Potassium, calcium, magnesium intakes linked to reduced risk of dementia

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

FoodConsumer

By David Liu, PHD

 (foodconsumer.org) -- A new study in Journal of American Geriatrics Society suggests that taking potassium, calcium and magnesium supplements or eating foods high in these minerals may help prevent some forms of dementia, but not Alzheimer's disease.

The study led by M. Ozawa of Kyushu University om Fukuoka Japan and colleagues showed that all-cause dementia was 48 percent, 36 percent, and 37 percent less likely among people with highest intakes of potassium, calcium, and magnesium, respectively, compared to those who had low levels.

A total of 1081 community dwelling Japanese people without dementia aged 60 or older participated in the study in which 303 participants were found to have all-cause dementia including 98 vascular dementia and 166 Alzheimer's disease during a 17-year follow-up.

Participants who had highest intakes of potassium, calcium and magnesium were 80 percent, 77 percent and 74 percent less likely to develop vascular dementia, respectively, compared to those who had lowest intakes.

But these minerals were not associated with risk of Alzheimer's disease.

The researchers concluded that high dietary intakes of potassium,calcium, and magnesium reduce risk of all cause dementia, particularly vascular dementia in the general Japanese population.

Alzheimer's disease is a major form of dementia affecting an estimated 5 million Americans. There is no cure for Alzheimer's but research suggests that the disease is preventable.

Sharp as a Tack at 90: Here is Why

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

HealthDay News

Elderly people who experience no decline in memory have certain brain characteristics that differ from their peers who show more typical age-related memory loss, new research reveals.

Scientists from Northwestern University's Cognitive Neurology and Alzheimer's Disease Center identified 12 people aged 80 and older who did as well or better on memory tests as people who were 20 to 30 years younger. Researchers dubbed them "SuperAgers."

MRI scans showed that the cortex of SuperAgers was thicker than a comparison group of people aged 80 and older. The cortex is the outer layer of the brain involved in memory, attention and other thinking abilities.

A thinning cortex suggests a loss of brain cells, or gray matter, explained senior study author Emily Rogalski, an assistant research professor at Northwestern.

Brain scans also showed that people in their 80s and 90s who exhibited more typical memory declines (though not the marked decline associated with Alzheimer's disease or other thinking impairments, researchers said) had a thinner cortex.

Brain scans also showed that people in their 80s and 90s who exhibited more typical memory declines (though not the marked decline associated with Alzheimer's disease or other thinking impairments, researchers said) had a thinner cortex.

"The SuperAgers looked more like the middle-aged controls, despite being 20 to 30 years older," Rogalski said. "We didn't see any significant atrophy or brain cell loss."

The study is published in the current issue of the Journal of the International Neuropsychological Society.

Some degree of forgetfulness is a common complaint among the elderly, Rogalski said. "These complaints are so widespread that it's come to be thought of as a normal part of aging," she noted.

Many prior studies have shown that brain atrophy and loss of thinking abilities go hand in hand, said Dr. Russell Swerdlow, director of the Alzheimer's Disease Center at the University of Kansas.

This study is unique in that it starts with people with exceptionally good memories for their age, and then looks at what makes their brains different, he said.

He noted, however, that the study shows a correlation between good memories in later life and a thicker cortex and larger brain volume, but it doesn't show cause-and-effect. What is unknown is if retaining brain volume protects thinking abilities, or if maintaining thinking abilities protects brain volume.

"It could be that those whose brains are better 'built to last' structurally are probably those brains that are better built to last from a functional perspective, or that those who are exercising their brains may have less atrophy," he said.

At the same time, SuperAgers also had a larger cingulate cortex, another brain region also involved in attention and memory, than even the middle-aged participants. What's unknown is if SuperAgers were born with a more prominent cingulate cortex or if that region resisted atrophy in later life, according to the study.

With studies like this, one thing people want to know is what it takes to be among the SuperAgers. Unfortunately, there aren't yet any clear answers, Rogalski said.

"Genetics are likely to play a role. And, in general, a healthy lifestyle is supportive of good memory," Rogalski said. "But in our experience, some of our SuperAgers have been smoking a pack of cigarettes for the last 20 years. Others have never touched them. Some go to the gym three to five days a week. Others don't exercise. Some are still working and others have never worked. It seems there might be more than one route to being a SuperAger."

More information

The U.S. National Institutes of Health has more on the brain.

