How to lower your risk of Alzheimer’s

Alzheimer’s disease is the most common form of dementia, accounting for between 50 and 80 % of all cases. Researchers are closer than ever to finding a cure, but sometimes prevention is the best medicine.

There are some easy things you can do to prevent developing Alzheimer’s:

• Add cinnamon to your diet – consuming a teaspoon of this spice has been shown to block the production of proteins in the brain that contribute to the onset of Alzheimer’s.

• Drink apple juice – it boosts the production of a chemical compound in the brain associated with learning, memory, mood and muscle movement.

• Drink coffee – it acts as an anti-inflammatory that can block cholesterol buildup in the brain. One large study showed that men and women who drank three to five cups of coffee a day reduced their chances of dementia by 65 percent.

• Socialize more – studies show that a busy social life can improve your cognitive abilities.

• Protect your vision – your eyes are a good indicator of how your brain is functioning. Preserving your vision can actually cut your dementia risk by 63 percent.

• Meditate – this will lower your blood pressure and reduce stress, and it increases blood flow to the brain, which is why researchers believe it helps us retain mental acuity as we age.

• Eat a Mediterranean diet – a diet rich in leafy greens, fish, fruit, nuts and a little red wine can cut your dementia risk in half because it’s chock full of brain-protecting antioxidants.

Taking steps to prevent dementia now will help cut your risk of developing Alzheimer’s disease as you age.

Living at Home With Dementia

Most people with dementia who live at home have multiple unmet health and welfare needs, any number of which could jeopardize their ability to remain home for as long as they desire.

The researchers say routine assessments of patient and caregiver care needs coupled with simple fixes in the areas of safety -- grab bars in the bathroom, carpets safely tacked down to prevent falls, guns locked away -- and basic medical and supportive services could go a long way toward keeping those with dementia from ending up in a nursing or assisted-living facility. "Currently, we can't cure their dementia, but we know there are things that, if done systematically, can keep people with dementia at home longer," says study leader Betty S. Black, Ph.D., an associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine. "But our study shows that without some intervention, the risks for many can be quite serious."

Previous research has shown that greater unmet needs among people with dementia are predictive of nursing home placement and death. Caregiver stress also foretells of nursing home admission for people with dementia. The new study also finds most caregivers have multiple unmet needs, including lack of access to resources and referrals to support services and education about how to best care for their loved one.

Black says that paying for needs assessments and putting into place preventive safety measures isn't always feasible, and programs like Medicare don't typically cover them. "If they did," she says, "it may be far more cost-effective than long-term nursing home care."

An estimated 5.4 million people in the United States have Alzheimer's disease and other types of dementia, and 70 percent are cared for in the community by family members and friends. Most have mild to moderate dementia.

For the study, Black and her colleagues performed in-home assessments and surveys of 254 people with dementia living at home in Baltimore and also interviewed 246 of their informal, non-professional caregivers. They found that 99 percent of people with dementia and 97 percent of their caregivers had one or more unmet needs. Ninety percent were safety-related. More than half of the patients had inadequate meaningful daily activities at a senior center or at home, and one-third still needed a dementia evaluation or diagnosis.
Unmet needs fell into many categories including safety, health, meaningful activities, legal issues and estate planning, assistance with activities of daily living and medication management, Black says.

More than 60 percent of people with dementia in the study needed medical care for conditions related or unrelated to their dementia, a problem considering that those with dementia are more likely to have other serious illnesses for which they may eventually be hospitalized, Black says.
"This high rate of unmet medical care need raises the possibility that earlier care could prevent hospitalizations, improve quality of life and lower the costs of care at the same time," she says. Interestingly, unmet needs were significantly greater in those with higher cognitive function, most likely because many of them did not realize they had dementia and were not yet being closely cared for or monitored, Black says.

The researchers also found that African-Americans, those with lower income, those who were more independent in their basic daily living activities such as being able to feed and clothe themselves and those with more symptoms of depression had higher levels of unmet needs. Caregivers with less education and more symptoms of depression also had significantly more unmet needs. This suggests that identifying and treating depression in people with dementia and their caregivers may enable them to address their other unmet needs.

Divorce & Other Life Stressors Linked with Dementia

Common life stressors — such as divorce, widowhood or losing a job — may increase the risk of dementia later in life, a new study of women in Sweden suggests.

