Mrs Jeanette Maitland claims her husband, Ken, 72, who died of a dementia related illness last week, was robbed of his dignity by the constant stream of new people arriving at their home.

Patients with dementia can find new faces and voices distressing.

Mrs Maitland said she was told her husband’s care would be provided by a core group of at most 10 people. She began writing down the names of Mr Maitland’s carers and the list rapidly ran into dozens, eventually reaching treble figures.

Mrs Maitland, of Aberdeen, said: “Each time a new face came, so I kept writing, writing, writing, until we’re here where we are today with 106 carers.

“Anyone who knows anything about dementia will know that suffers can live in fear a large part of the time.

“Obviously, the more regular the voice, the more regular the regime, the constancy of it all helps them to relax and be calm.

Jeanette Maitland

“Where is respect for his dignity?”

Professor June Andrews of Stirling University’s Dementia Centre, described Aberdeen City Council’s approach as “bad care,” adding: “It is absolutely unacceptable because of the kind of disruption that is caused to people with dementia if they are faced with too many people.

“This not only happens at home in people’s houses, but also in hospitals.”

The council promised to investigate the case.

Article source: http://www.dailyexpress.co.uk/posts/view/321075/Dementia-sufferer-had-106-carers-in-a-year/

Common variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimer’s disease, but the gene’s role in the disease has been unclear. Now, researchers funded by the National Institutes of Health have found that in mice, having the most risky variant of ApoE damages the blood vessels that feed the brain.

The researchers found that the high-risk variant, ApoE4, triggers an inflammatory reaction that weakens the blood-brain barrier, a network of cells and other components that lines brain’s brain vessels. Normally, this barrier allows nutrients into the brain and keeps harmful substances out.

The study appears today in Nature, and was led by Berislav Zlokovic, M.D., Ph.D., director of the Center for Neurodegeneration and Regeneration at the Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles.

“Understanding the role of ApoE4 in Alzheimer’s disease may be one of the most important avenues to a new therapy,” Dr. Zlokovic said. “Our study shows that ApoE4 triggers a cascade of events that damages the brain’s vascular system,” he said, referring to the system of blood vessels that supply the brain.

The ApoE gene encodes a protein that helps regulate the levels and distribution of cholesterol and other lipids in the body. The gene exists in three varieties. ApoE2 is thought to play a protective role against both Alzheimer’s and heart disease, ApoE3 is believed to be neutral, and ApoE4 confers a higher risk for both conditions. Outside the brain, the ApoE4 protein appears to be less effective than other versions at clearing away cholesterol; however,inside the brain, exactly how ApoE4 contributes to Alzheimer’s disease has been a mystery.

Dr. Zlokovic and his team studied several lines of genetically engineered mice, including one that lacks the ApoE gene and three other lines that produce only human ApoE2, ApoE3 or ApoE4. Mice normally have only a single version of ApoE. The researchers found that mice whose bodies made only ApoE4, or made no ApoE at all, had a leaky blood-brain barrier. With the barrier compromised, harmful proteins in the blood made their way into the mice’s brains, and after several weeks, the researchers were able to detect loss of small blood vessels, changes in brain function, and a loss of connections between brain cells.

“The study demonstrates that damage to the brain’s vascular system may play a key role in Alzheimer’s disease, and highlights growing recognition of potential links between stroke and Alzheimer’s-type dementia,” said Roderick Corriveau, Ph.D., a program director at NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research. “It also suggests that we might be able to decrease the risk of Alzheimer’s disease among ApoE4 carriers by improving their vascular health.”

The researchers also found that ApoE2 and ApoE3 help control the levels of an inflammatory molecule called cyclophilin A (CypA), but ApoE4 does not.  Levels of CypA were raised about five-fold in blood vessels of mice that produce only ApoE4. The excess CypA then activated an enzyme, called MMP-9, which destroys protein components of the blood-brain barrier. Treatment with the immunosuppressant drug cyclosporine A, which inhibits CypA, preserved the integrity of the blood-brain barrier and lessened damage to the brain. An inhibitor of the MMP-9 enzyme had similar beneficial effects. In prior studies, inhibitors of this enzyme have been shown to reduce brain damage after stroke in animal models.