Why is diagnosing the cause of dementia important

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

FCA

©Family Caregiver Alliance

What does it mean when someone is said to have dementia? For some people, the word conjures up scary images of “crazy” behavior and loss of control. In fact, the word dementia describes a group of symptoms that includes short-term memory loss, confusion, the inability to problem-solve, the inability to complete multi-step activities such as preparing a meal or balancing a checkbook, and, sometimes, personality changes or unusual behavior. Saying that someone has dementia does not offer information about why that person has these symptoms. Compare it to someone who has a fever: the person is ill from the fever, but the high temperature does not explain the cause or why this person is ill. Does any loss of memory signify dementia? Isn’t memory loss a normal part of aging? We often hear that because someone is old, memory problems are “just natural” and are to be expected.  But we know thatserious memory loss is not a normal part of aging, and should not be ignored. On the other hand, families might assume that a loved one’s noticeable loss of memory must be caused by Alzheimer’s disease. In many instances, Alzheimer’s is, in fact, the problem. But other conditions also can cause memory and cognitive problems severe enough to interfere with daily activities. These conditions can affect younger as well as older people. A clear diagnosis is needed. Certain conditions can cause reversible dementias. These include medication interactions, depression, vitamin deficiencies or thyroid abnormalities.  It is important that these conditions be identified early and treated appropriately so that symptoms can be improved. The irreversible dementias are known as degenerative dementias, and Alzheimer’s disease is the most common.  There are a number of other degenerative dementias, however, that may look like Alzheimer’s, but have distinct or different features which need special attention and different treatment. Reversible and irreversible dementias are described in more detail below. Importance of Obtaining a Diagnosis The diagnosis of dementia requires a complete medical and neuropsychological evaluation. The process is first to determine if the person has a cognitive problem and how severe it is. The next step is to determine the cause in order to accurately recommend treatment and allow patients and caregivers to plan for the future. A medical evaluation for dementia usually includes the following: Review of history or onset of symptoms Medical history and medications Neurological exam Laboratory tests to rule out vitamin deficiencies or metabolic conditions Brain Imaging   Mental status testing (also called cognitive or neuropsychological testing) The process of diagnosing dementia has become more accurate in recent years, and specialists are able to analyze the large amount of data collected and determine if there is a problem, the severity, and, often, the cause of the dementia. Occasionally, there may be a combination of causes or it may take time to monitor the individual to be sure of a diagnosis. Determining whether the cause is a reversible or irreversible condition guides the treatment and care for the affected person and family. Reversible Dementias Deteriorating intellectual capacity may be caused by a variety of diseases and disorders in older persons. An illness and/or a reaction to medication may cause a change in mental status.  These are sometimes called “pseudodementias.” Detecting the underlying cause of changes through medical evaluation may lead to a determination that the cause is reversible or treatable. Examples of conditions that can cause reversible symptoms of dementia include: Reactions to medications. Adverse drug reactions are one of  the most common reasons older persons experience symptoms that mimic dementia. All medications, prescriptions, over-the-counter pills and herbal remedies should be monitored by a physician to reduce the possibility of side effects. Endocrine abnormalities. The conditions of low or high thyroid levels, parathyroid disturbances or adrenal abnormalities can cause confusion that mimics dementia. Metabolic disturbances. Confusion or appetite, sleep and emotional changes can be caused by medical conditions including renal and liver failure, electrolyte imbalances (blood chemistry levels), hypoglycemia (low blood sugar), hypercalcemia (high calcium), and diseases of the liver and pancreas. Emotional Distress. Depression or major life changes such as retirement, divorce or loss of a loved one can affect one’s physical and mental health.  A physician should be informed about major stressful life events. Vision and Hearing. Undetected problems of vision or hearing may result in inappropriate responses and be misinterpreted.  Hearing and eye exams should be performed. Infections. Confusion can be a symptom of infection—such as a urinary tract infection (UTI)—and needs to be brought to the attention of the physician. Nutritional Deficiencies. Deficiencies of B vitamins (folate, niacin, riboflavin and thiamine) can produce cognitive impairment. Degenerative (Irreversible) Dementias If reversible dementias are ruled out and it is determined that the person has a degenerative or irreversible dementia, it is important that families and medical personnel  seek the cause of the problem. This will help ensure that the person affected receives proper medical care, and families can plan their caregiving and find appropriate support and resources. The following are the most common degenerative dementias: Alzheimer’s Disease. Alzheimer’s Disease is the most common cause of dementia in people over 65, although the disease also occurs in people much younger. Alzheimer’s affects approximately 50 percent of those over 85. Presently, researchers cannot definitely say what causes the disease, and there is no cure.  