In the study, experiencing such psychosocial stressors in midlife was linked with a 21 % increased risk of developing  Alzheimer's disease, and a 15 %  increased risk of developing any type of dementia, over nearly four decades. The findings held even after the researchers took into account factors that may affect dementia risk, such as smoking habits, alcohol consumption and a family history of mental illness.

People who were exposed to psychosocial stressors were also at increased risk of experiencing prolonged periods of distress (or feelings of irritability, tension, nervousness, fear, anxiety or sleep disturbances). However, such distress could not fully explain the link between psychosocial stressors and dementia, meaning that the association may, in part, be due to biological factors that change in response to experiencing stressors, the researchers said.

"More studies are needed to confirm these results and investigate whether more interventions, such as stress management and behavioral therapy, should be initiated in individuals who have experienced psychosocial stressors," the researchers, from the University of Gothenburg.

Researchers analyzed information from 800 Swedish women who periodically underwent testing between 1968 and 2005. At the study's start, participants were asked whether they had experienced any of 18 psychosocial stressors, including whether their spouse or close relative had a mental illness or abused alcohol, or whether they or their husband had lost a job. Medical records and other information from psychiatric examinations were used to determine whether participants developed dementia over a 38-year period.

About a quarter of participants said they had experienced one psychosocial stressor, 23 % experienced two stressors, 30 % experienced three stressors and 16 %  experienced four stressors. The most common stressor was mental illness in a first-degree relative.

During the study period, about 20 % (153 people) developed dementia, 104 of whom developed Alzheimer's disease.

Psychological stress has been linked with increased production of inflammatory factors in the brain, and with an increased frequency of cardiovascular disease, and these, in turn, may be risk factors for dementia, the researchers said.

Exercise Beneficial for Dementia

Exercise may benefit older people with dementia by improving their cognitive functioning and ability to carry out everyday activities.

Due to people living longer, rates of dementia are expected to rise sharply in the coming decades. Dementia affects the brain in different ways and is associated with effects on memory and personality. It is thought that exercise might be useful in treating dementia or slowing its progression, through improvements in the ability to carry out everyday tasks and positive effects on mental processes such as memory and attention, collectively described as cognitive functioning. Exercise may therefore indirectly benefit family caregivers and the healthcare system by reducing some of the burden of dementia.

The study updates a Cochrane review carried out in 2008, when only four trials on the effects of exercise in older people with dementia were available. In the updated review, data from eight trials involving 329 people showed that exercise could improve cognitive functioning. Data from six studies involving 289 people showed that exercise could improve the ability of older people with dementia to carry out daily activities, such as walking short distances or getting up from a chair.

"In our previous review, we were unable to draw any conclusions about the effectiveness of exercise in older people with dementia, due to a shortage of appropriate trials," said researcher, Dorothy Forbes, an Associate Professor of Nursing who works at the University of Alberta in Edmonton, Alberta. "Following this new review, we are now able to conclude that there is promising evidence for exercise programs improving cognition and the ability to carry out daily activities. However, we do still need to be cautious about how we interpret these findings."

The researchers remain cautious because there were substantial differences among the results of individual trials. In addition, they did not find enough evidence to determine whether exercise improved challenging behaviours or depression in older people with dementia. They were unable to come to any conclusions regarding quality of life, or benefits for family caregivers and health systems, because there was not enough evidence.

However, the researchers suggest that if more evidence becomes available in future, it may help to address the question of whether exercise can help people with dementia remain at home for longer. "Clearly, further research is needed to be able to develop best practice guidelines to enable healthcare providers to advise people with dementia living at home or in institutions," said Forbes. "We also need to understand what level and intensity of exercise is beneficial for someone with dementia."

Brain Imaging Differences in Infants at Genetic Risk for Alzheimer's

Researchers from Brown University and Banner Alzheimer's Institute have found that infants who carry a gene associated with increased risk for Alzheimer's disease tend to have differences in brain development compared to children without the gene.

The researchers imaged the brains of 162 healthy infants between the ages of two months and 25 months. All of the infants had DNA tests to see which variant of the APOE gene they carried. Sixty of them had the E4 variant that has been linked to an increased risk of Alzheimer's. Using a specialized MRI technique, the researchers compared the brains of E4 carriers with non-carriers. They found that children who carry the APOE-E4 gene tended to have increased brain growth in areas in the frontal lobe, and decreased growth in areas in several areas in the middle and rear of the brain. The decreased growth was found in areas that tend to be affected in elderly patients who have Alzheimer's disease.