“These findings point to cyclophilin A as a potential new drug target for Alzheimer’s disease,” said Suzana Petanceska, Ph.D., a program director at NIH’s National Institute on Aging (NIA), which also funded Dr. Zlokovic’s study. “Many population studies have shown an association between vascular risk factors in mid-life, such as high blood pressure and diabetes, and the risk for Alzheimer’s in late-life. We need more research aimed at deepening our understanding of the mechanisms involved and to test whether treatments that reduce vascular risk factors may be helpful against Alzheimer’s.”

Alzheimer’s disease is the most common cause of dementia in older adults, and affects more than 5 million Americans. A hallmark of the disease is a toxic protein fragment called beta-amyloid that accumulates in clumps, or plaques, within the brain. Gene variations that cause higher levels of beta-amyloid are associated with a rare type of Alzheimer’s that appears early in life, between age 30 and 60.

However, it is the ApoE4 gene variant that is most strongly tied to the more common, late-onset type of Alzheimer’s disease. Inheriting a single copy of ApoE4 from a parent increases the risk of Alzheimer’s disease by about three-fold. Inheriting two copies, one from each parent, increases the risk by about 12-fold.

Dr. Zlokovic’s study and others point to a complex interplay between beta-amyloid and ApoE4. On the one hand, beta-amyloid is known to build up in and damage blood vessels and cause bleeding into the brain. On the other hand, Dr. Zlokovic’s data suggest that ApoE4 can damage the vascular system independently of beta-amyloid. He theorizes that this damage makes it harder to clear beta-amyloid from the brain. Some therapies under investigation for Alzheimer’s focus on destroying amyloid plaques, but therapies designed to compensate for ApoE4 might help prevent the plaques from forming, he said.

This research was funded by grant NS034467 from NINDS, and grants AG023084, AG039452 and AG013956 from NIA.

NINDS (http://www.ninds.nih.gov) is the nation’s leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease — a burden borne by every age group, by every segment of society, by people all over the world.

NIA (http://www.nia.nih.gov) leads the federal government effort conducting and supporting research on aging and the health and well-being of older people. NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer’s Disease Education and Referral (ADEAR) Center at http://www.nia.nih.gov/Alzheimers.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers
and is a component of the U.S. Department of Health and Human Services. NIH
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Article source: http://www.nih.gov/news/health/may2012/ninds-16.htm

Main Category: Alzheimer’s / Dementia
Also Included In: Genetics;  Stroke
Article Date: 18 May 2012 – 0:00 PDT

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Common variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimer’s disease, but the gene’s role in the disease has been unclear. Now, researchers funded by the National Institutes of Health have found that in mice, having the most risky variant of ApoE damages the blood vessels that feed the brain.

The researchers found that the high-risk variant, ApoE4, triggers an inflammatory reaction that weakens the blood-brain barrier, a network of cells and other components that lines brain’s brain vessels. Normally, this barrier allows nutrients into the brain and keeps harmful substances out.

The study appears in Nature, and was led by Berislav Zlokovic, M.D., Ph.D., director of the Center for Neurodegeneration and Regeneration at the Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles.

“Understanding the role of ApoE4 in Alzheimer’s disease may be one of the most important avenues to a new therapy,” Dr. Zlokovic said. “Our study shows that ApoE4 triggers a cascade of events that damages the brain’s vascular system,” he said, referring to the system of blood vessels that supply the brain.

The ApoE gene encodes a protein that helps regulate the levels and distribution of cholesterol and other lipids in the body. The gene exists in three varieties. ApoE2 is thought to play a protective role against both Alzheimer’s and heart disease, ApoE3 is believed to be neutral, and ApoE4 confers a higher risk for both conditions. Outside the brain, the ApoE4 protein appears to be less effective than other versions at clearing away cholesterol; however, inside the brain, exactly how ApoE4 contributes to Alzheimer’s disease has been a mystery.

