL cholesterol, and poor control of blood sugar, a sign of impending diabetes – tended to perform worse on memory and thinking skills tests than those without these issues. Performing poorly on such tests is often an indicator of an increased risk of Alzheimer’s and other forms of dementia. The findings appeared in Neurology, the medical journal of the American Academy of Neurology.

Metabolic syndrome has long been linked to an increased risk of heart attacks. It is not an actual disease but rather a group of symptoms. The findings support a growing body of evidence that factors like a large waistline and high blood pressure – whether in midlife or beyond — may be linked to diminishing thinking skills and possibly even Alzheimer’s disease.

“Our study sheds new light on how metabolic syndrome and the individual factors of the disease may affect cognitive health,” said study author Christelle Raffaitin, M.D., of the French National Institute of Health Research in Bordeaux. “Our results suggest that management of metabolic syndrome may help slow down age-related memory loss, or delay the onset of dementia.”

At the start of the study, researchers evaluated the 4,323 women and 2,764 men and found that 16 percent had metabolic syndrome. All the participants were given memory tests two and four years later.

Those with metabolic syndrome were 20 percent more likely to have a decline in thinking and memory skills than those without the syndrome. Two factors in particular were linked to declining memory: higher triglycerides and low HDL, or “good” cholesterol. Having diabetes was also linked to memory problems, although high blood sugar levels were not.

The authors propose that taking steps to reduce metabolic syndrome may help to ward off or slow down mental decline in old age. Increasingly, Alzheimer’s is seen as a disease that may take years or even decades to develop. Taking measures to slow cognitive decline could, potentially help to keep thinking sharp and postpone the onset of full-blown Alzheimer’s by many years.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: C. Raffaitin, MD, C. Feart, PhD, M. Le Goff, MSc, et al: “Metabolic Syndrome and Cognitive Decline in French Elders: The Three-City Study.” Neurology, Feb 2, 2011, Vol. 76, pages 518-525.

Scientists are moving closer to diagnosing Alzheimer’s disease at an earlier stage using special brain scans. The scans, which are not routinely available in doctors’ offices, should make it easier to know for sure whether someone has Alzheimer’s earlier in its course, when treatments may be more effective and patients can better plan for the future. Currently, the only way to get a definitive diagnosis is to examine the brain after death during an autopsy.

The imaging technique picks up the presence in the brain of plaques, which are made up of clumps of beta-amyloid protein fragments. Plaques are a telltale sign that someone has Alzheimer’s, though their role in the disease is not well understood. Someone may have dementia, but if they do not have plaques, their dementia is due to a condition other than Alzheimer’s.

Between 10 and 20 percent of people who are given a diagnosis of Alzheimer’s turn out not to have the disease when their brains are examined at autopsy. And doctors miss the diagnosis of Alzheimer’s in about a third of patients with early disease and only mild memory loss and other symptoms. Someone who comes to the doctor’s office complaining of depression, for example, may actually be in the early stages of Alzheimer’s.

The imaging techniques involve the use of positron emission tomographic, or PET, scans. They use various dyes that latch on to particles of beta-amyloid in the brain, making it possible to see plaques on the brain scans in living people.

Most recently, an advisory panel to the US Food and Drug Administration recommended approval of an imaging technique developed by Avid Radiopharmaceuticals, pending further study of the technique. The company has developed a brain dye called florbetapir F 18 that attaches to beta-amyloid, which then lights up on PET scans.

In a recent study, florbetapir-PET imaging was performed on the brains of 35 men and women who were in hospice or long-term care facilities and nearing the end of their lives, about half of whom were thought to have Alzheimer’s. Their brains were then examined after they died, to see if the PET scans in the living people were consistent with the findings on autopsy.

In almost all the cases, the living brain scans matched the autopsy findings. One patient who was thought to have Alzheimer’s actually had dementia of other causes. Two others turned out to have Alzheimer’s, though they were given other diagnoses while alive.

Similar scans were performed on 74 young and healthy individuals under age 50. Presumably, their brains would be relatively free of plaque, which turned out to be the case. The study appeared in the Journal of the American Medical Association.

The findings give new weight that such scanning techniques will prove effective in diagnosing Alzheimer’s definitively at earlier stages. Scientists need to do further study to determine how much plaque defines a diagnosis, and doctors need to be trained in carrying out and interpreting test results.

The technique is also being used to assess the effects of various Alzheimer’s drugs in development. By monitoring brain plaques, researchers can determine whether an experimental drug is working by preventing the buildup of beta-amyloid in the brain. Current medications for Alzheimer’s may ease symptoms for a time but do not stop the downward progression of disease.

Additional work needs to be done to evaluate the accuracy of the technique. And doing PET scans with brain dyes is an expensive procedure that cannot be routinely performed in a doctor’s office. Still, the findings add another piece of the puzzle to diagnosing Alzheimer’s disease at earlier stages, potentially allowing patients, family members and doctors to plan for the future more effectively.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Christopher M. Clark, MD;  Julie A. Schneider, MD; Barry J. Bedell, MD, PhD; et al: “Use of Florbetapir-PET for Imaging Beta-Amyloid Pathology.” Journal of the American Medical Association, Vol. 305 (No. 3), January 19, 2011, pages 275-283.

Nutrition scientists continue to extol the virtues of a Mediterranean diet, the traditional diet from Italy, Greece and other countries that border the Mediterranean Sea. The diet, high in fruits and vegetables and healthy fats like olive oil, along with modest amounts of red wine and little red meat, may curb heart disease and prolong life – and keep your mind sharp and free of Alzheimer’s disease in old age, studies suggest.

Now a large new study from Rush Medical College in Chicago provides the strongest evidence to date that a Mediterranean style diet may be good for the brain. Researchers studied 3,790 men and women ages 65 and older, tracking them over many years beginning in 1993. They were given regular questionnaires about the foods they ate, along with tests of memory and thinking skills every three years.

Those seniors who adhered to a Mediterranean diet most strictly scored higher on mental acuity and memory tests than those who didn’t eat much of the heart-healthy foods. Overall, those who stuck most closely to a Mediterranean diet were two years younger in “brain age” than their peers who didn’t follow such a diet. The findings held even after adjusting for risk factors like age, sex, race, years of education and participation in mentally stimulating activities.

The researchers caution that they could not account for all the many factors that may contribute to cognitive decline in old age. Food surveys, in which people fill out what they eat, can be unreliable, though the researchers used scientifically validated methods to analyze the results, and the study involved a large number of people.

