Thursday, December 26, 2013

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.

Wednesday, December 18, 2013

Why Women Are More Likely to Have Alzheimer's Disease?

Changes in the brain that happen after menopause may make women vulnerable to Alzheimer's disease, recent research suggests.


The hypothesis may explain why women are twice as likely to develop Alzheimer's disease after age 65 compared with men, the researchers say. (About 17 % of women in the U.S. over age 65 have Alzheimer's, compared with 9 % of men.)

Traditionally, researchers have believed that women's increased risk of Alzheimer's disease was due to the fact that women live longer, said Roberta Diaz Brinton, a professor of pharmacology, biomedical engineering and neurology at the University of Southern California's School of Pharmacy. However, women only live about four years longer than men, and Alzheimer's develops over decades, Brinton said.

Now, research from Brinton and colleagues suggests that, as women age, their brains experience a shift in the way they use energy. A woman's risk of Alzheimer's disease may, in part, be determined by how well it adapts to this energy shift, Brinton said.

"Just like the woman is going through a reproductive shift," Brinton said, "the brain is undergoing adaptations as well."

Brinton's studies on mice have shown that, during menopause, the cell's powerhouses, called mitochondria, become less efficient at producing energy. In addition, cells start to use fuel sources other than glucose, which is a sign that the energy system is not working well, Brinton said. The brain has the highest energy requirement of any organ in the body, using 20 % of the body's fuel, she said.

In a 2011 study, Brinton and colleagues removed the ovaries of mice and found that the subsequent loss of ovarian hormones such as estrogen harmed the mitochondria.

In both people and mice, declines in the brain's energy production have been shown to precede the development of Alzheimer's disease, Brinton said.

"Over time, the reduction in the ability to generate sufficient energy for the brain leads to, ultimately, an increased risk of developing Alzheimer's disease," Brinton said.

Brinton and colleagues are now conducting a clinical trial to see if a drug that promotes estrogen activity in the brain reduces cognitive difficulties in women going through menopause. The drug does not promote estrogen activity in other parts of the body, such as the breast, where the hormone has been shown to increase the risk of cancer.

The largest trial of estrogen therapy in postmenopausal women did not find that the therapy reduced the risk of Alzheimer's disease, Brinton said. But that may be because there's a window of time when the therapy is effective, Brinton said.

"If you treat a woman at age 65, her brain is no longer estrogen-responsive," Brinton said. The time to provide an estrogen therapy for cognitive benefits could be during menopause, when women are still experiencing symptoms, Brinton said.

Brinton said changes in brain metabolism likely increase the risk of Alzheimer's disease in men as well. However, men tend to experience hormonal changes, a stage known as andropause, later in life than women, Brinton said.

Tuesday, December 10, 2013

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.

Friday, December 6, 2013

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."

Monday, November 25, 2013

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."

Wednesday, November 20, 2013

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.

Thursday, November 14, 2013

Can changes in the eyes help diagnose Alzheimer’s disease?


Diagnosing someone with Alzheimer’s disease can be a long and complicated process.  In addition to reviewing a patient’s full medical history, doctors must also subject individuals to expensive brain scans or invasive surgical procedures in order to be fully certain of the disease’s presence.

But now, there may be an easier way to spot the brain-wasting condition.  Researchers from Georgetown University Medical Center (GUMC) and the University of Hong Kong have found that it may be possible to diagnose Alzheimer's simply by screening for changes in two very important organs: the eyes.

“We’re looking for biomarkers for early disease [recognition], partly for our new clinical studies focusing more on prevention of Alzheimer’s… and to test new drugs,” study author Dr. R. Scott Turner, director of the Memory Disorder Program at GUMC.  “We’re hoping to incorporate this as a new biomarker for drug trials and potentially for screening and prognosis.”

Currently, there are two leading biomarkers that physicians can utilize to diagnose Alzheimer’s.  One is the buildup of beta-amyloid plaques in the brain, which can be observed through positron emission tomography (PET) or computed tomography (CT) scans.  The other involves measuring changes in protein levels of the cerebrospinal fluid – the liquid surrounding the brain and spinal cord.

However, brain imaging scans can be expensive for patients, and in order collect samples of the cerebrospinal fluid, doctors must administer a spinal tap, which can be a very invasive procedure.

Hoping to find a simpler biomarker, Turner and his colleagues decided to analyze the relationship between the eyes and dementia.  According to Turner, the retina serves as a direct extension of a person’s brain.