Dr. Zlokovic and his team studied several lines of genetically engineered mice, including one that lacks the ApoE gene and three other lines that produce only human ApoE2, ApoE3 or ApoE4. Mice normally have only a single version of ApoE. The researchers found that mice whose bodies made only ApoE4, or made no ApoE at all, had a leaky blood-brain barrier. With the barrier compromised, harmful proteins in the blood made their way into the mice’s brains, and after several weeks, the researchers were able to detect loss of small blood vessels, changes in brain function, and a loss of connections between brain cells.

“The study demonstrates that damage to the brain’s vascular system may play a key role in Alzheimer’s disease, and highlights growing recognition of potential links between stroke and Alzheimer’s-type dementia,” said Roderick Corriveau, Ph.D., a program director at NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research. “It also suggests that we might be able to decrease the risk of Alzheimer’s disease among ApoE4 carriers by improving their vascular health.”

The researchers also found that ApoE2 and ApoE3 help control the levels of an inflammatory molecule called cyclophilin A (CypA), but ApoE4 does not. Levels of CypA were raised about five-fold in blood vessels of mice that produce only ApoE4. The excess CypA then activated an enzyme, called MMP-9, which destroys protein components of the blood-brain barrier. Treatment with the immunosuppressant drug cyclosporine A, which inhibits CypA, preserved the integrity of the blood-brain barrier and lessened damage to the brain. An inhibitor of the MMP-9 enzyme had similar beneficial effects. In prior studies, inhibitors of this enzyme have been shown to reduce brain damage after stroke in animal models.

“These findings point to cyclophilin A as a potential new drug target for Alzheimer’s disease,” said Suzana Petanceska, Ph.D., a program director at NIH’s National Institute on Aging (NIA), which also funded Dr. Zlokovic’s study. “Many population studies have shown an association between vascular risk factors in mid-life, such as high blood pressure and diabetes, and the risk for Alzheimer’s in late-life. We need more research aimed at deepening our understanding of the mechanisms involved and to test whether treatments that reduce vascular risk factors may be helpful against Alzheimer’s.”

Alzheimer’s disease is the most common cause of dementia in older adults, and affects more than 5 million Americans. A hallmark of the disease is a toxic protein fragment called beta-amyloid that accumulates in clumps, or plaques, within the brain. Gene variations that cause higher levels of beta-amyloid are associated with a rare type of Alzheimer’s that appears early in life, between age 30 and 60.

However, it is the ApoE4 gene variant that is most strongly tied to the more common, late-onset type of Alzheimer’s disease. Inheriting a single copy of ApoE4 from a parent increases the risk of Alzheimer’s disease by about three-fold. Inheriting two copies, one from each parent, increases the risk by about 12-fold.

Dr. Zlokovic’s study and others point to a complex interplay between beta-amyloid and ApoE4. On the one hand, beta-amyloid is known to build up in and damage blood vessels and cause bleeding into the brain. On the other hand, Dr. Zlokovic’s data suggest that ApoE4 can damage the vascular system independently of beta-amyloid. He theorizes that this damage makes it harder to clear beta-amyloid from the brain. Some therapies under investigation for Alzheimer’s focus on destroying amyloid plaques, but therapies designed to compensate for ApoE4 might help prevent the plaques from forming, he said.

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A poor sense of smell may be one of the earliest signs of Alzheimer’s. Now, researchers have shown that the offending culprit may be beta-amyloid, a protein that builds up in a toxic form in the brains of those with the disease.

Working with laboratory mice that had been bred to develop a disease that resembles Alzheimer’s in people, the scientists from Case Western Reserve University School of Medicine showed that removing the plaque-forming protein restores the animals’ sense of smell.  Researchers believe that the smell centers of the brain may be among the first areas affected by toxic beta-amyloid, followed by brain areas critical for memory and thinking.

