News on Alzheimer's Disease
Exercise May Stave off Mental Decline
(Source: HealthDay News)
Two new studies show that exercise appears to help prevent and improve mild cognitive impairment. Researchers found that people who did moderate physical activity in mid-life or later had a reduced risk of mild cognitive impairment and that six months of high-intensity aerobic exercise improved cognitive function in people with mild cognitive impairment. The Mayo Clinic team said exercise may guard against mild cognitive impairment through production of nerve-protecting compounds, increased blood flow to the brain, improved development and survival of neurons, and decreased risk of heart and blood vessel diseases.
For Older Adults, Participating in Social Service Activities Can Improve Brain Functions
(Source: John Hopkins School of Public Health)
Volunteer services, such as tutoring children, can help older adults delay or reverse declining brain function, according to researchers at the Johns Hopkins Bloomberg School of Public Health. Using functional magnetic resonance imaging (fMRI), the researchers found that seniors participating in a youth mentoring program made gains in key brain regions that support cognitive abilities important to planning and organizing one's daily life. The study is the first of its kind to demonstrate that valuable social service programs, such as Experience Corps - a program designed to both benefit children and older adults' health - can have the added benefits of improving the cognitive abilities of older adults, enhancing their quality of life. "We found that participating in Experience Corps resulted in improvements in cognitive functioning and this was associated with significant changes in brain activation patterns," said lead investigator Michelle Carlson, Ph.D. "Essentially the intervention improved brain and cognitive function in these older adults."
Higher Level of Protein Hormone Associated with Lower Risk of Dementia, Alzheimer's
(Source: American Medical Association)
Persons with higher levels of leptin, a protein hormone produced by fat cells and involved in the regulation of appetite, may have an associated reduced incidence of Alzheimer's disease and dementia, according to a newly published study. The researchers found that higher leptin levels were associated with a lower incidence of all-cause dementia and AD. The incidence of dementia decreased gradually across increasing levels of leptin: a person with a baseline leptin level in the lowest quartile group had a 25 percent risk of developing AD after 12 years of follow-up, whereas the corresponding risk for a person in the top quartile group was only 6 percent. "These findings are consistent with recent experimental data indicating that leptin improves memory function in animals through direct effects on the hippocampus and strengthens the evidence that leptin is a hormone with a broad set of actions in the central nervous system," the authors wrote.
Imaging Test Detects Process Likely to Progress into Alzheimer's
Source: American Medical Association)
Early Alzheimer's disease, detected by a compound that binds to brain plaques, appears likely to progress into symptomatic Alzheimer's disease with dementia, according to a report. "The concept of preclinical Alzheimer's disease holds that the Alzheimer's pathologic process operates for many years before producing a clinically detectable impairment," the authors wrote. "A key corollary of this concept is that preclinical Alzheimer's is not benign and will eventually produce sufficient synaptic and neuronal damage to cause cognitive decline and other symptoms of Alzheimer's disease." "Many more individuals, studied for longer intervals and ideally through autopsy, will be needed to confirm or refute our observations," the authors wrote. "Nonetheless, this study provides support for the premise that preclinical Alzheimer's, detected either by the cerebrospinal fluid signature for Alzheimer's or here by elevated Pittsburgh Compound retention, predicts symptomatic Alzheimer's disease."
New Technique Detects Proteins That Make Us Age
(Source: University of Bath)
Scientists at the University of Bath have developed a technique that could be used to diagnose and develop treatments for age-related conditions like Alzheimer's disease, diabetes and cancer. In these diseases, proteins in the body react with sugars in a process called glycation. This modifies the protein's function and can trigger complications such as inflammation and premature aging. The team developed a technique that can detect glycated proteins and could in the future be used for diagnosing a whole range of diseases in patients.