The researchers emphasized that the findings do not mean that any of the children in the study are destined to develop Alzheimer's or that the brain changes detected are the first clinical signs of the disease. What the findings do suggest, however, is that brains of APOE-E4 carriers tend to develop differently from those of non-E4 carriers beginning very early in life. It is possible that these early changes provide a "foothold" for the later pathologies that lead to Alzheimer's symptoms, the researchers say. Information from this study may be an important step toward understanding how this gene confers risk for Alzheimer's, something that is not currently well understood.

"This work is about understanding how this gene influences brain development," said Sean Deoni, who oversees Brown University's Advanced Baby Imaging Lab and was one of the study's senior authors. "These results do not establish a direct link to the changes seen in Alzheimer's patients, but with more research they may tell us something about how the gene contributes to Alzheimer's risk later in life."

The APOE-E4 variant linked to Alzheimer's is present in about 25 percent of the U.S. population. Not everyone who carries the gene gets Alzheimer's, but 60 percent of people who develop the disease have at least one copy of the E4 gene.

The gene is thought to have several different roles in the blood and brain, some of which remain to be clarified. For instance, it has been shown to participate in regulation of cholesterol, a molecule that is involved in the development of gray matter and white matter brain cells. It has also been shown to participate in the regulation of amyloid, a brain protein that accumulates in Alzheimer's and is now being targeted by investigational treatments. Studies are needed to clarify the ways in which APOE-E4, human development, aging and other risk factors may conspire to produce the brain changes involved in Alzheimer's disease.

The researchers used an MRI technique developed at Brown's Advanced Baby Imaging Lab. The technique quiets the MRI machine to a whisper, enabling the brains of healthy babies to be imaged while they sleep without medication. The technique also enables imaging of both gray matter -- the part of the brain that contains neurons and nerve fibers -- and white matter, which contains the fatty material that insulates the nerve fibers. Both gray and white matter are thought to have a role in Alzheimer's. White matter growth begins shortly after birth and is an important measure of brain development.

"We're in a good spot to be able to investigate how this gene influences development in healthy infants," said Deoni, assistant professor of engineering at Brown. "These infants are not medicated and not showing any cognitive decline -- quite the opposite, actually; they're developing normally."

There is no reason to believe that the children won't continue to develop normally, Deoni said. There is no consistent evidence to suggest that E4 carriers suffer any cognitive problems or developmental delay. And the areas of increased growth raise the possibility that the gene might actually confer some advantages to infants early on. Ultimately, the researchers hope the findings could lead to new strategies for preventing a disease that currently affects more than 5.2 million people in the U.S. alone.
"It may sound scary that we could detect these brain differences in infants," said Dr. Eric Reiman, executive director of the Banner Alzheimer's Institute in Arizona and another senior author on the paper. "But it is our sincere hope that an understanding of the earliest brain changes involved in the predisposition to Alzheimer's will help researchers find treatments to prevent the clinical onset of Alzheimer's disease -- and do so long before these children become senior citizens."

Your Liver May Be 'Eating' Your Brain

People with extra abdominal fat are three times more likely than lean individuals to develop memory loss and dementia later in life, and now scientists say they may know why.

It seems that the liver and the hippocampus (the memory center in the brain), share a craving for a certain protein called PPARalpha. The liver uses PPARalpha to burn belly fat; the hippocampus uses PPARalpha to process memory.

In people with a large amount of belly fat, the liver needs to work overtime to metabolize the fat, and uses up all the PPARalpha — first depleting local stores and then raiding the rest of the body, including the brain, according to the new study. The process essentially starves the hippocampus of PPARalpha, thus hindering memory and learning, researchers at Rush University Medical Center in Chicago.

In another study, researchers at Boston University School of Medicine found that the greater the amount of belly fat, the greater the brain shrinkage in old age. The surprising discovery in the new study is that the hippocampus uses PPARalpha to process memory and learning, and that this is a possible reason for the connection between belly fat and dementia and/or memory loss.

Rush University researchers, led by neurological sciences professor Kalipada Pahan, raised mice that were deficient in PPARalpha. Some mice had normal PPARalpha in the liver but depleted PPARalpha in the brain, and had poor memory and learning abilities. Others had normal PPARalpha in the brain but not the liver, and showed normal memory, as expected. When the researchers injected PPARalpha into the hippocampus of PPARalpha-deficient mice, their learning and memory improved, Pahan said.