“Understanding smell loss, we think, will hold some clues about how to slow down this disease,� said Daniel Wesson, assistant professor of neuroscience at Case Western Reserve and lead investigator for the study, which was published in The Journal of Neuroscience.

Loss of the sense of smell can be caused by many conditions other than Alzheimer’s, including medications, viral illnesses or injuries to the olfactory systems. But a poor sense of smell has also long been recognized as an early sign of Alzheimer’s. It may also be an early sign of mild cognitive impairment, a form of memory loss that sometimes precedes Alzheimer’s. Not all people with Alzheimer’s lose their sense of smell.

The new research shows how and where in the brain this happens, and that the impairment is likely to be treatable.

Mice exposed to a very minute amount of beta-amyloid lost their ability to detect odors. Plaques made up of the toxic proteins appeared in the rodents’ brain areas responsible for smell long before they showed up in areas important for memory. The mice spent more time sniffing than usual but became incapable of remembering smells or telling the differences among odors in lab experiments.

The research team then sought to reverse the effects. The mice were given a drug that clears beta-amyloid from the brain. After two weeks on the drug, the mice could process smells normally. After withdrawal of the drug for one week, impairments returned.

Like the mice in the study, people with Alzheimer’s may have a poor sense of smell and be unable to detect common odors like natural gas or roses. But no drugs are currently available that clear beta-amyloid from the brain, though scientists continue to test new candidates.

“The evidence indicates we can use the sense of smell to determine if someone may get Alzheimer’s disease, and use changes in sense of smell to begin treatments, instead of waiting until someone has issues learning and remembering,� Dr. Wesson said. “We can also use smell to see if therapies are working.�

The researchers are continuing their research to determine how beta-amyloid spreads through the brain, and to find new ways to slow its spread and stop the progression of disease.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Disease Research at The Rockefeller University.

Source: The Journal of Neuroscience, Nov. 2, 2011. Case Western Reserve Medical School.

Article source: http://www.alzinfo.org/05/articles/diagnosis-and-causes/loss-smell-early-alzheimers-sign-reversed-lab

A new type of brain scan may help to detect Alzheimer’s early, using no radiation and at less cost than other techniques, researchers report. Doctors at the University of Pennsylvania’s Perelman School of Medicine have developed a form of magnetic resonance imaging, or MRI, that detects brain changes that signal Alzheimer’s disease. The doctors have developed a modification to the technique called arterial spin labeling, or ASL-MRI. Small studies show, this may be a useful way to diagnose probable early dementia.

MRI scans are routinely used in hospitals to check for tumors and other issues, and seniors with memory problems may undergo the procedure to rule out brain tumors, strokes or other problems that may be causing the deficits. If Alzheimer’s is suspected, they may then undergo another scanning procedure, such as a PET scan.

The advantage of the new ASL-MRI technique is that someone could undergo brain scanning in a single session to help determine whether Alzheimer’s may be present. The technique looks for changes in blood flow and the uptake of blood sugar, or glucose, in the memory centers of the brain. It requires about an additional 20 minutes compared to standard MRI scans.

“Increases or decreases in brain function are accompanied by changes in both blood flow and glucose metabolism,” explained Dr. John Detre, professor of Neurology and Radiology at Penn, who has worked on ASL-MRI for the past 20 years. “We designed ASL-MRI to allow cerebral blood flow to be imaged noninvasively and quantitatively using a routine MRI scanner.”

Studies show that the MRI method is similar in effectiveness to current PET scans that inject a radioactive dye to measure these brain changes. However, the ASL-MRI method uses no radiation and costs one-fourth as much.

“If ASL-MRI were included in the initial diagnostic work-up routinely, it would save the time for obtaining an additional PET scan, which we often will order when there is diagnostic uncertainty, and would potentially speed up diagnosis,” said Dr. David Wolk, Assistant Director of the Penn Memory Center and a collaborator on the research.