Symptoms differ from person to person, but declines in memory, thinking and ability to function gradually progress over of a period of years, ending in a severe loss of function. Ischemic Vascular Dementia (IVD). IVD is the second most common dementia, characterized by an abrupt loss of function or general slowing of cognitive abilities that interferes with what are called “executive functions” such as planning and completing tasks. When symptoms appear suddenly, the person has usually experienced a stroke. For others, the condition develops slowly with a gradual loss of function and/or thinking. Dementia with Lewy Bodies (DLB). Dementia with Lewy Bodies is a progressive degenerative disease that shares symptoms with Alzheimer’s and Parkinson’s.  People affected by this disease have behavioral and memory symptoms which can fluctuate, as well as motor problems which are commonly seen with Parkinson’s disease. Frontotemporal Dementia (FTD). FTD is a degenerative condition of the front (anterior) part of the brain, which can sometimes be seen on brain scans. The frontal and anterior temporal lobes of the brain control reasoning, personality, movement, speech, language, social graces and some aspects of memory. Symptoms may lead to misdiagnosis as a psychological or emotionally-based problem. FTD frequently occurs after age 40 and usually before age 65.  Symptoms appear in two seemingly opposite ways: some individuals are overactive, restless, distracted and disinhibited (showing poor social judgment), while others are apathetic, inert and emotionally blunted. Creutzfeldt-Jakob Disease. Creutzfeldt-Jakob Disease (CJD or Jakob-Creutzfeldt Disease) is a rapidly progressive, fatal brain disease. It is part of a family of diseases called transmissible spongiform encephalopathies, caused by an agent known as a prion (“pree-on”). This condition can be very difficult to diagnose as it has many different symptoms, including behavioral changes, movement changes, cognitive changes and general changes in well-being such as sleep problems, loss of appetite and headaches. Parkinson’s Dementia. Parkinsonism is the name given to a col-lection of symptoms and signs consisting of tremor, stiffness, slowness of movement, unsteady gait. Many neurological disorders have features of parkinsonism, including many of the dementias. When parkinsonism occurs without any other neurological abnormalities, and there is no recognizable cause, the disorder is termed Parkinson’s disease after the English physician who first described it fully in 1817. Progressive Supranuclear Palsy (PSP). People with PSP usually show a group of three symptoms, including the gradual loss of balance and trouble walking, loss of control of voluntary eye movements, and dementia. Although these features are considered to be the hallmarks of PSP, patients with this disorder also experience other symptoms common to degenerative diseases of the brain, including difficulties with movement, changes in behavior and difficulty with speech and swallowing. In part because it is relatively rare, PSP is frequently misdiagnosed as Parkinson’s Disease. How-ever, its treatment response and clinical symptoms are different, making an accurate diagnosis very important. Normal Pressure Hydrocephalus (NPH). Gait instability, urinary incontinence and dementia are the signs and symptoms typically found in patients who have NPH. Considered a rare cause of dementia, it primarily affects persons older than 60 years. The precise incidence of NPH is hard to determine because the condition does not have a formal, agreed-upon definition. Some physicians base the diagnosis strongly on radiographic evidence; another group of health care professionals relies more on clinical indications. Still others use a combination of signs and symptoms that they have found to be reliable. Traditionally, treatment is surgical implantation of a shunt to reduce the pressure caused by the build up of cerebrospinal fluid. Huntington’s disease (HD). Huntington’s disease is a fatal disease typically characterized by involuntary movements (chorea) and cognitive decline (dementia). It is caused by a genetic mutation that can be passed down from generation to generation. HD is an illness with profound neurological and psychiatric features affecting certain structures deep within the brain, particularly the basal ganglia, responsible for such important functions as movement and coordination. Structures responsible for thought, perception and memory are also affected, likely due to connections from the basal ganglia to the frontal lobe of the brain. As a result, patients may experience uncontrolled movements (such as twisting and turning), loss of intellectual abilities, and emotional and behavior disturbances. Mixed Dementias. At times, two of these conditions can overlap. This is commonly seen in Alzheimer’s disease and vascular dementia, and also in Alzheimer’s disease and Lewy Body dementia. There are no cures for degenerative or irreversible dementias, so medical treatments focus on maximizing the individual’s cognitive and functional abilities. Specific treatments for dementia vary depending on the cause of the dementia. Good communication with the primary care provider affects the well-being of the person with dementia as well as the well-being of the  caregiver.  Communicating your concerns clearly and describing the changes you may have observed will help guide the provider to investigate further.  In some cases, you may find yourself “educating” medical staff about your loved one’s symptoms. An accurate diagnosis begins a process of education for caregivers and families so that needs can be met and resources located and put to use. Irreversible dementia requires a level of care that increases as the disease progresses. Through education and the use of available resources, families can learn new skills to handle shifting care needs. Research into the cause and treatments for dementia continues at a rapid pace. We all look forward to new developments that someday may postpone, cure or even prevent these debilitating disorders. Excerpted from FCA's fact sheet Is This Dementia & What Does It Mean?  To view the entire text, go tohttp://caregiver.org/caregiver/jsp/publications.jsp?nodeid=345, or purchase a copy by sending $2.00 to Publication Orders, Family Caregiver Alliance, 180 Montgomery Street, Suite 1100, San Francisco, CA 94104.