“The retinas have neurons themselves that send projections straight into the brain,” Turner said. “…Those nerve cells are directly connected to the brain via the optic nerve….So when looking at the retina, it’s the easiest place to see the brain and its neurons.”

Turner also noted that there has been an established association between glaucoma and Alzheimer’s, though the mechanisms behind the relationship remain unclear.  Most studies examining this connection have revolved around the retinal ganglion cell layer, which is responsible for transmitting visual information through the optic nerve.  However, this cell layer relies on information it receives from another layer in the retina called the inner nuclear layer, which had never before been studied in relation to dementia.

With this knowledge in mind, the researchers analyzed a group of mice that had been genetically engineered to develop Alzheimer’s disease, observing the thicknesses of the six layers in their retinas. They found that there was significant loss in thickness to both the inner nuclear layer, which experienced an average 37 percent loss of neurons, and the retinal ganglion cell layer, which experienced an average 49 percent loss.

According to Turner, these two retinal layers may be most vulnerable to neuron loss because they are larger than the other layers.

“The larger the neuron, the more vulnerable it seems to be to injury,” Turner said.  “We looked at some of the other [smaller] neurons, and they didn’t lose much because they were presumably less vulnerable. So we think whatever is killing neurons in the brain is killing the bigger nerve cells in the retina.”

The next step, Turner said, is to see if this biomarker translates to humans with Alzheimer’s.  If similar changes in retinal thickness occur in people, then a simple, noninvasive procedure known as optical coherence tomography (OCT) can be used to measure loss of neurons in these layers.

“If this holds true with humans and seems to be predicative, it could be used for screening, diagnosis, prognosis, but probably more immediately, a research tool to test new drugs,” Turner said. “…But we should probably be looking at the retinal thickness of our Alzheimer’s patients.”

Wednesday, November 6, 2013

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.

Friday, October 25, 2013

Alzheimer's May Vary, Brain to Brain


Differences in plaque-forming structures in the brains of Alzheimer's patients may offer clues to why the disease can progress more rapidly or be less severe in some people, a new study suggests.

The research could spur the development of new imaging agents that highlight specific structures in the brain -- called beta-amyloid fibrils -- improving the reliability and specificity of diagnosis, according to Robert Tycko.  "Variations in disease may have a structural basis and be due to differences in the molecular structure of the fibrils," said Tycko, a senior investigator with the intramural research program of the U.S. National Institutes of Health.

The study represents an important advance in Alzheimer's research, an expert not involved with the study noted.

Beta-amyloid fibrils are responsible for the amyloid plaques seen in Alzheimer's disease, the most common form of dementia. Alzheimer's is the sixth leading cause of death in the United States and more than 5 million Americans have the disease, according to the Alzheimer's Association. For the research, the scientists took tissue from the brains of two deceased female Alzheimer's patients with different signs and symptoms of the disease. They extracted beta-amyloid from the tissue and used it as "seeds" to grow beta-amyloid fibrils. The investigators found that the same "seeds" -- the amino acid sequence -- could assemble into different molecular structures.

Using nuclear magnetic resonance and electron microscopy to visualize the beta-amyloid fibrils in the patients' brain tissue, the scientists discovered correlations between variations in the disease and differences in molecular structure.

"There are at least two different varieties [of amyloid structure] in Alzheimer's disease," Tycko said. "And certain fibril structures may be more likely than others to cause the disease."

Tycko explained that while the research team was able to determine that there are at least two structural varieties of Alzheimer's disease, they were unable to prove that there are correlations between variations in disease and molecular structure.

He said he hopes that the research will eventually lead to the ability to tell someone with memory loss whether or not the problem is likely to lead to a serious or fast-moving form of Alzheimer's.

One expert not involved with the research called the discovery a "technical tour de force."

"The research is a huge step forward," said Terrence Town, a professor of physiology and biophysics at the Keck School of Medicine at the University of Southern California. "They have accomplished something we have been trying to do for a decade."

For years, researchers have been focusing on something smaller than a fibril, called an oligomer, considered to be especially toxic to the brain, Town explained. "Now this paper is drawing attention to something different: fibrils."

The findings will help researchers focus on the fibrils, ideally working toward developing ways to identify and diagnose people in the earliest stages of the disease, Town said.

Thursday, October 17, 2013

Popular Asian spice can cure Alzheimer's disease


Nature is full of various herbs and spices that protect against disease and even treat and cure it. And according to Chris Kilham, turmeric root -- also known in its extract form as curcumin -- is one such powerful spice that appears to both prevent the onset of Alzheimer's disease and even cure it.

