In terms of health care expenses and lost wages of both patients and their caregivers, the cost of Alzheimer's disease nationwide is estimated at over $100 billion per year.
Stimulating The Brain's Immune Response May Provide Treatment For Alzheimer's Disease
January 27, 2011
Adapted from the University of South Florida
A new target for the prevention of adverse immune responses identified as factors in the development of Alzheimer's disease (AD) has been discovered by researchers at the University of South Florida's Department of Psychiatry and the Center of Excellence for Aging and Brain Repair.
Their findings are published online in the Journal of Neuroscience.
The CD45 molecule is a receptor on the surface of the brain's microglia cells, cells that support the brain's neurons and also participate in brain immune responses.
Previous studies by the USF researchers showed that triggering CD45 was beneficial because it blocked a very early step in the development of Alzheimer's disease. In the present study, the researchers demonstrated in Alzheimer's mouse models that a loss of CD45 led to dramatically increased microglial inflammation.
Although the brain's immune response is involved in Alzheimer's disease pathology, "this finding suggests that CD45 on brain immune cells appears critically involved in dampening harmful inflammation," said study senior author Jun Tan, M.D., Ph.D., a professor of psychiatry and Robert A. Silver chair at the Rashid Laboratory for Developmental Neurobiology, USF Silver Child Development Center and research biologist for Research and Development Service at the James A. Haley Veteran's Hospital.
The investigators also found an increase in harmful neurotoxins, such as A beta peptides, as well as neuron loss in the brains of the test mice.
"In short, CD45 deficiency leads to increased accumulation of neurotoxic A beta in the brains of old Alzheimer's mice, demonstrating the involvement of CD45 in clearing those toxins and protecting neurons," Dr. Tan said. "These findings are quite significant, because many in the field have long considered CD45 to be an indicator of harmful inflammation. So, researchers assumed that CD45 was part of the problem, not a potential protective factor."
The next step is to apply these findings to develop new Alzheimer's disease treatments, said Paula Bickford, Ph.D., a professor in the USF Department of Neurosurgery and senior career research scientist at the James A. Haley Veteran's Hospital.
"We are already working with Natura Therapeutics, Inc. to screen for natural compounds that will target CD45 activation in the brain's immune cells," Dr. Bickford said.
We have some very interesting Alzheimer's disease research news to share with you:
Non-Invasive Brain Scan And Blood Test Are Future Candidates To Assess Risk And Monitor Progression Of Alzheimer's Disease American Health Assistance Foundation
It is complicated to predict the risk for healthy individuals to develop dementia. If an individual does experience a problem with memory and brain function, it is difficult to determine whether it is Alzheimer's disease. Two studies published in the January 19, 2011 issue of the Journal of the American Medical Association describe methods developed to detect a hallmark of Alzheimer's disease—beta-amyloid protein—in the brain and blood. Both tests are not commercially available, but are important breakthroughs in the push for early detection and monitoring of this debilitating disease. [
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PROGRAMS RANGING from meals-on-wheels to caregivers services will continue to be provided by the Ocean County Department of Senior Services in 2011.
"Our seniors deserve these comprehensive and diverse services to ensure that they can enjoy the best possible quality of life," said Freeholder Director Joseph H. Vicari.
Services including outreach to the homebound elderly, volunteer friendly visitors, telephone reassurances, health screening and education are all included in the contracts scheduled to be approved by the Board during its January 19 meeting.
The 36 competitive contracts total more than $2.3 million. The Meals-on-Wheels and Congregate meal programs are expected to deliver more than 317,600 meals to senior citizens in the New Year, Vicari said.
The nutrition program awards to Community Services, Inc. were approved earlier and the Kosher Home Delivered Meals are among the contracts up for approval on January 19.
"These meals are often a lifeline for the frail and disabled, bringing not only nutritional value but also social contact," Vicari said. "About 60% of home delivered meals clients are at high nutritional risk."
Other contracts include transportation, legal services, caregiver services, care management, benefits screening, chore services and a host of others.
"More than a quarter of Ocean County's population is over the age of 60, including more than 75,000 people aged 75 and older," Vicari said. "Providing beneficial programs and services for the older adult population continues to be a priority for the Ocean County Board of Chosen Freeholders."