Aging: Understanding Hippocampal Sclerosis

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

ScienceDaily — The population of aged persons worldwide is expanding rapidly, and it is becoming increasingly clear that there are many different diseases that affect the minds of these individuals. Researchers at the University of Kentucky are breaking new ground in the ongoing project of identifying and defining those diseases most likely to affect an aged population. Dr. Peter Nelson of the University of Kentucky Sanders-Brown Center on Aging is the lead author on a paper soon to be published in the journal Brain; the paper deals with the little-understood but serious condition hippocampal sclerosis (HS-AGING).

Many different diseases may produce symptoms of dementia -- defined as cognitive decline and impaired memory -- in aged persons. Although Alzheimer's disease is probably the most recognized cause of dementia, HS-AGING also causes serious cognitive impairment in older adults. In those who live to a very advanced age (beyond the age of 95) HS-AGING is roughly as prevalent as Alzheimer's.

It is important for physicians and scientists to understand the unique pathology of HS-AGING, and to be able to differentiate it from other diseases, as it is only by making an accurate diagnosis that clinicians can hope to treat people who present with signs of cognitive decline.

Nelson, a neuropathologist, analyzed autopsy data from 1,100 individuals, each with substantial clinical data available from before death. The long-term clinical information was obtained through the University of Kentucky Alzheimer's Disease Center, the Nun Study and the Georgia Centenarian Study (all autopsies were performed at the University of Kentucky). The large numbers of patients and the high quality of the data enabled the research team to gather new clues about the prevalence and impact of HS-AGING.

"We and others have shown previously that HS-AGING has a strong impact on cognition. The goal of the new study was to define HS-AGING as a distinct disease entity," said Nelson.

"There were some surprises. The high prevalence of HS-AGING in individuals older than 95 was unexpected. In addition, by analyzing neuropathological data alongside clinical data, we were able to determine that there is a recognizable cognitive profile for individuals likely to develop HS-AGING," said Nelson.

In the future, clinicians may be able to utilize cognitive tests with increased accuracy to differentiate a diagnosis of HS-AGING from a general diagnosis of cognitive decline. Being able to pinpoint the cause of cognitive decline may lead to better and more accurate diagnosis and treatment of aging individuals who present with signs of dementia.

"This is an extremely exciting paper because it provides the largest study of HS-AGING in the literature to date, by far. These studies help to define the cognitive features, pathological features, and risk factors that correlate with HS-AGING," said Linda Van Eldik, director of the Sanders-Brown Center on Aging and co-author of the paper.

The next step for Nelson will be to use a grant from the NIH (through the Alzheimer's Disease Genetic Consortium) to study HS-AGING from a genomic approach.

"We want to show the specific genetic fingerprint of HS-AGING so that we can begin to develop ways of better diagnosing and curing the disease during life," said Nelson. "Our ultimate goal is to prevent or cure the disease, and a greater understanding of the disorder at the genetic and biological levels is critical. Dr. Nelson's studies are providing the essential foundation required for translating the science into new therapies for the Commonwealth of Kentucky and well beyond," summarized Van Eldik.

Peter Nelson is the recipient of a newly approved grant from the National Institutes of Health (NIH) to conduct a study of HS-AGING genetics.

Cocoa may improve brain function

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

WebMD

Having a cocoa-rich drink every day as part of a calorie-controlled and nutritionally-balanced diet could improve brain function in older adults, according to a new study.
The Italian study, published in the American Heart Association’s journal Hypertension, included 90 elderly people who already had mild cognitive impairment (MCI), which can include difficulty with memory, language, thinking or judgment.

For eight weeks they drank a cocoa drink that had high, medium or low amounts of antioxidants called flavanols and their diet was restricted to eliminate other sources of flavanols from foods and beverages. Those who had high and medium levels of flavanols in their drink did better on tests of attention and other mental skills, compared to people who had low amounts of flavanols.

Flavanols

Flavanols can be found in tea, grapes, red wine, apples and cocoa products and have been associated with a decreased risk of dementia. The researchers say flavanols may act on the brain structure and function directly by protecting neurons from injury, improving metabolism and their interaction with the molecular structure responsible for memory. Indirectly, flavanols may help by improving brain blood flow.

Flavanols "could be one element of a dietary approach to the maintaining and improving not only of cardiovascular health, but also specifically brain health", write the researchers, including Giovambattista Desideri of Italy's University of L'Aquila.

However, he cautions that the results of the study may not apply to everyone with MCI. The study population was generally in good health without known cardiovascular disease so it would not be completely representative of all mild cognitive impairment patients. In addition, only some clinical features of mild cognitive impairment were explored in the study.

Alzheimer's

Dr Laura Phipps at Alzheimer’s Research UK said via e-mail: "Cocoa-based treatments for brain function would likely have patients queuing out the door, but this small study of flavanols is not yet conclusive. It’s not clear from the research whether other factors may have been responsible for the improvements seen in the group of people who took part.