"People who develop Alzheimer's disease get a sticky plaque in the brain called amyloid beta," explained Kilham to Dr. Manny Alvarez in a recent Fox News interview. Such plaques either develop as a result of Alzheimer's, or they are the direct cause of it. But either way, they are directly related to the degenerative process.

However studies show that turmeric actually eliminates these plaques, both when they are first starting to form and even during the late stages of their advancement.

"What we have in turmeric is something that appears to inhibit the development of Alzheimer's disease…and actually help to reduce the occurrence of plaque in the brain if you have it," noted Kilham. "We know in animal studies, when animals actually have amyloid beta plaque in their brains and they're given turmeric root…that plaque is reduced."

Observational studies have also shown that people groups who eat large amounts of turmeric virtually never get Alzheimer's.

"In countries where people consume a lot of [turmeric], there's a very low incidence of Alzheimer's disease," emphasized Kilham. "In India and Southeast Asia, it's a rare disease. And [in the U.S.] it's very, very common."

According to Kilham, drug companies are hard at work trying to develop drug versions of turmeric, but he recommends eating real turmeric whenever possible, and taking turmeric extract supplements if eating the spice in food is not an option.

"A challenge that we face is that drug companies…can't patent turmeric root," he said. "So they will continue to try to develop something else. [But] eating turmeric, eating its extracts…appears to be protective against one of the most horrific and debilitating diseases we know."

Thursday, October 10, 2013

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.

Friday, October 4, 2013

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.

Thursday, September 26, 2013

Lifestyle changes may reverse aging in cells

Lifestyle changes may turn back the biological clock, and reverse aging on a cellular level.
In a pilot study, researchers found that men who ate a better diet, exercised moderately and led a less stressful lifestyle over a few years, had an increase in the length of their telomeres the caps at the ends of chromosomes that protect them from deterioration.

Telomeres get shorter each time cells divide. When they have shrunk to a certain length, a cell may die or stop dividing.

In the study, 10 men were asked to adopt a plant-based diet, do moderate exercise and stress-reducing activities such as meditation and yoga. They participated in weekly group meetings, as a way to promote social support. Another group of 25 men were not asked to make any changes to their lifestyle, and served as the control group.

The researchers measured the length of the telomeres in the participants' white blood cells at the start of the study, and again after five years.

In the group who made lifestyle changes, telomere length increased significantly, by an average of 10 %, but in the control group, telomere shortened by an average of 3 %. Telomeres are often likened to the plastic tips at the end of shoelaces that keeps them from unraveling. It was recently discovered that telomeres can lengthen too, and delay cells' ageing.

"A number of studies have shown that as telomeres get shorter, the risk of premature death and most chronic disease, from heart disease to cancer, even dementia goes up," said study researcher Dr. Dean Ornish, clinical professor of medicine at the University of California, San Francisco.

"So as our telomeres get shorter, in a sense, our lives get shorter," Ornish said. "This is the first study showing that lifestyle changes may actually increase the length of telomeres."

The discovery of telomere function in cell aging, along with the enzyme that builds telomeres won the 2009 Nobel Prize in medicine for three scientists, including Elizabeth Blackburn, also of UCSF, who also worked on the new study.

Exactly how lifestyle changes may affect telomere length is not known, the researchers said. Telomere length is controlled by multiple mechanisms, including the activity of its enzyme, telomerase. It is thought that higher telomerase activity increases telomeres length. But the researchers didn't find an increase in the enzyme in this study, and didn't test for other possible mechanisms.

All men in the study were diagnosed with low-risk prostate cancer, and had decided not to undergo conventional treatments with surgery or radiation. However, the study was not designed to detect the effects of lifestyle changes on the participants' prostate cancer, the researchers said. It is likely that the findings about lifestyle changes extend to other groups of people as well, they said.

"The implications of these findings in all likelihood extends to all men, not just those with prostate cancer, as well as to women," Ornish said.

The results also showed a clear trend: the more positive changes the participants made to their lifestyles, the greater the increase in their telomere length.

The number of participants was too small to prove a cause and effect relationship, the researchers said. However, despite the small size of the study, the difference between groups was highly significant, they said.

Larger trials are needed to see whether lifestyle changes could significantly reduce people's risk of dying early, and contracting chronic diseases, Ornish said.

Friday, September 13, 2013

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.