"Further research must be conducted to see how we could potentially maintain normal PPARalpha in the [human] brain in order to be resistant to memory loss,"  PPARalpha thus provides a new avenue to explore in searching for a treatment or cure for Alzheimer's disease, dementia, and related memory-loss and cognition problems, Pahan said.

Down Syndrome and Alzheimer's Disease Risk

Down syndrome increases the risk of Alzheimer’s disease. People with Down syndrome may experience health problems as they age that are similar to those experienced by older people in the general population. The presence of extra genetic material found among persons with Down syndrome may lead to abnormalities in the immune system and a higher susceptibility to certain illnesses, such as Alzheimer's, leukemia, seizures, cataracts, breathing problems, and heart conditions.

People with Down syndrome also experience premature aging. That is, they show physical changes related to aging about 20 to 30 years ahead of people of the same age in the general population. As a result, Alzheimer's disease is far more common in people with Down syndrome than in the regular population. Adults with Down syndrome often are in their mid to late 40s or early 50s when Alzheimer's symptoms first appear. People in the general population don't usually experience symptoms until they are in their late 60s.

The symptoms of Alzheimer's disease may be expressed differently among adults with Down syndrome. For example, in the early stages of the disease, memory loss is not always noted. In addition, not all symptoms ordinarily associated with Alzheimer's disease will occur. Generally, changes in activities of daily living skills are noted, and the person with Down syndrome may begin to have seizures when he or she never had them before. Changes in mental processes - such as thinking, reasoning, and judgment - also may be present, but they often are not commonly noticeable because of limitation of the individual's functioning in general.

Estimates suggest that 25% or more of individuals with Down syndrome over age 35 show the signs and symptoms of Alzheimer's-type dementia. The percentage increases with age. The incidence of Alzheimer's disease in people with Down syndrome is estimated to be three to five times greater than that of the general population.

A Potential New Strategy to Address Dementia

Alzheimer's disease affects millions of people worldwide. As a result of an increase in life expectancy, the number of patients with dementia is expected to increase dramatically. Due to the lack of effective treatments that can slow down or reverse the progression of AD, preventive measures to lower the prevalence rate of AD by means of managing potential or actual risk factors is a reasonable clinical strategy. In this respect, identifying treatable factors which are able to promote cognitive deterioration would have important practical implications.

In a recent study, a research group from the Neurological Clinic of Università Politecnica delle Marche, Ancona, Italy described an interesting association between the presence of sleep-disordered breathing and AD. 

The study, coordinated by Mauro Silvestrini and Leandro Provinciali with Laura Buratti as principal investigator, found that a significant percentage of AD patients suffer from Obstructive Sleep Apnea Syndrome (OSAS), a common but largely underdiagnosed respiratory disorder that causes people to temporarily stop breathing during their sleep. Most importantly, the presence of this nocturnal disorder leads to unfavorable changes in cerebral blood flow that are well recognized promoters of cognitive decline onset and progression. Based on these findings, detecting and treating OSAS before it becomes severe enough to cause irreversible effects on cerebral circulation should be considered a very promising clinical approach for AD.

Newly Identified Antibodies Effectively Treat Alzheimer's-Like Disease in Mice

Alzheimer's disease is characterized by the accumulation of particular toxic proteins in the brain that are believed to underlie the cognitive decline in patients.

A new study conducted in mice suggests that newly identified antibody treatments can prevent the accumulation of one of these of these toxic components, called tau proteins. The findings suggest that these antibodies may provide a basis for a promising therapy for patients with Alzheimer's disease and other neurodegenerative disorders.

In the brains of patients with Alzheimer's disease and several other neurodegenerative conditions, tau proteins aggregate together and become tangled, a process that interferes with the brain's function and can cause many of the symptoms that patients experience.

Investigators led by Drs. David Holtzman and Marc Diamond of Washington University School of Medicine in St. Louis conducted studies in mice to reveal potential treatments to block this process. "We have identified anti-tau antibodies that can strongly reduce tau pathology, decrease tau accumulation, and improve cognitive function in a mouse model of a neurodegenerative disease called frontotemporal dementia," explains Dr. Holtzman. "Similar tau pathology is seen in Alzheimer's disease, implying that this could be an exciting treatment for a large number of patients."