This early-stage trial took place over a very short period, and it would be useful to see more long-term studies to investigate the lasting effects. Ultimately we would need to see the results of large-scale trials to know whether cocoa flavanols could help prevent or delay dementia.

"While we do not yet have a sure-fire way to prevent dementia, the best evidence for lowering your risk is to eat a healthy, balanced diet with plenty of fruit and vegetables. Regular exercise, keeping your blood pressure and cholesterol in check and not smoking have also been shown to reduce the risk of dementia."

Neurologist and Alzheimer's disease researcher Dr Marc Gordon of the Feinstein Institute for Medical Research in New York says: "People need to be very careful about making broad-based dietary changes based on one study."

The Italian study was supported by a grant from Mars Inc, which also supplied the powdered cocoa drinks that were used.

Caring for a loved one with mesothelioma

Caregivers and health care professionals here is some information that you will find most useful.

As a health care professional, you no doubt have cared for people with a wide range of illnesses. As a caregiver, you may have cared for a loved one with one particular sickness. Sometimes things do not make sense about a person’s illness

Your loved one or client may have dementia, heart disease, lung problems or some other disease. How do you know what to expect from person(s) you are caring for?

As a health care professional, you are trained to look for certain things. As a caregiver you and your loved one’s doctor are a team wanting the best for this person. If you and your doctor see symptoms that might indicate an illness caused by contamination of a foreign substance, you may need the services of a lawyer so you can get compensation to help pay for medical costs of the illness.

If, for example, your loved one or client has mesothelioma caused by asbestos, you may want to seek the help of a mesothelioma lawyer. Using him will not cure your loved one or client, but you can get the financial help you need and deserve.

Research Shows Glymphatic System Flushes Away Most Alzheimer's Plaque

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Scientific American

The brain can be a messy place. Thankfully, it has good plumbing: Scientists have just discovered a cleansing river inside the brain, a fluid stream that might be enlisted to flush away the buildup of proteins associated with Alzheimer's, Huntington's and other neurodegenerative disorders.

The researchers, based at the University of Rochester (U.R.), University of Oslo and Stony Brook University, describe this new system in the journal Science Translational Medicine today. The study adds to the evidence that the star-shaped cells called astrocytes play a leading role in keeping the nervous system in good working order.

In most of the body, a network of vessels carry lymph, a fluid that removes excess plasma, dead blood cells, debris and other waste. But the brain is different. Instead of lymph, the brain is bathed in cerebrospinal fluid. For decades, however, neuroscientists have assumed that this fluid simply carries soluble waste by slowly diffusing through tissues, then shipping its cargo out of the nervous system and eventually into the body's bloodstream. Determining what's really going on has been impossible until recently.

In this study, researchers led by U.R. neuroscientist Maiken Nedergaard have identified a second, faster brain-cleansing system. Nedergaard an expert in non-neuronal brain cells called glia, has long suspected that these cells might play a role in brain cleansing.

Nedergaard and colleagues studied live mice with holes drilled into their skulls to gain an unobstructed view. To see how waste is carried by cerebrospinal fluid in a living mouse, they injected the mice with radioactive molecules that could be traced using laser-scanning technology.

The molecules' journey began after being injected into the subarachnoid space, a cavity between membranes covering the brain and spinal cord. The researchers observed that, like a river, cerebrospinal fluid carried these molecules rapidly along specific channels. Glial cells along the outside of arteries form these channels, creating a flume for cerebrospinal fluid that follows the brain's blood vessels. In addition, the researchers found that these glial cells mediate the channel's activity, assisting the flow of fluid through the channel.

From channels alongside arteries, the tracer-bearing fluid then passes through brain tissues. At the other end of tissues, it flows into similar channels along veins. The fluid follows these veins then either returns to the subarachnoid space, enters the bloodstream or eventually drains into the body's lymphatic system. The researchers christened the network the "glymphatic" system, a nod to both glial cells and its functional similarity to the lymphatic system.

U.R. neuroscientist and lead author Jeff Iliff notes several surprises in the study: "I didn't think we would see these jets of fluid going through the brain," Iliff says. In addition, he explains that previous conception of cerebrospinal fluid's role in waste removal suggested that the process was one-way, sending particle-carrying fluid from the brain into the body. Instead, they observed a recycling, as much as 40 percent of the fluid returned to the brain.

As a test of their work, the researchers injected proteins called amyloid beta into mice's brains. In Alzheimer's, this protein—present in all healthy brains—can accumulate and clump, developing into cell-damaging plaque. The researchers compared mice with a normal glymphatic system to those with a disabled gene that prevented glial cells from assisting in the fluid flow. They found that in the normal mice, the protein rapidly cleared from the brain along these channels, but amyloid removal diminished in the gene-altered animals.