The Office of Senior Services serves as a clearinghouse, teaming up seniors with programs that can help make a difference in their daily lives, Vicari said.
The office will oversee a total of 52 contracts with 22 governmental and non-profit agencies in 2011 totaling over $5.3 million.
This year, 536,411 units of service will be provided to 35,379 persons.
Access to information and assistance is a major focus for the Office of Senior Services, said D. Jane Maloney, director of the Ocean County Office of Senior Services.
"Our seniors need to know they can come to us and we can match them up with the appropriate services," Maloney said. "Over 12,000 individuals called or visited us in 2010 and our Outreach sites plan to provide this assistance to over 18,000 individuals in 2011."
For further information regarding services call Office of Senior Services at 732-929-2091 or 1-800-668-4899.
American Health Assistance Foundation Unveils New WebsiteTo Teach Kids About Macular Degeneration
December 7, 2010
The American Health Assistance Foundation (AHAF) today announced a new educational website, Children’s Corner™ for Macular Degeneration, to teach children about the degenerative disease through stories, interactive games, and sharing activities.
The Children’s Corner for Macular Degeneration is the first in a series of children’s websites that AHAF is developing for age-related diseases, including Alzheimer’s disease and glaucoma.
“As the holiday season begins, we are pleased to launch this educational website that offers a unique and innovative approach to helping family members better understand this difficult disease,” said Stacy Haller, AHAF president and CEO. “Age-related macular degeneration affects 11 million Americans, and the Children’s Corner provides a much-needed resource to bring about increased sensitivity.”
This inaugural site will teach general understanding about the disease and provide kids with ways to help their friend or family member. The Children’s Corner, (www.childrenscorner.org) includes age-appropriate content that enables learning through stories, games, and collaborative features such as an e-scrapbook and message board. Educational resources are also provided for students, teachers, and health-care professionals.
Age-related macular degeneration is a leading cause of vision loss in Americans 60 years of age and older. The projected cost of age-related macular degeneration in the United States will be $845 million in 2020.
Funding for the website was made possible in part through a healthcare charitable contribution from the Pfizer Foundation.
About the American Health Assistance Foundation
The American Health Assistance Foundation (www.ahaf.org) is a non-profit organization dedicated to finding cures for age-related and degenerative diseases by funding research worldwide on Alzheimer’s disease, macular degeneration, and glaucoma and also provides the public with free information about these diseases, including risk factors, preventative lifestyles, current treatments, and coping strategies.
Disclaimer:The information provided in this section is a public service of the American Health Assistance Foundation, and should not in any way substitute for the advice of a qualified healthcare professional and is not intended to constitute medical advice. Although we take efforts to keep the medical information on our website updated, we cannot guarantee that the information on our website reflects the most up-to-date research. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. The American Health Assistance Foundation does not endorse any medical product or therapy.
Some of the content in this section is adapted from other sources, which are clearly identified within each individual item of information.
7.3 million people in the U.S. have intermediate age-related macular degeneration and are at substantial risk for vision loss.
Omega-3s In Fish, Seafood May Protect Seniors' Eyes
December 6, 2010
Adapted from the American Academy of Ophthalmology
Seniors interested in lifestyle choices that help protect vision will be encouraged by a Johns Hopkins School of Medicine study, and people concerned about glaucoma can take heart from work on early detection by the University of Miami Miller School of Medicine. Both studies are published in the December issue of Ophthalmology, the journal of the American Academy of Ophthalmology.
Researchers at Wilmer Eye Institute, Johns Hopkins School of Medicine, wanted to know how the risk of age-related macular degeneration (AMD) would be affected in a population of older people who regularly ate fish and seafood, since some varieties are good sources of omega-3 fatty acids. A diet rich in omega-3s probably protects against advanced AMD, the leading cause of blindness in whites in the United States, according to the Age-Related Eye Disease Study (AREDS) and other recent studies. High concentrations of omega-3s have been found in the eye's retina, and evidence is mounting that the nutrient may be essential to eye health. The new research, led by Sheila K. West, Ph.D., was part of the Salisbury Eye Evaluation (SEE) study.