The studies compared the MRI technique and the specialized PET scan results using flurodeoxyglucose, or FDG, a radioactive tracer. In one, published in the journal Alzheimer’s and Dementia, doctors compared images from 13 patients diagnosed with Alzheimer’s and 18 age-matched controls. Both methods proved equally effective in detecting signs of early Alzheimer’s.  In the second study, published in the journal Neurology, data from 15 AD patients were compared to 19 age-matched healthy adults. The patterns of reduction in cerebral blood flow were nearly identical to the patterns of reduced glucose metabolism by the PET scan and showed reductions in brain gray matter typical of Alzheimer’s disease.

“Given that ASL-MRI is entirely noninvasive, has no radiation exposure, is widely available and easily incorporated into standard MRI routines, it is potentially more suitable for screening and longitudinal disease tracking than FDG-PET,” said the Neurology study authors.

Early diagnosis of Alzheimer’s in the doctor’s office has long been a goal for those who treat dementia. Increasingly, experts believe that Alzheimer’s is a disease that begins many years before symptoms like memory loss and personality changes become apparent. Treatment of the disease may be most effective in these early stages, before damage to the brain has become extensive. In addition, a simple test to measure brain function would be useful for researchers to test and monitor new treatments.

Additional studies of this new MRI technique will focus on larger sample sizes, including patients with mild cognitive impairment and other kinds of brain problems.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: American Academy of Neurology. Musiek ES, Chen Y, Korczykowski M, et al: “Direct Comparison of Flurodeoxyglucose Positron Emission Tomography and Arterial Spin Labeling Magentic Resonance Imaging in Alzheimer’s Disease.” Alzheimer’s and Dementia, Oct. 20, 2011, epub ahead of print. 

Article source: http://www.alzinfo.org/05/articles/diagnosis-and-causes/type-brain-scan-detect-alzheimers-early

Related MedlinePlus Page

By Julie Steenhuysen

CHICAGO (Reuters) – The U.S. government launched a national plan to address Alzheimer’s disease on Tuesday with funding for a first prevention study in high-risk patients and tests on an insulin nasal spray that has shown promise in earlier studies.

The trials, funded by grants of $16 million and $7.9 million respectively, are initial steps in the National Alzheimer’s Plan, a sweeping effort to find an effective way to prevent or treat Alzheimer’s by 2025 and improve the care of those already afflicted with the brain-wasting disease.

“This is our roadmap that will help us meet our goal to prevent and effectively treat Alzheimer’s disease by 2025,” Human Services Secretary Kathleen Sebelius told scientists at an Alzheimer’s summit at the National Institutes of Health in Bethesda, Maryland.

“The goal of the new law is to give us the kind of clear, national focus and attention on Alzheimer’s that we’ve given to other diseases,” Sebelius told the meeting, which was relayed by webcast, referring to the National Alzheimer’s Project Act signed by President Barack Obama last year.

Experts predict that without more effective drugs, the number of Americans with Alzheimer’s will double by 2050 and annual related healthcare costs could soar to more than $1 trillion.

The fatal form of dementia affects about 5.1 million Americans today and current treatments address symptoms, but cannot prevent the disease or stop its progression.

Sebelius said progress had so far proven elusive.

“We’ve yet to harness the right formula for drug development and clinical-trial results continue to be disappointing,” she said. “We’ve yet to find effective treatments or proven ways to prevent Alzheimer’s disease, and that’s the ultimate goal.”

Among the immediate actions will be funding for a study involving an antibody drug that attacks amyloid — a protein thought to be a cause of Alzheimer’s — in an international study of people who are genetically predisposed to develop the disease early.

The second will test the use of an insulin nasal spray to restore memory in patients with Alzheimer’s.

An earlier, small study of the latter approach by Suzanne Craft of the University of Washington published last year showed memory improvements in people with mild to moderate Alzheimer’s or a pre-Alzheimer’s condition called amnestic mild cognitive impairment.