*Iliff hypothesizes that a faulty glymphatic system may bear the blame for the over-accumulation of proteins seen in Alzheimer's, amyotrophic lateral sclerosis, Huntington's and other neurodegenerative disorders—and further study may even reveal a way to dispose of these clumps.

Jaleel Miyan, a neurobiologist at the University of Manchester in England who did not participate in this research, stressed the significance of this finding by characterizing the analogy with the lymphatic system as inadequate: "What they have demonstrated is actually far more extensive and important to CSF [cerebrospinal fluid] biology." The study clarifies discrepancies in past research and may lead to a better understanding of the functioning of the glymphatic system as a possible cleanser of the neural toxins that inevitably accrete and do damage as we age.

HiV drug may slow memory loss

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

WebMD

By Brenda Goodman, MA
WebMD Health News

A drug that's already been approved by the FDA for use in HIV patients may also help slow the decline of memory and mental function experienced by people who are in the early stages of Alzheimer's disease.

The drug, Egrifta, stimulates the release of human growth hormone from the brain's pituitary gland. It was approved by the FDA in 2010 to help correct the abnormal distribution of body fat that often occurs in patients who live with HIV.

A new study published in the Archives of Neurology suggests it may also slowmemory loss in people who have mild cognitive impairment (MCI), a condition that often precedes full-blown Alzheimer's disease.

For the study, researchers assigned adults between the ages of 55 and 87 to get either nightly injections of Egrifta or a placebo for five months. Some were healthy and showed no evidence of memory problems on a battery of mental function tests. Others showed MCI, or memory loss that was worse than expected for their age but was not yet severe enough to interfere with daily living.

A total of 137 patients -- 76 who were healthy and 61 with MCI -- finished the study. Researchers brought them back to the lab four times: at the start of the study, then at weeks 10, 20, and then another 10 weeks after the nightly shots stopped.

At each visit, their blood was drawn. In addition, they took a battery of tests that measured different skills used in mental processing and short-term recall of words, shapes, and facts. Researchers also asked them about their mood and sleeping patterns.

In both healthy adults and those with MCI, those taking Egrifta fared better than their counterparts who took placebo injections.

Healthy adults saw their executive function improve by about 200% over their peers who got a placebo. Executive function refers to the brain's ability to manage attention and concentration, to switch between thoughts, and use working memory to plan and strategize tasks.

Adults with MCI still saw their executive function slip over the five months of the study, but their declines were not as large as those in the placebo group.

"Their expected decline was cut in half," says researcher Laura D. Baker, PhD, apsychiatrist at the University of Washington School of Medicine in Seattle.

By the end of the study, people on the drug were also better able to recall words and details of stories a bit better than people on the placebo, though the differences between the groups were not significant.

How Egrifta Works

Egrifta is a close copy of a chemical that's already made by the body called growth-hormone-releasing hormone. As the name implies, it stimulates the production of human growth hormone (HGH). Human growth hormone, in turn, triggers the release of a whole cascade of other hormones including insulin and its close cousin, insulin-like growth factor.

How Egrifta Works continued..

Insulin is probably best known for its role in regulating blood sugar, but it also has important work in the brain. In the brain, insulin stimulates the growth of new nerves and protects existing nerves from damage. Insulin levels in the brain fall with age, and previous studies have found that they're especially low in the brains of patients with Alzheimer's and other kinds of dementia.

The same group of researchers involved in the study has been testing whether inhaled insulin can reverse memory loss in Alzheimer's patients.

Egrifta may boost insulin in the brain less directly, and that could be a good thing, Baker says.

"What's so nice about this particular strategy is that it stimulates a whole cascade of hormone activities. Once this whole cascade is stimulated, it behaves normally, as it does when we're younger adults. So all we're kind of doing is boosting the system and letting it do what it does best," she says.

"It also shuts itself off when levels of one hormone or another get too high," Baker tells WebMD, so the levels always stay within a more normal range.

Risk, Side Effects, and Cost to Be Considered

Should a larger, longer study confirm the benefits of the medication for patients with early memory loss, it wouldn't come cheap.

Baker says that given at the dosages used in the study, the drug costs about $750 a day, or more than $22,500 for a 30-day supply.

"Of course that's not feasible," she says. "No health plan would ever pay for this."

She says drug companies are hard at work trying to find a way to make a less expensive version.

Side effects were reported by 68% of people on Egrifta -- twice the rate of adverse events experienced by those on the placebo injections. Side effects were mostly mild. They included skin reactions like itching, redness, and stinging around the injection site. It was also common for people to report increased joint pain and stomach upset.

There are already products at vitamin and health foods stores that claim to boost growth-hormone-releasing hormone, but Baker cautions that they could do so dangerously.

But, she says, there is a far less expensive and less risky way to get virtually the same degree of benefit as was seen with this pricey drug: Exercise.