To make their discovery, the researchers used a screening technique to sift through numerous antibodies to isolate those that could prevent uptake of tau aggregates by cells and block subsequent intracellular tau aggregation. They then infused three anti-tau antibodies into the brains of diseased mice over three months. While the anti-tau antibodies markedly reduced tau accumulation and improved cognitive deficits in the animals, a control antibody not directed against tau had no beneficial effects. The findings further support work suggesting that spread of tau aggregates between cells is an important mechanism underlying tau-mediated disease.

This study, which is the first to report the effects of direct infusion of anti-tau antibodies into the brain, has important implications for the design of therapeutic antibodies for patients struggling with some of the most debilitating brain diseases. "In addition to the near-term implications for passive vaccination of patients, it suggests that therapies designed to target propagation of protein aggregation between cells could be very effective," says Dr. Diamond.

Coconut oil can stop dementia and Alzheimer's disease

You can prevent (and reverse) dementia, Alzheimer's disease, ALS, multiple sclerosis, plus many other neurodegenerative disorders by eating coconut-related foods. This is not just a "health nut" making these claims - it's all backed by scientific research and touted by many natural healthcare professionals like, Dr. Bruce Fife and Dr. Russell Blaylock.

Discover a natural way to keep your brain energized by killing (unwanted) bacteria; balancing hormones; maintaining healthy blood sugar levels and eliminating brain inflammation. The scientific data is crystal clear - coconut foods can dramatically improve brain chemistry; cognitive function plus much more - very quickly! Don't miss our next show about the power of coconut oil.

Memory loss and mental disorders are caused by chronic inflammation and excess oxidative stress

When we experience excessive, free radical damage - it prevents the brain from utilizing glucose. Simply put, when the brain does not get enough glucose - brain cells degenerate and die. This loss of brain matter can destroy memory and motor skills - depending on which area of the brain is damaged.

The key to all of these neurodegenerative diseases is a lack of energy. Obviously, a poor diet filled with processed foods will not supply adequate energy for the brain. But, did you know, that many of the prescription drugs for health problems like, Parkinson's disease actually interfere with the brain's ability to utilize glucose?

Look it up yourself - drugs cause breathing problems (apnea); loss of coordination; drowsiness; headaches; muscle pains; nausea; shaking; confusion; anxiety and, even, memory loss! Clearly, this is not the best protocol for people suffering with brain issues.

Eating coconut oil can improve memory and reverse Alzheimer's disease.

Dementia Risk Tied to Blood Sugar Level, Even With No Diabetes

A joint Group Health-University of Washington (UW) study in the New England Journal of Medicine has found that higher blood sugar levels are associated with higher dementia risk, even among people who do not have diabetes.

Blood sugar levels averaged over a five-year period were associated with rising risks for developing dementia, in this report about more than 2,000 Group Health patients age 65 and older in the Adult Changes in Thought (ACT) study.

For example, in people without diabetes, risk for dementia was 18 percent higher for people with an average glucose level of 115 milligrams per deciliter compared to those with an average glucose level of 100 mg/dl. And in people with diabetes, whose blood sugar levels are generally higher, dementia risk was 40 percent higher for people with an average glucose level of 190 mg/dl compared to those with an average glucose level of 160 mg/dl.

"The most interesting finding was that every incrementally higher glucose level was associated with a higher risk of dementia in people who did not have diabetes," said first author Paul K. Crane, MD, MPH, an associate professor of medicine at the UW School of Medicine, adjunct associate professor of health services at the UW School of Public Health, and affiliate investigator at Group Health Research Institute.

"There was no threshold value for lower glucose values where risk leveled off."
"One major strength of this research is that it is based on the ACT study, a longitudinal cohort study, where we follow people for many years as they lead their lives," said senior author Eric B. Larson, MD, MPH, a senior investigator at Group Health Research Institute who also has appointments at the UW Schools of Medicine and Public Health. "We combine information from people's research visits every other year with data from their visits to Group Health providers whenever they receive care. And this gave us an average of 17 blood sugar measurements per person: very rich data."

These measurements included blood glucose (some fasting, some not) and glycated hemoglobin (also known as HbA1c). Blood sugar levels rise and fall in peaks and valleys throughout each day, but glycated hemoglobin doesn't vary as much over short intervals. R. Walker, MS

R. Hubbard, PhD Combining glucose and glycated hemoglobin measures into a composite measure required special statistical techniques, which Drs. Crane and Larson's co-authors Rod Walker, MS, a biostatistician, and Rebecca Hubbard, PhD, an associate investigator, both from Group Health Research Institute, had developed. (Dr. Hubbard is also an affiliate assistant professor of biostatistics at the UW School of Public Health.) These sophisticated statistical models required specialized data on the relationships between glycated hemoglobin and glucose levels, and they used data generated by co-author David M. Nathan, MD, a professor of medicine at Harvard Medical School and director of the Diabetes Center at Massachusetts General Hospital.