FUNDING

Funding for the new initiatives will come from $50 million the Obama administration has set aside for the National Alzheimer’s Plan for fiscal 2012.

Another $100 million has been earmarked for fiscal 2013, including $80 million for research, $4.2 million for public awareness, $4 million for provider education, $10.5 million in caregiver support, and $1.3 million to improve data collection.

The national plan, called for in the National Alzheimer’s Project Act signed by President Barack Obama last year, and drafted by the Department of Health and Human Services (HHS), reflects the input of 3,600 people or organizations.

“The plan addresses every aspect of what it is to confront Alzheimer’s disease,” Sebelius told scientists at the summit.

It includes development of new training for doctors, a public education campaign, including TV advertisements and a website — www.alzheimers.gov — to help families and carers find services and support.

Dr. R. Scott Turner of Georgetown University Medical Center’s Memory Disorders Program applauded the announcement.

“These steps offer a ray of hope for those affected by Alzheimer’s,” Turner said. “We need a robust awareness campaign specifically targeting participation in research studies.”

He said many clinical trials were moving at a glacial pace because of a lack of study volunteers nationwide.

“We need more people with Alzheimer’s disease and their families to consider participating in research,” he said.

Sebelius said the plan was a national one, not a federal one, because it would require efforts from both public and private sectors to address the burden of Alzheimer’s disease.

“This is a strong plan that promises important progress when implemented,” said Harry Johns, president and chief executive of the Alzheimer’s Association. “For all Americans – not just the more than 5 million living with Alzheimer’s and their 15 million caregivers today – this plan is an historic achievement.”

Some have criticized the 2025 goal for a treatment as being too ambitious given the state of the science, and it was the subject of lengthy debate in the advisory council tasked with helping to write the national plan.

“We had people saying it was overly ambitious and we had people who said it wasn’t ambitious enough,” said Don Moulds, principal deputy assistant secretary for planning and evaluation at HHS, in a telephone interview.

Moulds said there was concern that an earlier goal might skew research funding into treatments that might be easy hits, but not game-changing treatments. In the end, the 2025 target was the earliest date a significant treatment could be found.

Although work was already going on to find a treatment for Alzheimer’s, Moulds said the national plan and its specific targets and timelines would help focus the government’s efforts.

“It’s a huge initiative and a very ambitious step in the right direction,” he said.

(Reporting by Julie Steenhuysen; Editing by David Brunnstrom)

Article source: http://www.nlm.nih.gov/medlineplus/news/fullstory_125218.html

Main Category: Alzheimer’s / Dementia
Also Included In: Caregivers / Homecare;  Seniors / Aging
Article Date: 16 May 2012 – 0:00 PDT

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A new study from the Regenstrief Institute and Indiana University has found that, at time of death, individuals with dementia are more likely to be living at home than in a nursing home. This contradicts the commonly held view that most individuals with dementia in the United States eventually move to nursing homes and die there.

“Transitions in Care for Older Adults With and Without Dementia” appears online in advance of publication in the May 2012 issue of the Journal of the American Geriatrics Society.

Most individuals with dementia, even advanced dementia, die of a physical condition such as heart disease, cancer or pneumonia. This study is the first to track movement of individuals with dementia until death regardless of whether the cause of death was recorded as dementia or as another condition.

The study follows these individuals to determine where they receive care and in what order. Rather than finding individuals with dementia progressing on a straight line from home to hospital to nursing home as presumed, the researchers found that individuals with dementia go back and forth. The number and direction of transitions in care can be numerous and follow no determined path.

“This is a study on what it is like to live with dementia over a five- to 10-year period,” said Regenstrief Institute investigator Christopher Callahan, M.D., Cornelius and Yvonne Pettinga Professor in Aging Research at Indiana University School of Medicine and director of the Indiana University Center for Aging Research. “You probably won’t proceed on a straight line from home to hospital to nursing home. You will experience multiple transitions as you progress from mild to moderate to advanced dementia.”