The findings, which appeared in the American Journal of Clinical Nutrition, bolster a growing body of evidence that a heart-healthy Mediterranean diet is good for the brain. Earlier, smaller studies have reported that healthy people who follow a Mediterranean diet lower their risk of developing Alzheimer’s disease. And those with Alzheimer’s who followed such a diet lived longer than their peers who did not. Earlier research has also shown that a Mediterranean diet may cut the risk of strokes, cancer, diabetes and possibly other illnesses as well.

Doctors are not sure why a Mediterranean diet may be good for the brain. One possibility is that such a diet reduces a risk for blood vessel disease, which may contribute to the risk for Alzheimer’s disease. A Mediterranean diet helps cut down on inflammatory substances in the body, too, and inflammation has increasingly been tied to heart disease and possibly Alzheimer’s as well. Fruits, vegetables and red wine are also high in cell-protecting antioxidants.

Key components of the Mediterranean diet include:

• An abundance of fiber-rich fruits, vegetables, cereals, nuts and beans;
• Choosing “good” fats like olive or canola oil, rather than butter or lard, and limiting dairy products like high-fat cheese and milk;
• Eating moderate amounts of fish and poultry, rather than red meat; and
• Drinking a glass or two of red wine a day.

Many other factors besides diet, including the genes you inherit and advancing age, play an important role in who ultimately develops Alzheimer’s. Still, the findings suggest that lifestyle factors can have an impact on Alzheimer’s risk. Eating a heart-healthy diet, along with getting regular exercise and keeping weight down, may help keep the brain young.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: Tangney CC, Kwasny MJ, Li H, Wilson RS, Evans DA, Morris MC: “Adherence to a Mediterranean-type dietary pattern and cognitive decline in a community population.” American Journal of Clinical Nutrition, Dec. 22, 2010.

Scientists have long been studying beta-amyloid, the sticky protein that builds up in the brains of those with Alzheimer’s disease. Everyone makes beta-amyloid, but in those with Alzheimer’s disease, the protein accumulates to toxic levels, eventually forming clumps in the brain called plaque that may play a part in damaging brain cells critical for thinking and memory.

But does this buildup of plaque occur in Alzheimer’s patients because they make too much beta-amyloid? Or are they unable to clear the sticky protein that naturally forms, the way healthy people do?

Researchers now have a better answer to these questions. It appears that those with Alzheimer’s make perfectly normal amounts of beta-amyloid. The problem is that they are unable to clear it from their brains.

“Clearance is impaired in Alzheimer’s disease,” said Dr. Randall Bateman, assistant professor of neurology at Washington University School of Medicine in St. Louis, who led the study that appeared in the journal Science. The findings could have important implications for diagnosis and treatment of Alzheimer’s, as researchers work to find treatments that can speed clearing of beta-amyloid from the brain.

In the study, researchers compared a group of 12 men and women with early Alzheimer’s disease with 12 healthy peers. Both groups produced beta-amyloid at the same average rate; the protein, at very low levels, seems to play an important role in keeping brain cells from becoming overexcited and firing abnormally. But compared to the healthy controls, those with early Alzheimer’s were 30 percent less able to clear the protein that accumulated in the brain.

The scientists estimate that over 10 years, enough beta-amyloid would accumulate in the brain to form the telltale plaques that damage brain areas crucial for thinking and memory.

“These findings may help point us toward better diagnostic tests and effective therapies. The next question is what is causing the decreased clearance rate,” Dr. Bateman said. “These findings support the idea that impaired beta-amyloid clearance is fundamentally linked to Alzheimer’s disease.”

Pathologists have long recognized beta-amyloid as a component of the plaques that riddle the brains of those with Alzheimer’s. One way the brain clears beta-amyloid is to move it into the spinal fluid, where it is broken down and disposed of. Understanding how this occurs could lead to new drugs and treatments that speed the process, before damage to the brain becomes extensive.

In those with Alzheimer’s, however, this process is impaired. Levels of beta-amyloid rise as the protein gets “stuck” in the brain, meaning that less of the substance moves into the spinal fluid. That’s one reason why studies have found that lower levels of beta-amyloid in the spinal fluid may be an early indicator of Alzheimer’s disease.

Many believe that accumulation of abnormal levels of beta-amyloid in the brain initiates a cascade of events leading to the death of brain cells and ultimately to dementia. In the rare, early-onset forms of Alzheimer’s that are linked to genetic mutations, there is a marked increase in beta-amyloid production. In the more common, late-onset form of Alzheimer’s, the mechanisms leading to increased beta-amyloid levels are not well understood.

Prior studies suggest several possible explanations for the slower clearance of beta-amyloid in late-onset Alzheimer’s. One possibility is that as beta-amyloid accumulates, it acts as a sink for more of the protein, trapping it within the brain. The researchers believe that sorting out these mechanisms is likely to help speed the development of new drugs for the disease.

“Abnormal protein deposits within the brain are a hallmark not only of Alzheimer’s disease, but of many neurological disorders. With knowledge about how these proteins accumulate, we may be able to slow that process and reduce the damage to the brain,” said Roderick Corriveau, Ph.D., a program director at the National Institute of Neurological Disorders and Stroke.

Fisher Scientists Discover New Ways to Rid Cells of Alzheimer Protein, click here for full article.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source:

Kwasi G. Mawuenyega, Wendy Sigurdson, Vitaliy Ovod, et al: “Decreased Clearance of CNS Beta-Amyloid in Alzheimer’s Disease.” Science, published online December 9, 2010.

High levels of high-density lipoprotein, or HDL, the so-called “good” cholesterol, appear to protect against Alzheimer’s disease, according to a new report. The findings come from a study of older adults living in New York City who were followed for about four years.

Previous studies have shown that high levels of HDL seem to protect against heart attacks and strokes. Hence the name “good” cholesterol. The new findings, publishing in the Archives of Neurology, from the American Medical Association, suggest HDL has protective effects, not just for the heart, but for the brain as well.

In the study, researchers at Columbia University’s Taub Institute for Research on Alzheimer’s and the Aging Brain studied 1,130 seniors living in northern Manhattan. None had Alzheimer’s at the start of the study. All were given blood tests to assess their cholesterol levels, including levels of HDL.

During the follow-up period, 101 of the participants developed Alzheimer’s; their average age was 83. Men and women who had the highest HDL levels, measuring 55 milligrams per deciliter of blood or higher, developed 60 percent fewer cases of Alzheimer’s disease than those with the lowest HDL levels, of 38 milligrams or less. The protective effect persisted even after the researchers considered such Alzheimer’s risk factors as age, education levels and genes that predispose to the disease.