"We completed a study last year testing exercise for brain function in people with mild cognitive impairment," Baker says. "We had the same improvements in executive function. We used the same tests in both studies, and we saw the same benefits."

How much exercise is needed to get the benefit? In her previous study, which was published in 2010 in the Archives of Neurology, people engaged in aerobic exercisefor 45 to 60 minutes at least four days of the week for six months.

"Up to this point, this is the most potent way to slow things down or improve cognition," she says.

Single brain trauma affects an enzyme associated with Alzheimer's disease

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Here is a great dementia resource for caregivers and healthcare professinals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Tufts Now

By 

News Staff

A study, performed in mice and utilizing post-mortem samples of brains from patients with Alzheimer’s disease, found that a single event of a moderate-to-severe traumatic brain injury (TBI) can disrupt proteins that regulate an enzyme associated with Alzheimer’s. The paper, published in the Journal of Neuroscience, identifies the complex mechanisms that result in a rapid and robust post-injury elevation of the enzyme BACE1 in the brain. These results may lead to the development of a drug treatment that targets this mechanism to slow the progression of Alzheimer’s disease.

“A moderate-to-severe TBI, or head trauma, is one of the strongest environmental risk factors for Alzheimer’s disease. A serious TBI can lead to a dysfunction in the regulation of the enzyme BACE1. Elevations of this enzyme cause elevated levels of amyloid-beta, the key component of brain plaques associated with senility and Alzheimer’s disease,” says first author Kendall Walker, postdoctoral associate in the department of neuroscience at Tufts University School of Medicine (TUSM). 

Moderate-to-severe TBIs are caused most often by traumas such as severe falls or motor vehicle accidents that result in a loss of consciousness. Not all traumas to the head result in a TBI. According to the Centers for Disease Control and Prevention, each year 1.7 million people sustain a TBI. Concussions, the mildest form of a TBI, account for about 75 percent of all TBIs. Studies have linked repeated head trauma to brain disease, and some previous studies have linked single events of brain trauma to brain disease, such as Alzheimer’s. Alzheimer’s disease currently affects as many as 5.1 million Americans and is the most common cause of dementia in adults age 65 and over.

Building on her previous work, Giuseppina Tesco, an assistant professor of neuroscience in the School of Medicine, led a research team that first used an in vivo model to determine how a single episode of TBI could alter the brain. In the acute phase (first two days) following injury, levels of two intracellular trafficking proteins (GGA1 and GGA3) were reduced, and an elevation of BACE1 enzyme level was observed.

Next, in an analysis of post-mortem brain samples from patients with Alzheimer’s disease, the researchers found that GGA1 and GGA3 levels were reduced while BACE1 levels were elevated in the brains of Alzheimer’s disease patients compared to the brains of people without Alzheimer’s disease, suggesting a possible inverse association.

In an additional experiment using a mouse strain genetically modified to express the reduced level of GGA3 that was observed in the brains of Alzheimer’s disease patients, the team found that one week following traumatic brain injury, BACE1 and amyloid-beta levels remained elevated even when GGA1 levels had returned to normal. The research suggests that reduced levels of GGA3 were solely responsible for the increase in BACE 1 levels and therefore the sustained amyloid-beta production observed in the sub-acute phase, or seven days, after injury.

“When the proteins are at normal levels, they work as a clean-up crew for the brain by regulating the removal of BACE1 enzymes and facilitating their transport to lysosomes within brain cells, an area of the cell that breaks down and removes excess cellular material. BACE1 enzyme levels may be stabilized when levels of the two proteins are low, likely caused by an interruption in the natural disposal process of the enzyme,” said Tesco, who is also member of the neuroscience program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts.

“We found that GGA1 and GGA3 act synergistically to regulate BACE1 post-injury. The identification of this interaction may provide a drug target to therapeutically regulate the BACE1 enzyme and reduce the deposition of amyloid-beta in Alzheimer’s patients,” she continued. “Our next steps are to confirm these findings in post-mortem brain samples from patients with moderate-to-severe traumatic brain injuries.”

Butter Flavoring Linked to Alzheimer’s Disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Food Poisoning Alert

A new study published in Chemical Research in Toxicology showed that the butter flavoring diacetyl (DA) increases the type of protein clumping linked to Alzheimer’s disease. The chemical is found in many processed foods, including microwave popcorn, snack foods, baked goods, and margarine. In fact, the researchers say that diacetyl is “ubiquitous” in the modern diet.

The study’s authors are troubled about chronic exposure that industry workers have to DA. That exposure may lead to long-term neurological damage. DA easily traversed the blood-brain barrier, which usually keeps substances from entering the brain itself. Scientists do not know if consuming DA in products like microwave popcorn can cause problematic levels of the chemical in the body.

Diacetyl’s structure is similar to other substances that makes beta-amyloid proteins clump in the brain. That clumping is indicative of Alzheimer’s disease. In addition, DA prevented a protective protein that helps keep nerve cells healthy from reaching the brain.