One Form of Vitamin E May Protect Brain after Stroke
(Source: Ohio State University)
Blocking the function of an enzyme in the brain with a specific kind of vitamin E can prevent nerve cells from dying after a stroke, new research suggests. In a study using mouse brain cells, scientists found that the tocotrienol form of vitamin E, an alternative to the popular drugstore supplement, stopped the enzyme from releasing fatty acids that eventually kill neurons. “Our research suggests that the different forms of natural vitamin E have distinct functions. The relatively poorly studied tocotrienol form of natural vitamin E targets specific pathways to protect against neural cell death and rescues the brain after stroke injury," said Chandan Sen, Ph.D.
Reduced anti-psychotic use in older adults with dementia
(Source: American Medical Association)
The use of atypical antipsychotics to treat elderly patients with dementia appears to have decreased following a 2005 Food and Drug Administration (FDA) advisory regarding the risks of these medications in this population, according to a report in the Archives of Internal Medicine. An overall decline in the use of atypical medications began within one month of the FDA advisory. Medications mentioned included clozapine, risperidone, olanzapine, and paliperidone. And although they are less likely to cause neurological adverse effects associated with conventional or "typical" antipsychotics, some reports have linked atypical antipsychotics to strokes, diabetes and other severe adverse events. "The residual use in the population at risk and the decrease in the use of atypical antipsychotics in the general population, who were not targeted by the warning, raise the question as to whether the effect and specificity of FDA regulatory actions could be enhanced," the authors concluded. "Targeting specific segments of patients and physicians (e.g., high prescribers) and further customizing and evaluating the impact of regulatory actions may improve their impact at minimizing the risks associated with select prescription medications."
Researchers Suggest Brain Cell Rescue for Alzheimer's
(Source: Alzheimer's Research Trust)
Cambridge scientists report that nerve cells damaged by Alzheimer's disease might be able to be rescued, if caught in time. Alzheimer's disease causes nerve cells in the brain to die, resulting in problems with memory, speech and understanding. Little is known about how the nerve cells die, but new research has revealed how they first lose the ability to communicate with each other, before deteriorating further. Dr. Michael Coleman explained, "This is very important for treatment because in normal adult life nerve cell connections constantly disappear and reform, but can only do so if the supporting parts of the cell remain. Our results suggest a window in which damaged connections between brain cells could recover under the right conditions." Rebecca Wood, Chief Executive of the Alzheimer's Research Trust, said: "This is an exciting development which could lead to new treatments, and demonstrates the excellence of British dementia research. If it's possible to rescue severely damaged brain cell connections, we could perhaps slow or halt the progression of Alzheimer's. Further research is urgently needed if we are to offer hope to the 700,000 people in the UK who live with dementia."
Brain-shielding Chemical Found in Sea Algae
(Source: ANSA)
Italian scientists report that a chemical found in seaweed may shield the brain against the devastating effects of Alzheimer's. Dr. Giovanni Scapagnini, Molise University (Italy), reported that a number of seaweed varieties contain large amounts of a chemical called homotaurine, which may protect the brain against the corrosion observed in people with Alzheimer's. Scapagnini and colleagues gave homotaurine to about 2,000 patients. After 18 months, they found the chemical had ''greatly reduced'' the presence of brain toxins thought to be a factor in the onset of this degenerative disease. ''It also helps to preserve the hippocampus, an area of the brain associated with long-term memory and one of the first to show signs of damage," he added.
Brain Plaques Linked to Increased Alzheimer's Risk
(Source: Washington University in St. Louis)
Researchers at Washington University have shown that brain plaques in apparently healthy individuals are associated with increased risk of diagnosis with Alzheimer's disease years later. "We don't have enough data yet to definitively say that people who scan positive for these brain plaques have pre-symptomatic Alzheimer's disease, but something is clearly going on that does not bode well for the health of their aging brains," said Dr. John Morris.