Professional medical guidelines recommend that men raise HDL levels that are under 40 milligrams per deciliter, and that women increase HDL numbers under 50 milligrams. An HDL of 60 milligrams or higher is considered optimal.

Regular exercise, and especially aerobic activities like walking, dancing or running, are thought to boost levels of “good” HDL cholesterol. Other studies have shown that regular exercise may likewise reduce the risk of developing Alzheimer’s later in life. Exercise also improves cardiovascular function, including blood flow to the brain. In addition, a heart-healthy Mediterranean diet, rich in fish, nuts and healthy oils like olive oil, is also recommended to keep the brain healthy into old age.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source:

Christiane Reitz; Ming-Xin Tang; Nicole Schupf; Jennifer J. Manly; Richard Mayeux; José A. Luchsinger: “Association of Higher Levels of High-Density Lipoprotein Cholesterol in Elderly Individuals and Lower Risk of Late-Onset Alzheimer Disease.” Archives of Neurology, Vol. 67 (No. 12), pages 1491-1497.

Every year, some 750,000 Americans suffer from sepsis, a life-threatening ailment that many have never heard of. The condition, sometimes called “blood poisoning” though no poison is involved, is an inflammatory response to serious infection that can cause damage to multiple tissues and organs. New findings show that the condition may lead to loss of memory and thinking skills that, when severe, may mimic the symptoms of Alzheimer’s disease.

Earlier this year, a study from the University of Washington in Seattle found that older men and women who receive critical care in the hospital are more likely to suffer from memory loss and cognitive decline than their peers who are not hospitalized and an earlier study, led by researchers at Beth Israel Deaconess Medical Center and Hebrew Senior Life in Boston, found that an episode of delirium, marked by agitation, confusion and hallucinations, rapidly accelerates cognitive decline and memory loss in Alzheimer’s patients.

In the current study, researchers at the University of Michigan Medical School in Ann Arbor sifted through data from more than 27,000 men and women over 50 who were part of the Health and Retirement Study, an ongoing national health survey of American residents. Among the study participants, nearly 1,200 had been hospitalized for severe sepsis, a critical condition that requires intensive medical care and that can damage the skin, kidneys, lungs and other organs.

The researchers followed the sepsis patients for up to eight years and found that the condition was not just bad for the body. Many of those who had severe sepsis showed thinking and memory problems that were similar to those of Alzheimer’s and other forms of dementia.

“An episode of severe sepsis, even when survived, may represent a sentinel event in the lives of patients and their families, resulting in new and often persistent disability, in some cases even resembling dementia,” the authors wrote.

The researchers found that the prevalence of moderate to severe cognitive impairment increased 10.6 percentage points among patients who survived severe sepsis. Their odds of acquiring moderate to severe cognitive impairment were more than three times higher than those who didn’t have sepsis, including those who were admitted to the hospital for other medical problems.

“Cognitive and functional declines of the magnitude seen after severe sepsis are associated with significant increases in caregiver time, nursing home admission, depression, and mortality,” the authors wrote. “These data argue that the burden of sepsis survivorship is a substantial, under-recognized public health problem with major implications for patients, families and the health care system.” The study was published in the Journal of the American Medical Association.

The authors added that given published dementia and sepsis incidence rates for those ages 65 years or older in the United Slates, their results suggest that nearly 20,000 new cases per year of moderate to severe cognitive impairment in the elderly may be attributable to sepsis.

Unlike Alzheimer’s, sepsis is a curable condition, though it remains a leading cause of death in hospitals. Symptoms include fever, chills, difficulty breathing and general weakness. The condition can rapidly worsen, making immediate hospitalization and prompt treatment with fluids and antibiotics critical.

The findings point to the need for prompt medical care for serious infections in those with or without Alzheimer’s disease. They also point to the need for long-term follow-up, since even if the infection is successfully treated, there may be long-term damage to the brain and body.

In an editorial accompanying the study, Dr. Derek Angus of the University of Pittsburgh School of Medicine noted that the findings “…can help physicians when assessing care options and discussing outcomes with patients and families.” Researchers aren’t sure why sepsis may contribute to cognitive decline, but by raising awareness of the issue, the hope is that doctors and family members will be more aware of the risk of thinking and memory problems during and after hospital stays.

A trip to the hospital, with its strange sights and sounds and change in routine, can lead to confusion and agitation in any patient. The problem may be especially challenging for someone with Alzheimer’s disease. If hospitalization is needed, experts recommend that family members and loved ones stick close by whenever possible to help ease the transition.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source:

Theodore J. Iwashyna; E. Wesley Ely; Dylan M. Smith; et al.  “Long-term Cognitive Impairment and Functional Disability Among Survivors of Severe Sepsis.” Journal of the American Medical Association, Vol. 304(16), Oct. 27, 2010, pages 1787-1794.

Derek C. Angus: “The Lingering Consequences of Sepsis: A Hidden Public Health Disease?” Journal of the American Medical Association, Vol. 304(16), Oct. 27, 2010, pages 1833-1834.

Fisher Center Scientists Show That Anti-Inflammatory Drugs Reduce Effectiveness of SSRI Antidepressants

Scientists at the Fisher Center for Alzheimer’s Disease Research at The Rockefeller University, led by Paul Greengard, Ph.D., and Jennifer Warner-Schmidt, Ph.D., have shown that anti-inflammatory drugs, which include ibuprofen, aspirin and naproxen, reduce the effectiveness of the most widely used class of antidepressant medications, the selective serotonin reuptake inhibitors, or SSRIs, taken for depression, obsessive-compulsive disorder and anxiety disorders. This surprising discovery, published online this week in the Proceedings of the National Academy of Sciences, may explain why so many depressed patients taking SSRIs do not respond to antidepressant treatment and suggests that this lack of effectiveness may be preventable. The study may be especially significant in the case of Alzheimer’s disease. Such patients commonly suffer from depression and unless this can be treated successfully, the course of the illness is likely to be more severe. Depression in the elderly is also a risk factor for developing Alzheimer’s disease and researchers have suggested that treating depression in the elderly might reduce the risk of developing the disease.