So should people try to eat less sugar -- or foods with a lower "glycemic index"? Not necessarily, Dr. Crane said: "Your body turns your food into glucose, so your blood sugar levels depend not only on what you eat but also on your individual metabolism: how your body handles your food." But he does suggest that taking walks couldn't hurt: The ACT study has previously linked physical activity to later onset and reduced risk of dementia, including Alzheimer's disease.

Furthermore, Dr. Crane emphasized that these results come from an observational study: "What we found was that people with higher levels of glucose had a higher risk of dementia, on average, than did people with lower levels of glucose," he said. "While that is interesting and important, we have no data to suggest that people who make changes to lower their glucose improve their dementia risk. Those data would have to come from future studies with different study designs."

Common Blood Pressure Drugs May Help Slow Dementia

Older adults with dementia who use certain blood pressure medications may have a slower rate of mental decline, new research suggests. The study found that dementia patients on particular ACE inhibitors showed a somewhat slower decline in memory and other mental skills than patients not on the drugs. And dementia patients who were newly started on the drugs had, on average, a small improvement in the first six months.

The drugs linked to the benefit are known as centrally acting ACE inhibitors, which means they cross from the blood into the brain.

However, the findings do not mean that people with dementia should be started on those ACE inhibitors, according to a neurologist who was not involved with the research. The study was not a clinical trial set up to test the effects of ACE inhibitors, noted Dr. Gayatri Devi, of Lenox Hill Hospital in New York City. Instead, she said, it was an "observational" study, where researchers followed more than 350 older adults with Alzheimer's or other forms of dementia -- about one-quarter of whom happened to be on ACE inhibitors. Those types of studies cannot prove that a drug is the reason for a particular benefit. "And there are past studies that have contradicted this one, and have not shown a benefit of ACE inhibitors," Devi said. On the other hand, the findings support the "larger message" that better cardiovascular health -- including controlling blood pressure and cholesterol levels -- can benefit the brain as well, she said.

Previous studies have linked better blood pressure control -- and various classes of blood pressure drugs -- to both a lower risk of developing dementia and a slower progression of the disease. Currently, no treatments exist to prevent or modify dementia. "The blood pressure medication that's best for you is the one that most effectively controls your blood pressure," Devi said. "People respond differently to the different classes of blood pressure drugs." The study included 361 dementia patients, average age 77, who completed standard tests of memory, planning and other mental abilities. Of those, 85 were already on a centrally acting ACE inhibitor, and 30 more started on one during the study period. On average, test scores declined by 1.8 points every six months among patients who were already on ACE inhibitors. That compared with 2.1 points for patients not on the drugs. Among patients who newly started an ACE inhibitor, test scores typically rose 1.2 points in the first six months -- which was as long as that group was followed. The rest of the study patients were tracked for about a year-and-a-half.

Those are small differences in test scores. But if they persisted over years, that could add up to a significant difference in dementia patients' rate of decline, said Dr. William Molloy, one of the researchers on the study. Clinical trials are needed to confirm whether certain ACE inhibitors do, in fact, slow down dementia, according to Molloy, a professor of gerontology and rehabilitation at University College Cork in Ireland. He said he does not think the benefit linked to ACE inhibitors is explained by better blood pressure control. There is animal research showing that ACE inhibitors that cross into the brain may have a stronger effect on brain functioning than ACE inhibitors that do not breach the blood-brain barrier. One possibility, Molloy said, is that the drugs reduce inflammation in the brain. But another expert not involved in the study urged caution. "I don't think these findings should be used in any clinical decision-making," said Dr. Jacobo Mintzer, chair of the Alzheimer's Foundation of America's medical advisory board. "This study supports the general concept that controlling blood pressure and other cardiovascular risk factors could have an effect" on dementia progression, said Mintzer, of Roper St. Francis Healthcare in Charleston, S.C. But he agreed with Devi that the specific medication you take for high blood pressure should be the one -- or ones -- that best rein in your numbers.