Diabetes May Triple Risk of Dementia in Older People
(Source: Diabetes UK)
A UK study claims that some older people with mild memory-loss are three times more likely to develop dementia if they also have diabetes. Research by scientists at King's College London, investigated the connection between mild cognitive impairment (MCI) in older people and dementia. The scientists followed 61 people aged 65 or over who had MCI over a period of four years. Sixteen of the participants had diabetes. After four years, 19 developed dementia, two reverted to normal cognitive levels, and 40 remained stable. Of those who progressed to dementia, seven had diabetes. "We have already seen a number of previous studies linking Type 2 diabetes to cognitive impairment and dementia and we already know that Type 2 diabetes is considered to be a risk factor for Alzheimer's disease," said Dr. Iain Frame, Director of Research at Diabetes UK. "This study is interesting because it considers the association between Type 2 diabetes and the progression from mild cognitive impairment to dementia. Although the number of participants in the study is quite small, the researchers have suggested that such a link exists."
Diet High in Methionine Could Increase Alzheimer's Risk
(Source: Temple University) 12-17
A diet rich in methionine, an amino acid typically found in red meats, fish, beans, eggs, garlic, lentils, onions, yogurt and seeds, could increase the risk of developing Alzheimer's disease, according to researchers at Temple University. "When methionine reaches too high a level, our body tries to protect itself by transforming it into a particular amino acid called homocysteine," said Dr. Domenico Praticograve;. "The data from previous studies show - even in humans - when the level of homocysteine in the blood is high, there is a higher risk of developing dementia." "We found that the mice with the normal diet had normal homocysteine levels, but the mice with the high methionine diet had significantly increased levels of homocysteine, very similar to human subjects with hyperhomocysteinemia," said Praticograve;. "The group with the high methionine diet also had up to 40 percent more amyloid plaque in their brains, which is a measurement of how much Alzheimer's disease has developed.
Long Life with Tight Plaques
(Source: Alzheimer Research Forum)
It is not just material goods that are best when they come in small packages, but amyloid-B (AB) as well. Researchers at The Salk Institute report that mice overproducing AB survive longer without disease symptoms when they tightly bundle the rogue peptide into dense plaques.
The work supports the idea that small, oligomeric forms of the peptide are the most toxic, and that keeping them under wraps is good for the brain. In this case, the ability to bundle and detox AB arises from knocking out one copy of the insulin-like growth factor 1 (IGF-1) receptor, a component of the insulin/IGF-1 signaling pathway. The work suggests that reducing insulin/IGF-1 signaling, for example, by eating drastically fewer calories, could be one way for humans to stave off AD.
Scaffold Regulating Protein Disposal Identified
(Source: Helmholtz Association of German Research Centers)
How does a cell manage to identify and degrade defective proteins and protect the body against serious diseases? Researchers in Germany have found a crucial piece in this puzzle. In an enzyme complex that plays a critical role in the quality control of proteins, they discovered a scaffold regulating the identification and disposal of various defectively produced proteins. Many cell proteins are produced, folded and routed in a cell organelle (a specialized subunit within a cell) called the endoplasmic reticulum. However, errors can occur: during the process proteins can be misfolded. Older proteins may also accumulate defects due to environmental stress. Proteins can lose their structure and fail to carry out their function. Diseases can develop, such as Alzheimer's orParkinson's. Defective proteins must therefore be detected in the cell and disposed of. The study sheds light on this puzzle. Researchers discovered the central and flexible scaffold of the enzyme complex, the subunit Usa1. Depending on what is required, it tethers specific modules of the complex, connecting them with each other.
Scientists Decode Memory-Forming Brain Cell Conversations
(Source: Medical College of Georgia) 12-18
The cell-to-cell communications between neurons, as memories are formed and recalled, have been decoded by Medical College of Georgia (MCG) scientists. Being able to recognize, in real time, the formation and recollection of a memory opens the door to objective, thorough memory studies and eventually better therapies, said Dr. Joe Tsien, neuroscientist and co-director of MCG's Brain and Behavior Discovery Institute. "It's a beginning, a first glimpse of a memory," said Dr. Tsien. "For the first time it gives us the ability to look at the brain dynamic and tell what kind of memory is formed, what are the components of the memory and how the memory is retrieved at the network level." The finding could help pinpoint the stages when memory formation is flawed and whether drugs are improving it.