In the recent study, investigators treated animal models with antidepressants in the presence or absence of anti-inflammatory drugs. They then examined how the models behaved in tasks that are sensitive to antidepressant treatment. The behavioral responses to antidepressants were inhibited by anti-inflammatory/analgesic treatments. They then confirmed these effects in a human population.  Depressed individuals who reported anti-inflammatory drug use were much less likely to have their symptoms relieved by an antidepressant than depressed patients who reported no anti-inflammatory drug use.  The effect was rather dramatic since, in the absence of any anti-inflammatory or analgesic use, 54% of patients responded to the antidepressant, whereas, success rates dropped to approximately 40% for those who reported using anti-inflammatory agents.

“The mechanism underlying these effects is not yet clear.  Nevertheless, our results may have profound implications for patients, given the very high treatment resistance rates for depressed individuals taking SSRIs,” noted Dr. Warner-Schmidt.  Dr. Greengard added, “Many elderly individuals suffering from Alzheimer’s disease also have arthritic or related diseases and as a consequence are taking both antidepressant and anti-inflammatory medications.  Our results suggest that physicians should carefully balance the advantages and disadvantages of continuing anti-inflammatory therapy in patients being treated with antidepressant medications.”

This is the third significant finding in nine months by Fisher Scientist in Dr. Greengard’s lab. Previously, Fisher Center researchers headed by Nobel laureate Dr. Paul Greengard in the Fisher laboratory at The Rockefeller University found two new ways to control beta-amyloid.  In September of 2010 published in Nature, they discovered a previously unknown function for a protein in the brain that stimulates the production of beta-amyloid which is known to contribute to the cause of Alzheimer’s. Controlling this protein, called gSAP, is a key and also has the advantage of not interfering with other life functions which caused the failure of many earlier drug trials. In another finding published in the FASEB Journal in March 2011, they also succeeded in accelerating the breakdown of accumulated beta-amyloid. They discovered that a process called autophagocytosis reduces the buildup of beta-amyloid in isolated cells and might be utilized to eliminate the buildup of beta-amyloid in the brains of Alzheimer’s patients. They discovered that a compound called SMER28 lowers the level of beta-amyloid found in nerve cells. According to Dr. Greengard, “the combination of inhibition of formation and acceleration of breakdown of beta-amyloid represents a new and powerful strategy for treating Alzheimer’s disease.”

“This is the third major finding by the Fisher Center scientists at the Greengard lab in only nine months,” says Kent L. Karosen, President of the Fisher Center for Alzheimer’s Research Foundation. “It’s quite amazing that their novel techniques are proving to be so prolific. This latest finding shows their success in not only one day ending Alzheimer’s, but in also having even broader implications for society.”

The Fisher Center for Alzheimer’s Research Foundation is a leading source of funding for Alzheimer’s research and education. They serve Alzheimer’s patients and their families by seeking to understand the causes of, discover a cure for, and improve the lives of people with Alzheimer’s disease. Nobel laureate Dr. Paul Greengard directs the Foundation’s team of internationally renowned scientists. Of the money raised by the Foundation, only 9 cents out of every dollar is used for overhead and administrative purposes. For more information about the Fisher Center for Alzheimer’s Research Foundation, click here.

Researchers are discovering subtle changes in different areas of the brain that may be early clues to the onset of Alzheimer’s. The findings could lead to earlier diagnosis of the disease, which doctors are coming to realize may affect the brain years before memory loss and thinking difficulties become prominent. Earlier diagnosis could in turn lead to more effective treatments, since drugs and other therapies may be most effective before the disease has extensively damaged the brain.

The findings were presented in two studies at the Neuroscience 2010 annual meeting in San Diego, a gathering of brain researchers sponsored by the Society for Neuroscience. “Identifying those at risk for Alzheimer’s and developing new treatments for nervous system disorders is a social imperative,” said Sam Sisodia, Ph.D., of the University of Chicago, an expert on the cellular biology of proteins implicated in Alzheimer’s disease. “These studies are evidence that we’re making real progress to overcome this tragic epidemic.”

In one study, researchers at the University of California, Los Angeles (UCLA), reported that people with Alzheimer’s disease exhibit striking structural changes in an area of the brain called the caudate nucleus. This brain structure is typically associated with movement disorders like Parkinson’s disease, rather than Alzheimer’s.

“Our finding suggests that Alzheimer’s disease produces broader damage in the brain than previously thought, including damage to areas not usually associated with the disease,” said lead author Sarah Madsen, a graduate student at the university.

For the study, the California researchers studied the brains of 400 elderly men and women. A quarter were healthy, a quarter had been diagnosed Alzheimer’s disease, and half had mild cognitive impairment, a condition that causes serious memory loss and sometimes leads to Alzheimer’s disease.

In those with Alzheimer’s, the caudate nucleus was 7 percent smaller than in those with intact memories. It was 4 percent smaller in those with mild cognitive impairment. It was also smaller in seniors who were older and overweight.

“Our finding suggests a gradual progression of brain tissue loss in the caudate nucleus as dementia becomes more severe,” said Ms. Madsen. “This brain area, which is associated with certain forms of learning and memory as well as motor control, is an important factor to consider when studying Alzheimer’s disease and in predicting how the disease will progress,” she said.

In another study, researchers at Rush University Medical Center in Chicago used MRI brain scans to locate brain changes that seemed to predict the onset of Alzheimer’s disease. MRI, or magnetic resonance imaging, is a form of scanning that uses magnetic tools rather than radiation. The experts did periodic scans on 52 seniors with mild cognitive impairment over six years. During that time, 23 were given a diagnosis of Alzheimer’s disease.

The researchers focused on an area that lies deep within the brain called the substantia innominata, which sends chemical signals to the cerebral cortex, the outer layer of the brain that plays a big part in reasoning and memory. The scans did not show any structural changes in the substantia innominata in those with memory problems, but they did show thinning in the cortical areas that receive signals from the SI in those who developed Alzheimer’s.

“Our findings support the notion that structural imaging techniques can be used to identify people at risk for developing Alzheimer’s disease,” said co-author Sarah George, a graduate student at Rush. “MRI screening appears to be a strong candidate for an early biomarker of Alzheimer’s disease.”

Researchers continue to focus on MRI and other imaging techniques in the hopes of finding ways to detect Alzheimer’s early. “”One of the main challenges in the field of Alzheimer’s disease is identifying individuals at risk of developing Alzheimer’s disease so that therapeutic interventions developed in the future can be given at the earliest stage before symptoms begin to appear,” Ms. George said.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: Neuroscience 2010 Annual Meeting, San Diego, Calif. http://www.sfn.org/am2010/index.aspx?pagename=abstracts_main

Men and women who are fluent in more than one language may be protected in part from the memory ravages of Alzheimer’s disease, a new study suggests. The findings add to a growing body of evidence that intellectual challenges like learning languages, playing musical instruments, reading or doing crossword puzzles may help keep the brain sharper for longer.