Diacetyl is a natural byproduct of fermentation and is also synthesized for use in the food industry. The United States Occupational Safety and Health Administration (OSHA) has written hazard communication guidance for the chemical. That guidance says that “a number of employees exposed to food flavorings containing diacetyl (FFCD) have developed serious respiratory illness presenting with persistent dry cough, wheezing, shortness of breath upon exertion, and fixed airways obstruction on spirometry. Several employees have been diagnosed with asthma or bronchiolitis obliterans.”

The National Institute for Occupational Safety and Health (NIOSH) has investigated the occurrence of severe lung disease in employees at microwave popcorn packaging plants and flavorings manufacturing facilities in 2003 and 2007. This latest research on the link between DA and Alzheimer’s Disease strengthens the concern about this chemical and the health of industry workers.

Alzheimer's Progression Slower After 80

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Here is a great dementia resource for caregivers and healthcare professinals,


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The Dementia Caregiver's Little Book of Hope [Kindle Edition

By Steven Reinberg
HealthDay Reporter

(HealthDay News) -- The deadly march of Alzheimer's disease is slower in people aged 80 or older than the younger elderly, researchers have found.

The risk of developing Alzheimer's disease increases with age, and by 85, the risk is about 50 percent. But those who develop the progressive brain disorder that late in life will experience a less aggressive disease than those whose symptoms appear at 60 or 70 years, according to investigators at the University of California, San Diego.

Lead researcher Dominic Holland from the university's neurosciences department said doctors will need to consider these findings when assessing older patients for Alzheimer's disease.

"Methods for early detection, which will rely on biomarkers as well as mental ability, will need to take into account the age of the individuals being assessed," he said. Because the "old" elderly may deteriorate at a slower pace than younger patients, doctors may not realize these people are suffering from Alzheimer's disease.

The findings also have implications for clinical trials evaluating potential Alzheimer's treatments and cost-of-care projections for different Alzheimer's patients, Holland and other experts say.

Currently, no effective treatments exist to slow or cure Alzheimer's disease, which gradually destroys brain cells and robs people of memory, and their ability to communicate and carry out everyday tasks.

The report was published Aug. 2 in the online journal PLoS One.

To study Alzheimer's disease progression, Holland and colleagues used data from the Alzheimer's Disease Neuroimaging Initiative study. They looked at more than 700 people aged 65 to 90, some with normal mental functioning, some with mild signs of dementia and others suffering from Alzheimer's.

Participants were tested every 6 or 12 months.

The researchers found that younger Alzheimer's patients lost their mental abilities faster than older patients.

These declines among younger patients paralleled the accelerated rate of brain tissue loss and the increase in a spinal-fluid indicator of Alzheimer's seen among the younger age group, compared with older patients, the study authors added.

The researchers aren't sure why Alzheimer's is more aggressive in younger patients. One explanation might be that the older patients have been declining at that slower rate over a longer time, with some unknown factor keeping symptoms at bay, they suggest.

Another possibility is that the older patients have dementia plus Alzheimer's, which might stall the full effect of Alzheimer's on the brain. But such a diagnosis must be made with an autopsy, which is the only way Alzheimer's is accurately diagnosed, Holland noted.

Alzheimer's disease currently affects an estimated 5.6 million Americans, and that number is expected to triple by 2050 as the baby boom generation ages.

The finding that the earlier one develops the disease, the more aggressive it is isn't good news for those younger elderly patients who will suffer the worsening loss of their mental abilities for a long time, Holland said.

Another expert said the findings may affect both health cost projections and clinical trials.

"This is an extremely important paper with implications for both the projections of cost of care for Alzheimer's disease and for planning clinical trials," said Dr. Sam Gandy, associate director of the Mount Sinai Alzheimer's Disease Research Center at the Mount Sinai School of Medicine in New York City.

If the clinical picture in the over-85 population is milder than what is typical in younger populations, those older patients would remain independent longer, and the projections for the economic burden to the health care system should be adjusted, he said.

"The annual cost now is $200 billion in the U.S.; the projection is $1 trillion annually by 2050," Gandy said.

"Maybe that $1 trillion is really only $500 to $750 billion. Still catastrophic, but it is worth considering this in projection," he added.

Equally important, if the rate of decline is slower in 85-year-olds than in 65-year-olds, that must be taken into account when recruiting for clinical trials, Gandy said.

For example, if all the patients receiving a drug were over 85 and all the patients receiving an inactive placebo were much younger, it might appear the drug was working when, in fact, the populations were improperly matched, Gandy pointed out.

"We have known that we wanted populations to be as identical as possible, but we didn't really know of this specific phenomenon before," he said.

More information

For more information on Alzheimer's disease, visit theAlzheimer's Association.