Tuesday, September 3, 2013

Toward an Early Diagnostic Tool for Alzheimer's Disease



Patients with Alzheimer's disease currently undergo neuropsychological testing to detect signs of the disease. The test results are difficult to interpret and are insufficient for making a definitive diagnosis. But as scientists have already discovered, activity in certain areas of the cerebral cortex is affected even in the early stages of the disease. Professor Falk, who specialises in biological signal acquisition, examined this phenomenon and compared the electroencephalograms (EEGs) of healthy individuals, individuals with mild Alzheimer's, and individuals with moderate cases of the disease. He found statistically significant differences across the three groups.

In collaboration with neurologists and Francisco J. Fraga, an INRS visiting professor specializing in biological signals, Professor Falk used an algorithm that dissects brain waves of varying frequencies. "What makes this algorithm innovative is that it characterizes the changes in temporal dynamics of the patients' brain waves," explains Professor Falk. "The findings show that healthy individuals have different patterns than those with mild Alzheimer's disease. We also found a difference between patients with mild levels of the disease and those with moderate Alzheimer's."

To validate the model in order to eventually develop an early diagnostic tool for Alzheimer's disease, Professor Falk's team is sharing their algorithm on the NeuroAccelerator.org online data analysis portal. It is the first open source algorithm posted on the portal and may be used by researchers around the world to produce additional research findings.

Alzheimer's disease accounts for 60% to 80% of all dementia cases in North America and is skyrocketing. This step toward the development of an early diagnostic tool that is non-invasive, objective, and relatively inexpensive is therefore welcome news for the research community.

Friday, August 23, 2013

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."

Wednesday, August 14, 2013

Breastfeeding proven to lower risk of Alzheimer's in moms.


As more research becomes available, it is increasingly clear that breastfeeding children provides infinitely more long-term health benefits to both baby and mom. Now, a new study shows that mothers who breast feed run a lower risk of developing Alzheimer's disease later in life.

The research  indicates the link may have something to do with key biological effects of breastfeeding. Scientists also found that breastfeeding for longer periods of time decreased overall risk.

Previous studies have established that breastfeeding can reduce a mother's risk of other diseases but until now little has been done to examine the impact of breastfeeding duration on Alzheimer's risk.

Biological changes could be responsible for the additional protection

Researchers from the University of Cambridge's Department of Biological Anthropology conducted the study using data gathered from a relatively small group of 81 women. But, they said, the correlation between breastfeeding and Alzheimer's was especially consistent and significant, though it was much less common in women who had a history of dementia in their family.

The findings could lead to new ways to combat what is being called a global Alzheimer's epidemic. Also, researchers note that the study could offer some indications as to why some people are more susceptible to developing the disease than others.

The study argues that there may be a number of biological reasons for the connection between Alzheimer's and breastfeeding. One theory is that breastfeeding deprives the body of the hormone, progesterone, compensating for high levels of progesterone which are produced during pregnancy.

Researchers note that progesterone is known to have a desensitizing effect on the brain's oestrogen receptors; it may also play a role in protecting the brain against Alzheimer's, they add.

Still another possibility: Breastfeeding boosts a woman's glucose tolerance by restoring her sensitivity to insulin following pregnancy, which in and of itself "induces a natural state of insulin resistance and Alzheimer's is characterized by a resistance to insulin in the brain," the Telegraph reported.

"Women who spent more time pregnant without a compensatory phase of breastfeeding therefore may have more impaired glucose tolerance, which is consistent with our observation that those women have an increased risk of Alzheimer's disease," Dr. Molly Fox, who led the study, said.

"Alzheimer's is the world's most common cognitive disorder and it already affects 35.6 million people. In the future, we expect it to spread most in low and middle-income countries. So it is vital that we develop low-cost, large-scale strategies to protect people against this devastating disease," she said.

Prior research has established that breastfeeding can lower a mum's risk of other diseases and a possible link between breastfeeding and cognitive decline later in life. But until now, little work has taken place on the effect on Alzheimer's of the length of time women breastfeed for.

More research is warranted, but so far, it's promising

The 81 women involved in the study were between 70 and 100 years old. Fox, along with Prof. Carlo Berzuini and Prof. Leslie Knapp interviewed the women; they discovered that "women who breastfed were less likely to have developed the disease and the threat fell still further for those with a longer history of breastfeeding," Cambridge said, in a press release.

Researchers said the link between breastfeeding and Alzheimer's was not affected by other factors such as the drinking and smoking history of the women, education history, age or other variables.