The study, from researchers at the Rotman Research Institute and York University in Toronto, Canada, reviewed the medical records of 211 people who were diagnosed with likely Alzheimer’s disease. About half spoke one language, while the others spoke two or more. They found that being bilingual delayed the onset of Alzheimer’s symptoms for as long as five years. The findings were published in the medical journal Neurology.

“We are not claiming that bilingualism in any way prevents Alzheimer’s or other dementias,” said the study leader Dr. Fergus Craik, “but it may contribute to cognitive reserve in the brain, which appears to delay the onset of Alzheimer’s symptoms for quite some time.” The “cognitive reserve” theory holds that educational pursuits like learning languages build up connections between nerve cells in the brain. When a disease like Alzheimer’s strikes and destroys parts of the brain, enough healthy cells and pathways remain intact to keep memory and thinking working longer.

The brains of people who speak two languages still show deterioration from Alzheimer’s effects on the brain. Bilingual people with Alzheimer’s, though, seem to have extra brain capacity that allows them to fend off symptoms like memory loss, confusion, and difficulties with problem solving and planning.

The researchers found that on average, bilingual patients were diagnosed with Alzheimer’s 4.3 years later than those who spoke only one language. Symptoms tended to crop up five years later in the multilingual group.

The study adds to mounting scientific evidence that suggests lifestyle factors can have an impact on Alzheimer’s onset. In addition to mental activity, regular exercise and a heart-healthy diet have been suggested as possible ways to help keep the mind and memory sharp into old age.

“Although a great deal of research is being focused on the development of new and more effective medications for Alzheimer’s disease, there are currently no drug treatments that show any effects on delaying Alzheimer’s symptoms, let alone delaying the onset of these symptoms by up to five years,” said Dr. Morris Freedman, another study leader.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: Craik FIM, Bialystok E, Freedman M.; Delaying the onset of Alzheimer disease: bilingualism as a form of cognitive reserve. Neurology. 2010;75:1726-1729.

Falls are a leading cause of broken hips and other serious injuries in the elderly, and those with Alzheimer’s are at particularly high risk of falling. Problems with vision, perception and balance increase as Alzheimer’s advances, making the risk of a fall more likely.

A study from the medical journal Age and Ageing found that seniors with Alzheimer’s are three times more likely to suffer from hip fractures than those without the disease. A broken hip is very painful and requires surgery and hospitalization, which can lead to further disorientation and disability for the person with Alzheimer’s. A broken hip increases the chances that the person with Alzheimer’s may no longer be able to be cared for at home. Furthermore, the study showed, those with Alzheimer’s who suffer a broken hip are more likely to die than those without dementia.

It’s therefore important that persons with Alzheimer’s and those who care for them take measures to prevent falls. Extra attention must also be given to those with Alzheimer’s who are undergoing rehabilitation follow a fall and fracture. Fall prevention is important for caregivers as well, since those who care for a loved one with Alzheimer’s must remain mobile and healthy in order to provide optimal care.

The National Center for Injury Prevention and Control, part of the federal Centers for Disease Control and Prevention, recommends a number of measures to reduce the chance of falls. Since about half of all falls occur in the home, the center recommends a number of steps to make the home safer.

• Remove things you can trip over, such as papers, books, clothes, and shoes, from stairs and places where you walk.
• Remove small throw rugs or use double-sided tape to keep the rugs from slipping.
• Keep items you use often in cabinets you can reach easily without using a step stool.
• Have grab bars put in next to your toilet and in the tub or shower.
• Use non-slip mats in the bathtub and on shower floors.
• Improve the lighting in your home. As you get older, you need brighter lights to see well. Lamp shades or frosted bulbs can reduce glare.
• Have handrails and lights put in on all staircases.
• Wear shoes that give good support and have thin non-slip soles. Avoid wearing slippers and athletic shoes with deep treads.

People with Alzheimer’s are particularly likely to have vision or perception problems. Busy patterns, for example, may make it difficult for the person with Alzheimer’s to navigate about a room. Or similar-colored furniture, tables and carpets may be hard to distinguish for the person with Alzheimer’s.

Other steps to reduce the likelihood of falls include getting regular exercise, which can help to improve balance, strength and agility. The ancient martial art of tai chi, for example, has been shown to improve balance and reduce the risk of falls. Ask your doctor about the best type of exercise for you or for someone with Alzheimer’s.  Keep in mind, some people with dementia may have difficulty learning a new kind of exercise.

Many medications, including blood pressure medicines, can cause dizziness when standing, lightheadedness or other problems that increase the risk of falls. If side effects are a problem, ask your doctor about medication alternatives.

Finally, regular vision checks are important at all ages, and particularly in seniors. Eye problems like cataracts, for example, can make it difficult to see and increase the chance of falls, but are easily corrected.

By ALZinfo.org. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: Nicole L. Baker, Michael N. Cook, H. Michael Arrighi and Roger Bullock: Hip fracture risk and subsequent mortality among Alzheimer’s disease patients in the United Kingdom, 1988–2007 Age and Ageing (2010) doi: 10.1093/ageing/afq146 First published online: November 18, 2010

In the largest study of its kind to date, a team of American researchers has identified four new genes that appear to be linked to Alzheimer’s in old age. Another group of researchers, working in Europe and with the first group, identified a fifth gene linked to the disease. The findings could shed new light on why people develop Alzheimer’s and open up new ways of treating the debilitating illness.

The American study was what’s known as a genome-wide association study, the gold standard in genetic research, and looked at the entire genetic makeup of more than 56,000 men and women, about a fifth of whom had Alzheimer’s disease. The European study also looked at tens of thousands of volunteers. Using gene chips and other novel technologies, they identified subtle differences between those with or without Alzheimer’s. Five genes were linked to late-onset Alzheimer’s, by far the most common form of the disease that typically arises after age 60.

“By comparing people diagnosed with Alzheimer’s with people free of disease symptoms, researchers are now able to discern elusive genetic factors that may contribute to risk of developing this very devastating disease,” said Dr. Richard J. Hodes, director of the National Institute on Aging, which sponsored the U.S. study. “We are entering an exciting period of discoveries in genetics that may provide new insights about novel disease pathways that can be explored for development of therapies.” The findings from both studies appeared in the scientific journal Nature Genetics.

Doctors have long known that Alzheimer’s disease runs in families. Having a family member with the disease increases the risk you will get it, and the disease is also more common in identical twins than in fraternal ones. But identifying genes has been elusive.