Food intake information with details on fish and shellfish consumed was collected over one year using a validated questionnaire for 2,391 participants aged 65 to 84 years who lived along Maryland's Eastern Shore. After dietary assessment was complete, participants were evaluated for AMD. Those with no AMD were classified as controls (1,942 persons), 227 had early AMD, 153 had intermediate-stage disease, and 68 had advanced AMD. In the advanced AMD group, the macular area of the retina exhibited either neovascularization (abnormal blood vessel growth and bleeding) or a condition called geographic atrophy. Both conditions can result in blindness or severe vision loss.
"Our study corroborates earlier findings that eating omega-3-rich fish and shellfish may protect against advanced AMD." Dr. West said. "While participants in all groups, including controls, averaged at least one serving of fish or shellfish per week, those who had advanced AMD were significantly less likely to consume high omega-3 fish and seafood," she said.
The study also looked at whether dietary zinc from crab and oyster consumption impacted advanced AMD risk, but no significant relationship was found. Zinc is also considered protective against AMD and is included in an AMD-vitamin/nutrient supplement developed from the AREDS study. Dr. West speculated that her study found no effect because the levels of zinc obtained from seafood/fish were low compared to supplement levels.
A side note: fish and shellfish were part of the normal diet of the study population, rather than added with the intention of improving health. The links between fish consumption, omega-3s and healthy lifestyles were not widely known in the early 1990s when the dietary survey was conducted. In fact, some of the study participants who consumed the most seafood were also smokers and/or overweight, two factors usually associated with AMD and other health risks.
Disclaimer:The information provided in this section is a public service of the American Health Assistance Foundation, and should not in any way substitute for the advice of a qualified healthcare professional and is not intended to constitute medical advice. Although we take efforts to keep the medical information on our website updated, we cannot guarantee that the information on our website reflects the most up-to-date research. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. The American Health Assistance Foundation does not endorse any medical product or therapy.
Some of the content in this section is adapted from other sources, which are clearly identified within each individual item of information.
Nearly half of all people age 85 years or older have some form of dementia.
Tau Disrupts Neural Communication Prior To Neurodegeneration
December 22, 2010
On behalf of our donors, Alzheimer's Disease Research (ADR), a program of the American Health Assistance Foundation (AHAF), recognizes Dr. Liao, an AHAF grantee, for his work on this important study.
Dr. Dezhi Liao and co]authors discovered that part of the memory loss from Alzheimerfs disease is not due to cell death, but caused by a buildup of tau protein in the parts of the nerve cell, called the gdendritic spines,h that are used to store memories. Specifically, tau is forced to go where it shouldnft by a change called phosphorylation. In a laboratory study, when the researchers used genetically-modified tau proteins that couldnft be phosphorylated, they also blocked the damaging tau protein buildup in rat nerve cells. In the future, a new drug could be developed to prevent this phosphorylation and stop tau from entering the dendritic spines, potentially halting the loss of memories in early stages of Alzheimerfs disease.
Adapted from Cell Press
A new study is unraveling the earliest events associated with neurodegenerative diseases characterized by abnormal accumulation of tau protein. The research, published by Cell Press in the December 22 issue of the journal Neuron, reveals how tau disrupts neuronal communication at synapses and may help to guide development of therapeutic strategies that precede irreversible neuronal degeneration.
Tau normally contributes to the supportive framework of proteins in the cell. It is well established that abnormal tau sometimes clumps into neuron-damaging filamentous deposits and that aggregates of tau with multiple phosphate groups attached are a defining feature of neurodegenerative disorders called gtauopathiesh, which include Alzheimerfs disease and other dementias.
gResearch has shown that healthy neurons have more tau in the axon and less in the cell body and dendrites, and that this gradient is reversed in neurodegenerative disorders like Alzheimerfs,h explains study author, Dr. Karen H. Ashe from the University of Minnesota. gAlthough studies have shown that accumulation of tau in dendrites induced neurodegeneration, they do not address how tau diminished brain function at preclinical disease stages preceding neurodegeneration.h
Dr. Ashe, co-author Dr. Dezhi Liao, and their colleagues investigated how tau induces early memory deficits and disrupts neuronal communication, prior to obvious neuron damage. The researchers found that early accumulation of hyperphosphorylated tau in dendrites and dendritic spines disrupted communication coming in from other neurons. Dendritic spines are sites where there is a synapse between two neurons. The phosphorylation state of tau played a critical role in mediating tau mislocalization and subsequent impairment of synaptic communication.