The university said its researchers hope the study will lead to more research into the relationship between the risk of Alzheimer's and the reproductive history of women.


Monday, August 5, 2013

Alzheimer's Progression


New research seeks to delineate just how Alzheimer's disease unfolds in the human brain.

Biological changes may happen earlier than scientists had previously thought, according to a new disease model. This suggests that early signs of risk could potentially become treatment targets long before symptoms of Alzheimer's begin to appear, the researchers said. "We're getting a better idea of what is happening during the asymptomatic [symptomless] phases of the disease," said Dean Hartley, director of science initiatives at the Alzheimer's Association, who was not involved with the new research.

The scientists behind the new research identified distinct but overlapping phases in the course of Alzheimer's disease, each detectable by biological "markers" showing physical changes in the brain. They also have refined their model to distinguish between these "biomarkers" of Alzheimer's disease and those of normal aging.

In the first phase of Alzheimer's, brain markers signaling changes in beta-amyloid protein show up first, the model suggests. Beta-amyloid plaques are protein pieces from the fatty membrane surrounding nerve cells that clump together, contributing to nerve dysfunction.

In the second phase of the disease, signs of degeneration and death of brain cells occur.

Symptoms of dementia are seen in the third phase of Alzheimer's disease, according to the new model.

The refined model should help researchers design better research, guide the selection of study participants, suggest the ideal time to begin treatment and help measure the impact of treatment, said Dr. Clifford Jack Jr.

In addition to beta-amyloid proteins, "tau" - another protein - also plays a role in Alzheimer's, creating what are called "neurofibrillary tangles." Jack said the changes in the brain created by tau seem to occur first, but amyloid aggregation, or clumping, accelerates the changes in tau and causes it to spread.

The central message is that tau and beta-amyloid plaque interact with each other in a synergistic way, said Jack, a professor of radiology and a neuroradiologist at the Mayo Clinic College of Medicine, in Rochester, Minn.

Alzheimer's disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. Symptoms typically appear after age 60, and about 5 million Americans may have the disease, according to the U.S. National Institute on Aging.

How could the model spark new ideas for treating Alzheimer's disease? "What really makes sense probably is a combined therapeutic approach where you target a point or points in tau and in the amyloid pathways simultaneously," Jack explained.

Just as people often take statins -- drugs that lower cholesterol -- to reduce their risk of heart disease, it could someday be possible that those at risk for Alzheimer's could take medication to help prevent it, Jack said. He envisions a "cocktail" or combination of drugs that could target different points in the molecular pathways of the disease, administered at an early age, depending on a person's risk for Alzheimer's disease.

The Alzheimer's Association's Hartley said he's excited about the revised model. "It suggests that some of the treatments we're using may be too late in the progression of the disease."

Two related studies were also scheduled for presentation at the meeting. Dr. Victor Villemagne at the University of Melbourne, in Australia, and colleagues followed about 200 people with and without signs of Alzheimer's disease over four years to estimate when beta-amyloid levels tend to become abnormal. The scientists concluded that Alzheimer's disease is a slow process, likely extending for more than 20 years.

The other study, led by Daniela Bertens at VU University Medical Center, in Amsterdam, Holland, provided more evidence that abnormal beta-amyloid is what triggers the development of Alzheimer's disease. The research included about 300 people with abnormal beta-amyloid, and followed them over four years, testing their cerebrospinal fluid for diagnostic signs of the disease.

Wednesday, July 31, 2013

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.

Tuesday, July 23, 2013

Cinnamon beats Alzheimers


The miracle spice cinnamon is the scented bark of a tropical evergreen tree, native to India and Sri Lanka. Cinnamon comes from an evergreen tree in Southeast Asia and is cultivated widely in Vietnam, China, Burma, and Laos for its bark and the oil processed from the bark. Once upon a time in ancient Rome, cinnamon was worth more than silver.

Cinnamon is harvested from the inner bark of the tree branches after scraping off the corky outer layer and then drying the bark. As it dries, the bark curls up into quills which are then cut into sticks to be ground into the spice form. Full of calcium and fiber, cinnamon is one of the oldest known spices, it is mentioned in the Bible and was used in ancient Egypt as medicine, beverage flavoring and an embalming agent.

According to traditional Chinese medicine, cinnamon helps improve the body's "fire."

Cinnamon - Not just a spice!