The first gene to be linked to late-onset Alzheimer’s was APOE-E4, identified in 1995. In the past several years, four other genes were identified. The latest research identified four new Alzheimer’s genes— called MS4A, CD2AP, CD33, and EPHA1 — and helped confirm the role of two other genes, BIN1 and ABCA7. The findings doubled the number of genes known to play a role in Alzheimer’s disease, bringing the total to 10. Other genes are associated with the far less common early-onset Alzheimer’s disease, which runs in families and arises in people younger than 50.

APOE-E4 appears to confer the greatest risk of developing Alzheimer’s in old age, typically between the ages of 60 and 80. Inheriting a copy of the gene from one parent doubles or triples the lifetime risk that you might get the disease, though having the gene by no means guarantees that you will get Alzheimer’s. Inheriting two copies of the gene, one from each parents, increases risk by five-fold.

None of the newer Alzheimer’s genes confer anywhere near the risk that the APOE gene does. Carrying the genes increases risk only slightly, and doctors are not proposing that you get tested for them. But all share common properties that shed new light on the development of Alzheimer’s and could open the way to new therapies for treating the disease.

All the genes appear to play a role in the way that the body processes cholesterol, a blood fat that is known to play a role in heart disease. They also appear to be linked to inflammation, which also plays a role in heart disease. Both inflammation and cholesterol metabolism are recognized as factors in Alzheimer’s and other types of dementia as well.

“This is the culmination of years of work on Alzheimer’s disease by a large number of scientists, yet it is just the beginning in defining how genes influence memory and intellectual function as we age,” said Dr. Gerard D. Schellenberg, a study leader from the University of Pennsylvania, one of the more than 44 medical centers involved in the research. “We are all tremendously excited by our progress so far, but much remains to be done, both in understanding the genetics and in defining how these genes influence the disease process.”

Now, the European and American groups are pooling their data to do an even larger study of the effects of genes on Alzheimer’s disease.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Sources: Paul Hollingworth, Denise Harold, Rebecca Sims, Amy Gerrish, et al: Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer’s disease. Nature Genetics, April 3, 2011.

Adam C Naj, Gyungah Jun, Gary W Beecham, Li-San Wang, et al: Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer’s disease. Nature Genetics, April 3, 2011.

Rush University, University of Pennsylvania, National Institute on Aging.

“The new gene data along with our recent findings could lead to an earlier detection of Alzheimer’s disease.  Our scientists are striving to find new treatments be able to introduce to individuals before the progression of Alzheimer’s disease begins,” says Kent L. Karosen President and CEO of the Fisher Center for Alzheimer’s Research Foundation.

For more information on the latest discoveries Nobel laureate Dr. Paul Greengard and his scientist at the Fisher Center for Alzheimer’s Disease Research laboratory, please visit:

Fisher Scientists Discover New Was to Rid Cells of Alzheimer Protein

New research points to a possible role for vitamin B12, a nutrient important for nerve and brain health, in the prevention of Alzheimer’s. People who had evidence of high levels of the vitamin in their blood appeared to be at lower risk of the disease.

But it’s too early to start gobbling vitamin supplements to ward off memory loss. Numerous studies have looked at the role of vitamins in brain health and found inconclusive results. Two rigorous studies earlier this year found that nutrients like B12 and folic acid, another B vitamin, did not protect against the disease.

Vitamin B12 is common in foods like eggs, meat, cheese, liver and fish. It is also found in brewer’s yeast, and some breakfast cereals are fortified with the vitamin as well. Vegetarians may need to watch their vitamin B12 levels to make sure they are getting enough. And many seniors are deficient in the vitamin, even if they eat animal products, because their bodies do not absorb it well. As a result, deficiencies may build up over years.

In the current study, published in Neurology, researchers from the Karolinka Institutet in Stockholm took blood samples from 271 Finnish men and women in their mid- to late-60s and 70s. None had Alzheimer’s or other serious memory problems at the study’s start.

By the end of the study period, seven years later, 17 people had been diagnosed with Alzheimer’s disease. Researchers measured blood levels of homocysteine, an amino acid that has been linked to heart disease, strokes and inflammation. The higher the levels of vitamin B12 somebody has, the lower the levels of homocysteine.

The researchers also looked at another related substance called holotranscobalamin, a protein found in the blood that transports vitamin B12 to cells and is necessary for B12 to be active. The chemical is sometimes also called “active B12” because it correlates with active levels of vitamin B12 in the blood.

The researchers found that as levels of homocysteine increased, the risk of Alzheimer’s disease increased modestly. But as levels of active B12 increased, the risk of Alzheimer’s decreased slightly. The results were independent of other Alzheimer’s risk factors like advancing age, low levels of education, smoking, high blood pressure and obesity. This could mean that prevention of B12 deficiency (which is common in the elderly) might reduce the risk of AD.

In this study, higher levels of folic acid, another B vitamin, did not appear to affect the risk of Alzheimer’s disease.

The authors noted that more research must be done to uncover the role of B vitamins and other nutrients in the onset of Alzheimer’s disease. Most dietary experts recommend a nutrient-rich diet containing an array of vitamins and minerals to protect against Alzheimer’s and other chronic ailments. In addition to a balanced diet, studies have found that moderate exercise, along with keeping weight under control and cholesterol and blood pressure in check during midlife, may be important for a healthy old age.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

B. Hooshman, MD, MSc; A. Solomon, MD, PhD; J. Kareholt, PhD; et al: “Homocysteine and Holotranscobalamin and the Risk of Alzheimer Disease.” Neurology ,Vol. 75, October 19, 2010, pages 1408-1414.

Sudha Seshadri, MD: “Beauty and the Best: B12, Homocysteine, and the Brain: A Bemusing Saga!” (editorial). Neurology, Vol. 75, Oct. 19, 2010, pages 1402-1403.

Measuring the levels of inflammatory proteins in the blood, combined with certain clinical features, can aid in the diagnosis of Alzheimer’s disease, according to a new report from the Texas Alzheimer’s Research Consortium. A blood test for Alzheimer’s that detects the disease at an early stage could be a boon for helping to managing the disease, since treatments may be most effective early on in the disease process.

Scientists now believe that Alzheimer’s may begin to damage the brain decades before memory loss and other symptoms become prominent. Definitive diagnosis can be made only after death, by studying the brain at autopsy. Early diagnosis could be especially helpful in testing new drugs, since they may help prevent deterioration of the brain before damage becomes extensive.