Promising Alzheimer's 'Drug' Halts Memory Loss

A new class of experimental drug-like small molecules is showing great promise in targeting a brain enzyme to prevent early memory loss in Alzheimer's disease, according to Northwestern Medicine® research.
Developed in the laboratory of D. Martin Watterson, the molecules halted memory loss and fixed damaged communication among brain cells in a mouse model of Alzheimer's.
"This is the starting point for the development of a new class of drugs," said Watterson, lead author of a paper on the study and the John G. Searle Professor of Molecular Biology and Biochemistry at Northwestern University Feinberg School of Medicine. "It's possible someday this class of drugs could be given early on to people to arrest certain aspects of Alzheimer's."
Changes in the brain start to occur ten to 15 years before serious memory problems become apparent in Alzheimer's.
"This class of drugs could be beneficial when the nerve cells are just beginning to become impaired," said Linda Van Eldik, a senior author of the paper and director of the University of Kentucky Sanders-Brown Center on Aging.

The novel drug-like molecule, called MW108, reduces the activity of an enzyme that is over-activated during Alzheimer's and is considered a contributor to brain inflammation and impaired neuron function. Strong communication between neurons in the brain is an essential process for memory formation.
"I'm not aware of any other drug that has this effect on the central nervous system," Watterson said.
"These exciting results provide new hope for developing drugs against an important molecular target in the brain," said Roderick Corriveau, program director at the National Institute of Neurological Disorders and Stroke, which helped support the research. "They also provide a promising strategy for identifying small molecule drugs designed to treat Alzheimer's disease and other neurological disorders."
Watterson and his collaborators have a new National Institutes of Health (NIH) award to further refine the compound so it is metabolically stable and safe for use in humans and develop it to the point of starting a phase 1 clinical trial.
In a key memory experiment in the study, mice brains were injected with beta-amyloid, whose increase is one hallmark of Alzheimer's in humans. One group of mice was then administered MW108 and another group was administered a placebo.
Next, each group of mice was taught environmental cues to learn how to swim through a water maze to find a resting platform. Then the mice were placed in a different arm of the maze and tested on their ability to remember the location of the platform based on the environmental cues.
The mice administered MW108 found the resting platform in the water maze as quickly as a control group of mice. The mice given the placebo made more mistakes and took longer to find the platform. They also had difficulty learning the location of the resting platform during the teaching phase.
"The results show the compound prevented the cognitive impairment," Van Eldik said..

Gene May Protect Against Alzheimer’s Disease

New research has identified a genetic mutation that may protect against both Alzheimer's disease and age-related declines in thinking and memory. And future drug treatments already in the pipeline may help prevent against both.

Amyloid protein plaques in the brain are seen in people with Alzheimer's disease. A gene for amyloid-beta precursor protein (APP) plays a key role in the formation of these plaques. Researchers from Reykjavik, Iceland, found that a mutation in this gene may help protect against Alzheimer's disease and age-related mental decline.

This mutation is rare, but, when present, confers about a 40% reduction in amyloid plaque-forming proteins. What's more, study participants between 80 to 100 years old without Alzheimer's disease who carry this mutation have better mental function than those without the mutation, the study shows.

Alzheimer's disease affects memory and thinking. Symptoms usually develop slowly and worsen with time. One in eight older Americans has Alzheimer's disease, making it the most common type of dementia in the U.S., according to the Alzheimer's Association.

New Chemical Approach to Treat Alzheimer's

Scientists developed a new chemical approach to help harness the natural ability of complex sugars to treat Alzheimer's disease.

The team used a new chemical method to produce a library of sugars, called heparan sulphates, which are known to control the formation of the proteins in the brain that cause memory loss.

Heparan sulphates are found in nearly every cell of the body, and are similar to the natural blood-thinning drug, heparin. Now scientists have discovered how to produce them chemically in the lab, and found that some of these sugars can inhibit an enzyme that creates small proteins in the brain.

These proteins, called amyloid, disrupt the normal function of cells leading to the progressive memory loss that is characteristic of Alzheimer's disease.

There are more than 800,000 people in the UK, and 50,000 in New Zealand living with dementia. Over half of these have Alzheimer's disease, the most common cause of dementia. The cost of these diseases to the UK economy stands at £23 billion, more than the cost of cancer and heart disease combined. Current treatments for dementia can help with symptoms, but there are no drugs available that can slow or stop the underlying disease.