Professor Daniel Fung, an expert in food science at Kansas State University, says cinnamon contains a compound that has the ability to kill bacteria. "If cinnamon can knock out E.coli 0157:H7, one of the most virulent food-borne microorganisms that exists today, it will certainly have antimicrobial effects on other common food-borne bacteria such as Salmonella and Campylobacter."

Now researchers from Tel Aviv University found that extracts from cinnamon bark inhibit the toxic amyloid polypeptide oligomers and fibrils that have been found in Alzheimer's Disease (AD) brain plaque formations. In animal models of Alzheimer's, cinnamon reduced s-amyloid plaques associated with the pathology of AD. Reduction of these proteins can improve mental cognition. In one model, cinnamon extract resolved AD associate reduced longevity, helped recover locomotion defects and completely abolished tetrameric species of plaque in the brain.

Other benefits of cinnamon are: anti-microbial actions, blood sugar balancing, improving colon health, boosting brain function. Cinnamaldehyde in cinnamon has been well researched for its effects on blood platelets which help the blood clot to stop bleeding. Platelets can also cause strokes if they clump together too much. Cinnamon has been shown to help prevent this deadly clumping. Cinnamon will stop vomiting and relieve feelings of nausea. Cinnamon also helps slow tumor growth while inhibiting inflammatory markers connected to cellular proliferation.

In a recent study, people reduced their blood sugar levels by as much as 29 percent with cinnamon in just 40 days. That's with NO drugs, NO diet changes - just plain old cinnamon!

Study volunteers who took a cinnamon extract showed significant decreases in fasting blood glucose and increases in lean muscle mass compared with the placebo group. Pre and post study analysis of the extract group revealed a statistically significant decrease in body fat and blood pressure.

Research found that cinnamon can have favorable effects on brain function. Participants in a study chewed cinnamon gum or even just smelled the sweet spice. Cognitive tests revealed that subjects who used cinnamon had better memory functions and could process information more quickly.

What kind and how much

Which is best: Ceylon cinnamon, Saigon cinnamon, cinnamomum zeylanicum or regular grocery store variety cinnamon? Interestingly, the grocery store variety known as cinnamomum cassia works the best in most research studies and clinical trials.

Drink cinnamon in tea or sprinkle a little cinnamon on your toast, cereal, oatmeal, or sliced apples. It not only tastes good, it lowers your blood sugar!

Taking two 500 mg capsules of cinnamon a day will help good cholesterol levels and taking two capsules with each meal can make a big difference in blood sugar and insulin levels for diabetics.

Wednesday, July 17, 2013

Alzheimer’s Aggression


Alzheimer’s aggression most often flares up during the later stages of Alzheimer’s disease. The person may become easily agitated, angry, and abusive - often for no apparent reason. The person may curse, hurl insults, and scream. Though verbal assaults are more common than physical assaults, a person with Alzheimer’s disease may throw things or resist care by pushing and hitting.

Why Does Alzheimer’s Aggression Occur? - No one knows for sure why Alzheimer’s patients become aggressive. Aggression may be a symptom of Alzheimer’s disease itself. It may also be a reaction to actions of others or to the environment around the person with Alzheimer’s disease.

Understand the Triggers of Alzheimer’s Aggression - Alzheimer’s aggression can flare up without warning. There may not be an obvious cause. However, often there are triggers that caregivers can look for. By knowing the triggers, you may be able to lower the frustration level of the person with Alzheimer’s disease. This can reduce the number of aggressive outbursts. Here are some common triggers of Alzheimer’s aggression:

Discomfort caused by lack of sleep, side effects from medication, or pain that the person is not able to describe
The surrounding environment, such as loud noises, busyness around the person, or clutter
Confusion caused by being asked too many questions at once, trying to understand complex instructions, or feeling the stress of caregivers

Tips to Reduce Alzheimer’s Aggression - Once you understand the triggers for Alzheimer’s aggression, you can take steps to prevent it. Try these suggestions:


  • Anticipate situations in which the person with Alzheimer’s may be uncomfortable, overstimulated, or confused.
  • Avoid asking too many questions at once, giving overly complicated instructions, and speaking negatively. That way, you are less likely to confuse and agitate the person you are caring for.
  • Limit the amount of loud noises, frenetic movement, and clutter.
  • Don’t contradict. Those with Alzheimer’s disease see a different reality than you do. Rather than challenge that reality, sit and listen. Ask questions about it.
  • Focus on the past. Alzheimer’s affects short-term memory. It’s often easier and less stressful for someone with Alzheimer’s disease to recall and talk about distant memories than it is for them to remember what they watched on TV the night before.
  • Use memory cues. As the disease progresses, remembering to do and how to do everyday tasks like brushing your teeth or getting dressed becomes more difficult. Reminder notes placed in key locations can help prevent frustration.