“There is clearly a need for reliable and valid diagnostic and prognostic biomarkers of Alzheimer’s disease,” the authors wrote, “and in recent years, there has been an explosive increase of effort aimed at identifying such markers.”

Scientists are studying a number of ways to detect Alzheimer’s at an earlier stage. They include brain scans to look for physical changes that may be indicative of Alzheimer’s, as well as spinal taps to measure proteins in the spinal fluid that may be characteristic of the disease. An accurate blood test, which could be done easily in a doctor’s office or clinic, would be an easier and more efficient way to measure the progress of the disease.

In the current study, published in the medical journal Archives of Neurology, researchers from Texas Tech University Health Sciences Center in Lubbock analyzed proteins in the serum of 197 patients diagnosed with Alzheimer’s. They measured levels of various proteins, including fibrinogen, which is involved in blood clotting; interleukin-10, an immune system chemical; and C-reaction protein, which is a marker for inflammation. They compared their results with 203 age-matched peers who did not have Alzheimer’s.

Using these measures, they were able to identify Alzheimer’s in 80 percent of those with the disease. They also excluded Alzheimer’s in more than 90 percent of those who were mentally intact.

Their predictive accuracy improved when they combined the blood test markers with other risk factors, like the person’s age, sex, education levels, and whether they carried the APOE-E4 gene, which raises the risk of developing Alzheimer’s. Using these clinical measures, they identified Alzheimer’s in 94 percent of those with the disease, and excluded it in 84 percent of healthy control.

While a test that is 100 percent accurate would be ideal, the findings show that scientists are growing closer at identifying Alzheimer’s at ever-earlier stages using standard laboratory tests. “The identification of blood-based biomarker profiles with good diagnostic accuracy would have a profound impact worldwide and requires further validation,” the authors concluded.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source:
Sid E. O’Bryant; Guanghua Xiao; Robert Barber; Joan Reisch; Rachelle Doody; Thomas Fairchild; Perrie Adams; Steven Waring; Ramon Diaz-Arrastia; for the Texas Alzheimer’s Research Consortium: “A Serum Protein–Based Algorithm for the Detection of Alzheimer Disease.” Archives of Neurology, Sept. 2010; Vol. 67 (No. 9): pages 1077-1081.

Identifying a cure for Alzheimer’s disease remains a major challenge. Few drugs are currently approved by the Food and Drug Administration to treat Alzheimer’s patients. Unfortunately none of these drugs halt progression of the disease and their impact on cognitive defects is minimal. On top of that, current strategies to reduce beta-amyloid, the plaque forming proteins found in the brain of Alzheimer’s patients, are associated with severe side effects. This limitation was highlighted recently by the failures of various clinical trials.

Two current discoveries by researchers at the Fisher Center for Alzheimer’s Disease Research laboratory under the direction of Nobel laureate Dr. Paul Greengard have now made it possible to prevent accumulation of beta-amyloid in nerve cells and in the brain. One involves inhibiting the formation of beta-amyloid. The second discovery involves stimulating the breakdown of beta-amyloid. According to Dr. Greengard, “the combination of inhibition of formation and acceleration of breakdown of beta-amyloid represents a new and powerful strategy for treating Alzheimer’s disease.”

In the first project, Dr. Greengard and researchers in his laboratory identified gamma-secretase activating protein (gSAP), and showed that it stimulates an enzyme called gamma secretase that is responsible for producing beta-amyloid. This discovery was published in the September 2 issue of the journal Nature. The process of inhibiting gSAP did not prove toxic to the cells in models of Alzheimer’s disease, a factor that has plagued many other experimental treatments that inhibit beta-amyloid. This discovery therefore opens a new door for research into highly specific anti-amyloid drugs that do not harm the body.

In the more recent study, published in the March 7, 2011 issue of the Journal of Federation of American Societies for Experimental Biology (FASEB), they succeeded in accelerating the breakdown of beta-amyloid. They discovered that a process called autophagy reduces the buildup of beta-amyloid in isolated cells and might be utilized to eliminate the buildup of beta-amyloid in the brains of Alzheimer’s patients. Autophagy is a process cells use to “clean out” the debris from their interiors, including unwanted materials such as the protein aggregates that are hallmarks of Alzheimer’s disease. The scientists discovered that a compound called SMER28 lowers the level of beta-amyloid found in nerve cells. This occurs because SMER28 stimulates autophagy, which then rids the cell of beta-amyloid.

“Our work demonstrates that small molecules can be developed as therapies, by activating autophagy, to prevent Alzheimer’s disease,” says Marc Flajolet, a research assistant professor in Greengard’s lab. “By increasing our understanding of autophagy, it may be possible to stimulate it, pharmacologically or naturally, to improve the quality of life for aging people.”

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Disease Research at The Rockefeller University.

Everyone becomes forgetful from time to time: forgetting where you placed the car keys, not remembering to pick up an item at the grocery store, forgetting to return a friend’s phone call. And as we age, most of us become increasingly forgetful. At least half of those over age 65 say that they are more forgetful than they were when they were younger, experiencing “senior moments” about things like where they put things or recalling somebody’s name.

But when does an ordinary memory lapse indicate something more serious, like early Alzheimer’s disease or another form of dementia? Can you brush it off as “just being forgetful,” or might it be mild cognitive impairment, a more pronounced form of memory loss that sometimes precedes dementia?

VIDEO: Understanding Alzheimer’s Disease

“We now know the early warning signs of Alzheimer’s disease can begin some 15 years before symptoms of mild cognitive impairment, or long before the beginning signs of a dementia surface,” said Dr. Barry Reisberg, director of the Fisher Alzheimer’s Disease Education and Resources Program at New York University Langone Medical Center. Because the onset of dementia can be so insidious, forgetfulness and other symptoms may develop over a period of many years.

Increasingly, research indicates that feeling you are forgetful may be cause for concern. A study conducted by Dr. Reisberg and colleagues found that seniors with subjective memory complaints are, over many years, 4.5 times more likely to develop mild cognitive impairment or dementia than those who do not have such memory complaints. That’s one reason why it’s important to pay attention for signs of being forgetful, and to seek medical attention about early signs of dementia and a possible dementia evaluation and work-up.

In order to distinguish the ordinary forgetfulness that comes with aging from more serious problems like Alzheimer’s disease, it helps to consider some key symptoms of mild cognitive impairment and the early stages of dementia.