While 74 percent of the time individuals with dementia go to a nursing home after hospitalization, they don’t remain there. Approximately a quarter will return to the hospital in less than a month. Many of the remainder will return home.

The researchers determined that a majority of care for those with dementia, even advanced dementia, is provided in the community by families.

“These results challenge previous assumptions,” said Dr. Callahan, who founded the IU Center for Aging Research in 1997. “Our findings will provide important information for all those concerned with managing the care of older adults – families, physicians, social workers, policy-makers, Medicare and Medicaid, insurance companies, hospital and nursing home administrators, as well as aging individuals. Caring for people living with dementia requires the attention of our entire health care system.”

More than 4,000 primary-care patients seen at Wishard Health Services, the public hospital division of the Health and Hospital Corporation of Marion County, participated in the study. Dr. Callahan sees patients at Wishard’s Health Aging Brain Center.

The research was funded by the National Institute on Aging through a Recovery and Reinvestment Act grant. Co-authors in addition to Dr. Callahan are Greg Arling, Ph.D.; Wanzhu Tu, Ph.D.; Marc B. Rosenman, M.D.; Steven R. Counsell, M.D.; Timothy E. Stump, M.A.; and Hugh C. Hendrie, MB, Ch.B., D.Sc. With the exception of Mr. Stump, all are with Regenstrief Institute, IU School of Medicine and IU Center for Aging Research. Mr. Stump is with the IU School of Medicine.
Indiana University School of Medicine

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Main Category: Alzheimer’s / Dementia
Article Date: 16 May 2012 – 11:00 PDT

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Obama’s healthcare goals have been controversial at best, and although anti-smoking campaigns and other public health and safety awareness drives have been successful, it’s always somewhat dubious when government starts creating grand plans and lofty goals. Nonetheless, Health and Human Services Secretary Kathleen Sebelius has released an ambitious and wide ranging national plan to fight Alzheimer’s disease.

The plan, known as The National Alzheimer’s Project Act (NAPA), which Obama signed into law in Feb 2012, includes five goals, such as development of treatment and prevention for Alzheimer’s disease and other associated dementias by 2025.

The announcement today is accompanied by National Institutes of Health (NIH) $50M in additional funding for 2012 to be directed at Alzheimer’s disease; more specifically, at high quality and up to date training for clinicians and a new public information campaign. The campaign is driven, as is often the case, in part by concern that with an aging population and numbers of American patients suffering from the disease expected to rise from the current 5.4 million to 16 million by 2050, burdening the healthcare system with costs project to soar to a trillion dollars.

In addition, President Obama has earmarked an extra $80M for the 2013 budget plan just for Alzeimer’s research in what he describes as a “jump start” to reach the 2025 goal. The provisions include improving public awareness of the disease ($4.2 million), supporting provider education programs ($4.0 million), investment in caregiver support ($10.5 million) and improving data collection ($1.3 million).

Secretary Sebelius announced :

“These actions are the cornerstones of an historic effort to fight Alzheimer’s disease … This is a national plan not a federal one, because reducing the burden of Alzheimer’s will require the active engagement of both the public and private sectors.”

The plans were presented at the Alzheimer’s Research Summit 2012: Path to Treatment and Prevention which was developed with input from experts in aging and Alzheimer’s disease issues. Calling for a comprehensive collaboration across federal, state and non-profit organizations drew comments from more than 3,600 people or organizations.

One of the more promising treatments that will be ramped up is the use of a drug that attacks a protein known as amyloid, thought to be a major contributor to the problems Alzheimer’s patients suffer from. Much of the funding will come from Genetech, the drug’s US manufacturer, which additional assistance from National Institutes of Health, as well as the Banner Alzheimer’s Institute in Phoenix.

A second trial will work with insulin inhalers, which appear to have the ability to restore some of the memories lost to the disease. The insulin treatment is particularly important, as Alzheimer’s has been linked to diabetes.