Caregiver Stress and Alzheimer’s Aggression - It’s not easy to care for a person with Alzheimer’s disease. The burden of round-the-clock care takes an emotional toll. Add to it the frustration and sadness of watching a loved one deteriorate. It’s not surprising that caregivers may feel isolated and depressed. Left unrelieved, these feelings can lead to abusive behavior toward the person with Alzheimer’s disease, from insults to physical injury.

If you are a caregiver, do yourself and the person you care for a favor. Seek help for yourself if you notice signs of depression, anxiety, sleeplessness, exhaustion, or irritability. Taking care of yourself will help you take better care of others.

Tuesday, July 9, 2013

Mechanism of Alzheimer's Therapy


Gammagard™ IVIg is a therapy that has been investigated for treatment of Alzheimer's. Despite small clinical studies that have reported efficacy of the approach, the mechanism of action is poorly understood.
The UK researchers set out to investigate the mechanism by which the treatment may act in the brain to lower amyloid deposition (amyloid deposits being a key pathology in Alzheimer's).

To conduct their investigation, researchers introduced IVIg directly into the brains of mice which carry a human gene causing them to develop amyloid plaques. They found that IVIg lowers amyloid deposits in the brains of the mice over the course of seven days. Their data suggest that the modulation of inflammation in the brain by IVIg is a key event that leads to the reduction in amyloid deposition.

The scientists hypothesize that the IVIg acts as an immune modulator, and this immune modulation is responsible for the reductions in amyloid pathology.

The data suggests that modulating the immune response in the brain may help ameliorate the Alzheimer's pathology. Researchers are currently investigating other ways to produce the same modulation of the immune response because the access of IVIg to the brain when administered peripherally is very limited.

Wednesday, July 3, 2013

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..

Friday, June 21, 2013

Steroids might slow Alzheimer’s disease progression


Anti-inflammatory drugs for treatment and prevention of Alzheimer’s disease have to date proved disappointing, including a large study of low-dose prednisone, but higher dose of anabolic steroids significantly reduced amyloid secretion in a small series of nondemented patients. In addition, there is a case report of a patient with amyloid angiopathy who had complete remission from two doses of dexamethasone, and very high dose steroids are already used for systemic amyloidosis. This paper presents the hypothesis that pulse-dosed intrathecal methylprednisolone or dexamethasone will produce detectable slowing of Alzheimer’s progression, additive to that obtained with cholinesterase inhibitors and memantine. 

A protocol based on treatment regimens for multiple sclerosis and central nervous system lupus is outlined, to serve as a basis for formulating clinical trials. Ultimately intrathecal corticosteroids might become part of a multi-agent regimen for Alzheimer’s disease and also have application for other neurodegenerative disorders.

Thursday, June 13, 2013

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.


Wednesday, June 5, 2013

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.

Wednesday, May 29, 2013

Preventing 'Traffic Jams' in Brain Cells




What you would see is a network of nerve cells called neurons, each with its own internal highway system for transporting essential materials between different parts of the cell.
When this biological machinery is operating smoothly, tiny motor proteins ferry precious cargo up and down each neuron along thread-like roadways called microtubule tracks. Brain cells are able to receive information, make internal repairs and send instructions to the body, telling the fingers to flex or the toes to curl.
But when the neuron gets blocked, this delicate harmony deteriorates. One result: diseases like Alzheimer's.

Understanding such blockages and how traffic should flow normally in healthy brain cells could offer hope to people with neurodegenerative diseases. Toward that end, a research team led by University at Buffalo biologist Shermali Gunawardena, PhD, has shown that the protein presenilin plays an important role in controlling neuronal traffic on microtubule highways, a novel function that previously was unknown.

Inside the nerves of fruit fly larvae, presenilin helped to control the speed at which molecular motors called kinesins and dyneins moved along neurons. When the scientists halved the amount of presenilin present in the highway system, the motors moved faster; they paused fewer times and their pauses were shorter.
Given this data, Gunawardena thinks that tweaking presenilin levels may be one way to free up traffic and prevent dangerous neuronal blockages in patients with Alzheimer's disease.