Forgetting a friend’s name or not remembering a lunch date is something that most people without dementia do from time to time. Someone with early dementia, though, might repeatedly forget names or plans, and forget all about the incident soon afterward. Curiously, while someone with early dementia may forget something that happened the previous evening, they may recall in detail events that happened in the more distant past, last year, say, or during their childhood.

At these early stages of dementia, family members, friends and colleagues may begin to notice that something seems wrong. Maybe your spouse or partner complains that you are forgetting social engagements at an increasing rate, or that you repeat questions often. Maybe colleagues at work have expressed concern when you forget to attend a meeting or send an important memo, or are unable to learn a new computer program. Such situations may, understandably, trigger feelings of anger and defensiveness. They can also produce anxiety, which can in turn make anyone even more forgetful. The anxiety may be particularly pronounced in someone in the early stages of dementia.

In addition to being forgetful, those in the early stages of dementia may also have problems with judgment and planning. Someone with early dementia might, for example, become distracted in preparing a recipe or forget the rules of a card game. People with dementia are also much more likely to have traffic accidents than those who do not have dementia. And while many of us are challenged when it comes to finances, someone with early dementia may find it impossible to do everyday chores, like balancing a checkbook, that they used to find easy.

READ: Clinical Stages of Alzheimer’s

READ: Top 10 Alzheimer’s Signs & Symptoms

As dementia progresses, people get even more forgetful. Someone with dementia might, for example, get lost in the neighborhood when driving home from the grocery store or forget what day it is. Those with dementia may forget simple words or replace them with strange substitutes, making them difficult to understand. Someone with dementia might also misplace things, like placing a cell phone in the refrigerator, or get confused while getting dressed. These behaviors are not common in someone without dementia.

Unusual changes in personality can also occur, like showing bursts of anger for no reason, becoming depressed or confused, or uncharacteristically clinging to a family member. And while many of us plop down on the couch to watch TV after a long day at work, someone with dementia may show little or no initiative in reaching out to friends and stare at the TV for hours or sleep all day.

Anyone who has concerns about being forgetful or has signs or symptoms like those described, particularly if they are over age 65, should speak with their doctor immediately. “If you are experiencing memory complaints, it is more important than ever to have honest conversations with your physician so he or she can monitor your symptoms and offer treatment therapies if applicable,” Dr. Reisberg said. “We often see patients who would gladly talk to their doctors if they felt they were in pain or experiencing other health issues, but conversations about memory are avoided, and this is a dangerous mistake.”

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While most people who are forgetful don’t have dementia, a professional assessment can aid families in determining if this is forgetfulness or possible dementia. In some cases, medications or other environmental factors may be contributing to somebody becoming forgetful. Dosages can be adjusted, or new treatments prescribed, to ease the memory problems. Medical and mental health conditions, like depression or a deficiency in vitamin B12, can also make someone forgetful. These conditions are treatable and reversible.

Even if the diagnosis is Alzheimer’s disease or another form of dementia, steps can be taken to improve quality of life. Counseling, for example, can help the person who has early dementia to assess situations like whether the patient should stay in his or her job. Taking steps like early retirement may ease anxiety and improve day-to-day functioning. Medications to ease symptoms can also be prescribed, and may be most effective, during the early stages of dementia and families can take the necessary legal and financial steps to plan more effectively for the future.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Disease Research at The Rockefeller University.

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If you need another reason to quit smoking, here it is: People who are heavy smokers in middle age have nearly double the risk of developing Alzheimer’s disease in old age, a new study reports. Smoking, long known to be hazardous to the lungs and heart, also appears to be bad for the brain and memory as well.

The relationship between smoking and Alzheimer’s is complex. Some earlier reports suggested that the nicotine in cigarettes may be protective against neurologic ailments like Parkinson’s disease and help keep the memory sharp. But nobody recommends smoking, which is linked to lung cancer, stroke and heart attacks, to ward off Alzheimer’s or other brain diseases.

The study, published in the Archives of Internal Medicine, involved 21,123 men and women who were in their 50s and enrolled in a health plan in Finland from 1978 to 1985. All completed a medical and lifestyle survey initially, then were assessed again 20 years later, when they were in their 70s.

During that time, about a fourth of the participants had been given a diagnosis of Alzheimer’s or another form of dementia. Those who smoked more than two packs a day in middle age were at especially high risk. Former smokers or those who smoked less than half a pack per day, though, did not appear to be at increased risk. Men and women were equally at risk, as were those of different races.

The researchers, from the University of Eastern Finland and Kuopio University Hospital, noted that smoking is known to contribute to vascular disease and can damage blood vessels throughout the body, including the brain. Smoking also stokes inflammation, which is increasingly believed to be important in the development of Alzheimer’s disease. “It is possible that smoking affects the development of dementia via vascular and neurodegenerative pathways,” they note.

Early studies on smoking and Alzheimer’s risk were of shorter duration, lasting only two to seven years. “To our knowledge, this is the first study evaluating the amount of midlife smoking on long-term risk of dementia and dementia subtypes in a large multiethnic cohort,” the researchers said.

Alzheimer’s is increasingly being viewed as a disease that may take 10 to 20 years, or longer, to develop. So there is increased focus on finding measures that may stop the disease process early, before damage to the brain becomes extensive and irreversible.

“Our study suggests that heavy smoking in middle age increases the risk of both Alzheimer’s disease and vascular dementia for men and women across different race groups,” the authors concluded. “The large detrimental impact that smoking already has on public health has the potential to become even greater as the population worldwide ages and dementia prevalence increases.”

The findings add further support to the recommendation to stop smoking to help keep the mind sharp. Middle-aged smokers appear to have worse memories than their peers who don’t smoke, a 2008 study found [Read the article: "Middle-Age Smokers May Have Worse Memories Than Those Who Don't Smoke"], and a poor memory at midlife increases the risk of Alzheimer’s in old age. Another study found that heavy smokers and drinkers got Alzheimer’s years earlier than those who don’t drink or smoke heavily. [Read the article, "Heavy Drinking, Smoking May Spur Onset of Alzheimer's"] And a large European study of seniors 65 and older in 2004 found that older men and women who smoked showed greater decline in memory than those who had never smoked. [Read the article, "Smoking Is Bad for Your Brain, Too"]

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source:

Minna Rusanen; Miia Kivipelto; Charles P. Quesenberry; Jufen Zhou; Rachel A. Whitmer: Heavy Smoking in Midlife and Long-term Risk of Alzheimer Disease and Vascular Dementia. Archives of Internal Medicine, posted online doi:10.1001/archinternmed.2010.393 and scheduled for print, Feb. 28, 2011.