The campaign is not only commendable but carries a certain amount of urgency and financial concern to avoid an epidemic of Alzheimer’s in the future. With several Presidents including Ronald Regan having suffered from the disease in their retirement, perhaps Mr. Obama is also privately hoping to ensure he can avoid their fate.

Written by Rupert Shepherd

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MONDAY, May 14 (HealthDay News) — Feeding tubes increase the risk of bed sores in bedridden dementia patients, according to a new study.

The finding challenges the long-held belief that providing nutrition through feeding tubes helps prevent bed sores or helps promote their healing in this group of patients, the authors of the Brown University-led study said.

The researchers did not look at how feeding tubes could cause bed sores (also called pressure ulcers), but they noted that feeding tubes can cause agitation in patients, who then have to be restrained and sedated. Feeding tubes also may increase the risk of diarrhea.

Together, these factors may cause and worsen bed sores, the researchers said.

The researchers examined data from nursing homes and Medicare claims in order to compare thousands of dementia patients. Among patients who did not initially have a bed sore, 35.6 percent with a feeding tube ended up with at least a stage 2 bed sore, compared with 19.8 percent of patients without a feeding tube.

A stage 2 bed sore is an open sore in the upper layer of the skin. A stage 4 bed sore is the most serious type.

After making statistical adjustments, the researchers concluded that patients with a feeding tube were 2.27 times more likely to develop a bed sore than those without a feeding tube. The risk of developing a stage 4 bed sore was 3.21 times higher for those with a feeding tube.

Among patients who already had a bed sore, short-term improvement in the sore occurred in 27.1 percent of patients with a feeding tube and in 34.6 percent of those without. Patients without a feeding tube were 0.7 times more likely to have an improvement in a sore than those with one, the researchers determined.

The study was published May 14 in the journal Archives of Internal Medicine.

“This study provides new information about the risks of feeding tube insertion in people with advanced [dementia],” lead author Dr. Joan Teno, a gerontologist and professor of health services, policy and practice in the Public Health Program at Brown, said in a university news release.

“We see a substantial risk of people developing a stage 2 and higher [bed sore],” she said. “We believe these risks should be discussed with family members before a decision is made to insert a feeding tube in a hospitalized nursing home resident with advanced [dementia].”

Article source: http://www.nlm.nih.gov/medlineplus/news/fullstory_125138.html

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FRIDAY, May 11 (HealthDay News) — Many elderly people with dementia live and die at home rather than in nursing homes, a new study has found.

The findings challenge the widely held belief that most dementia patients eventually move into and die in nursing homes, said Dr. Christopher Callahan, of the Indiana University School of Medicine and the Regenstrief Institute in Indianapolis, and colleagues.

The researchers followed about 1,500 dementia patients and found that 74 percent of those who went to a nursing home after being hospitalized didn’t remain. About one-quarter returned to the hospital in less than a month, but many others returned home.

Dementia patients did not move straight from home to hospital to nursing home, as the researchers expected. Instead, dementia patients moved back and forth between settings, which can make managing patient care even more complex and add stress for family caregivers.

The researchers also found that the majority of care for dementia patients is provided by families.

The study appears Friday in the Journal of the American Geriatrics Society.

“Our study is the first to track movement of individuals with dementia until death regardless of whether the cause of death was … dementia or another condition,” Callahan said in a journal news release. “A better understanding of the relationships between sites of care for older adults with dementia is fundamental to building better models of care for these vulnerable elders.”

The findings challenge beliefs “regarding the permanence of nursing-home care for persons with dementia,” Dr. Robert Kane, of the School of Public Health at the University of Minnesota in Minneapolis, and Dr. Joseph Ouslander, of the Charles E. Schmidt College of Medicine at Florida Atlantic University in Boca Raton, wrote in an accompanying editorial.

“More research is needed to understand how this impacts the quality of care for dementia patients and how we can improve care transitions and management for dementia patients and their families,” they noted.

Article source: http://www.nlm.nih.gov/medlineplus/news/fullstory_125091.html