Presenilin rides along neuronal highways in tiny organic bubbles called vesicles that sit atop the kinesin and dynein motors, and also contain a second protein called the amyloid precursor protein (APP). Presenilin participates in cutting APP into pieces called amyloid beta, which build up to form amyloid plaques in patients with Alzheimer's disease.
Such buildups can lead to cell death by preventing the transport of essential materials -- like proteins needed for cell repair -- along neurons.
The findings of the new study mean that presenilin may contribute to Alzheimer's disease in at least two ways: not just by cleaving APP, but also by regulating the speed of the molecular motors that carry APP along neuronal highways.


Tuesday, May 21, 2013

Sleep Apnea Linked to Alzheimer's




But this latest study also poses an interesting question: Could AD in its "preclinical stages" also lead to SDB and explain the increased prevalence of SDB in the elderly?
The study will be presented at the ATS 2013 International Conference.

"It's really a chicken and egg story," said Ricardo S. Osorio, MD, a research assistant professor at NYU School of Medicine who led the study. "Our study did not determine the direction of the causality, and, in fact, didn't uncover a significant association between the two, until we broke out the data on lean and obese patients."

When the researchers did consider body mass, they found that lean patientswith SDB did possess several specific and non-specific biomarkers of AD risk. Among obese patients , glucose hypometabolism was also found in the medial temporal lobe, but was not significant in other AD-vulnerable regions.
"We know that about 10 to 20 percent of middle-aged adults in the United States have SDB [defined as an apnea-hypopnea index greater than 5] and that the number jumps dramatically in those over the age of 65," said Dr. Osorio, noting that studies put the percentage of people over the age of 65 with SDB between 30 and 60 percent. "We don't know why it becomes so prevalent, but one factor may be that some of these patients are in the earliest preclinical stages of AD."

According to Dr. Osorio, the biochemical harbingers of AD are present 15 to 20 years before any of its currently recognized symptoms become apparent.

The NYU study enrolled 68 cognitively normal elderly patients (mean age 71.4±5.6, range 64-87) who underwent two nights of home monitoring for SDB and were tested for at least one diagnostic indicator of AD. The researchers looked at P-Tau, T-Tau and Aβ42 in CSF, FDG-PET (to measure glucose metabolism), Pittsburgh compound B (PiB) PET to measure amyloid load, and/or structural MRI to measure hippocampal volume. Reduced glucose metabolism in AD-vulnerable regions, decreased hippocampal volume, changes in P-Tau, T-Tau and Aβ42, and increased binding of PiB-PET are recognized as markers of risk for AD and have been reported to be abnormal in healthy subjects before the disease onset.
Biomarkers for AD risk were found only among lean study participants with SDB. These patients showed a linear association between the severity of SDB and CSF levels of the biomarker P-Tau and between SDB and glucose hypometabolism using FDG-PET, in the medial temporal lobe, the posterior cingulate cortex/precuneus and a composite score of all AD-vulnerable regions . Lean SDB patients also showed smaller hippocampi when compared to lean controls, but no differences were found in measures of amyloid burden such as decreased Aβ42 in CSF or PiB positive scans.

Friday, May 10, 2013

Turning Alzheimer's Fuzzy Signals Into High Definition

Scientists at the Virginia Tech Carilion Research Institute have discovered how the predominant class of Alzheimer's pharmaceuticals might sharpen the brain's performance

One factor even more important than the size of a television screen is the quality of the signal it displays. Having a life-sized projection of Harry Potter dodging a Bludger in a Quidditch match is of little use if the details are lost to pixilation.

The importance of transmitting clear signals, however, is not relegated to the airwaves. The same creed applies to the electrical impulses navigating a human brain. Now, new research has shown that one of the few drugs approved for the treatment of Alzheimer's disease helps patients by clearing up the signals coming in from the outside world.The discovery was made by a team of researchers led by Rosalyn Moran, an assistant professor at the Virginia Tech Carilion Research Institute. Her study indicates that cholinesterase inhibitors -- a class of drugs that stop the breakdown of the neurotransmitter acetylcholine -- allow signals to enter the brain with more precision and less background noise.

Alzheimer's disease affects more than 35 million people worldwide -- a number expected to double every 20 years, leading to more than 115 million cases by 2050. Of the five pharmaceuticals approved to treat the disease by the U.S. Food and Drug Administration, four are cholinesterase inhibitors. Although it is clear that the drugs increase the amount of acetylcholine in the brain, why this improves Alzheimer's symptoms has been unknown. If scientists understood the mechanisms and pathways responsible for improvement, they might be able to tailor better drugs to combat the disease, which costs more than $200 billion annually in the United States alone.