gThese findings capture what is likely the earliest synaptic dysfunction that precedes synapse loss in tauopathies and provide an important mechanistic link between tau phosphorylation and the mislocalization of tau to dendritic spines,h concludes Dr. Liao. gUnderstanding the key interactions that occur prior to neuronal loss will become increasingly important as preventative strategies shift the timing of interventions to pre-degenerative phases of disease,h adds Dr. Ashe. gThe aberrant mislocalization of tau proteins in dendritic spines might be a novel target in these strategies.h
Congress has passed legislation that prevents a 25 percent reduction in payments to Medicare physicians from taking effect on January 1. The bill, known as the Medicare and Medicaid Extenders Act of 2010, also prevents further cuts to physician payments effectuated under the Sustainable Growth Rate formula enacted by Congress in 1997, and maintains current Medicare physician payment rates through December 31, 2011. The Medicare and Medicaid Extenders Act also extends a number of other programs that were set to expire on December 31, including the Qualified Individual (QI) Program and the Medicare therapy caps exception process.The legislation extends QI, a Medicare Savings Program (MSP) that helps pay Part B premiums for individuals with incomes between 120 and 135 percent othe federal poverty level, until December 31, 2011. The legislation also extends for an additional year the Medicare therapy caps exception process, which allows consumers to apply for exceptions to the $1,860 coverage limit for combined speech and physical therapy services and the $1,860 coverage limit for occupational therapy services if such services are medically necessary.
Alzheimer’s disease is the most common form of dementia.
Preliminary Results Show That Walking May Slow The Progression Of Alzheimer's Disease
December 3, 2010
Adapted from the Radiological Society of North America
Walking may slow cognitive decline in adults with mild cognitive impairment (MCI) and Alzheimer's disease, as well as in healthy adults, according to a study presented today at the annual meeting of the Radiological Society of North America (RSNA).
"We found that walking five miles per week protects the brain structure over 10 years in people with Alzheimer's and MCI, especially in areas of the brain's key memory and learning centers," said Cyrus Raji, Ph.D., from the Department of Radiology at the University of Pittsburgh in Pennsylvania. "We also found that these people had a slower decline in memory loss over five years."
Alzheimer's disease is an irreversible, progressive brain disease that slowly destroys memory and cognitive skills. According to the National Institute on Aging, between 2.4 million and 5.1 million Americans have Alzheimer's disease. Based on current population trends, that number is expected to increase significantly over the next decade.
In cases of MCI, a person has cognitive or memory problems exceeding typical age-related memory loss, but not yet as severe as those found in Alzheimer's disease. About half of the people with MCI progress to Alzheimer's disease. "Because a cure for Alzheimer's is not yet a reality, we hope to find ways of alleviating disease progression or symptoms in people who are already cognitively impaired," Dr. Raji said.
For the ongoing 20-year study, Dr. Raji and colleagues analyzed the relationship between physical activity and brain structure in 426 people, including 299 healthy adults (mean age 78), and 127 cognitively impaired adults (mean age 81), including 83 adults with MCI and 44 adults with Alzheimer's dementia.
Patients were recruited from the Cardiovascular Health Study. The researchers monitored how far each of the patients walked in a week. After 10 years, all patients underwent 3-D MRI exams to identify changes in brain volume. "Volume is a vital sign for the brain," Dr. Raji said. "When it decreases, that means brain cells are dying. But when it remains higher, brain health is being maintained."
In addition, patients were given the mini-mental state exam (MMSE) to track cognitive decline over five years. Physical activity levels were correlated with MRI and MMSE results. The analysis adjusted for age, gender, body fat composition, head size, education and other factors.
The findings showed across the board that greater amounts of physical activity were associated with greater brain volume. Cognitively impaired people needed to walk at least 58 city blocks, or approximately five miles, per week to maintain brain volume and slow cognitive decline. The healthy adults needed to walk at least 72 city blocks, or six miles, per week to maintain brain volume and significantly reduce their risk for cognitive decline.
Over five years, MMSE scores decreased by an average of five points in cognitively impaired patients who did not engage in a sufficient level of physical activity, compared with a decrease of only one point in patients who met the physical activity requirement.
"Alzheimer's is a devastating illness, and unfortunately, walking is not a cure," Dr. Raji said. "But walking can improve your brain's resistance to the disease and reduce memory loss over time
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