New Book Looks At Long-Term Care And Uncertainties For Elderly Baby Boomers

The continued decline of the nursing home – once the mainstay care for the frail elderly – and an upsurge in popularity of assisted living will lead to many dramatic changes in long-term care, according to a University of Florida expert and editor of a new book on the subject.

“The American public has expressed a strong distaste for going to a nursing home because it smacks of a hospital-like, institutional way of living and receiving care,” said Stephen Golant, a UF geography professor and expert on elderly housing. “Assisted living has emerged as a highly attractive option for older persons who have experienced some physical or cognitive decline and feel less secure about receiving care in their own home.”

Yet there are few certainties about either the future of assisted living for the elderly or the huge number of baby boomers who stand to be its recipients, Golant said.

“Although baby boomers will constitute a large market, it is unclear what share will have impairments and chronic health problems that make them candidates for assisted living,” he said. “The emergence of an unexpected new medical or rehabilitation breakthrough, such as a cure or the discovery of a disease-controlling drug for Alzheimer’s disease – could result in a substantial decline in the number of elderly Americans who need such care.”

Golant and Joan Hyde, an assisted living provider and a senior fellow at the Gerontology Institute at the University of Massachusetts in Boston, are editors of the new book “The Assisted Living Residence: A Vision for the Future,” published this month by The Johns Hopkins University, which examines elderly housing and possible care trends over the next 20 to 30 years.

The biggest competitors to assisted living are daughters and daughters-in-law who provide most elderly caregiving and determine whether their loved ones can remain in their own homes, Golant said. But the availability and attitudes of the current generation of female offspring who must juggle work and family responsibilities are unclear, he said.

“We know that women have succeeded in being comfortable in going back to work even when they have a baby less than a year old and assigning that care to somebody else,” he said. “Now the question is how will they react when they confront the possibility of leaving their older parents?”

New technology may make that transition easier, Golant said. The development of sophisticated monitoring and surveillance devices that would allow grown children to track their parents’ daily movements on a computer screen from home or work, for example, would revolutionize attitudes about nursing home and assisted living facilities, he said.

“Suddenly some of the downsides of not living at home would be minimized because sons and daughters could feel very much involved with the caregiving experience of their mothers and fathers even without physically being there,” he said. “They could see parents in their rooms, walk with them to the dining hall and even communicate with them in real time.”

Businesses and social service agencies are preparing for the surge of aging baby boomers, an estimated seven out of 10 of whom are expected to require long-term care at some point after they reach the age of 65, Golant said. Many will also face the issue of a parent needing long-term care before reaching that stage themselves, he said.

Nursing homes are increasingly gearing their business toward acute episodes, such as strokes, which call for short rehabilitative recovery periods, Golant said. When they offer long-term care, nursing homes increasingly serve poorer people and are funded through the Medicaid program, while assisted living caters to private paying individuals with higher incomes or salable assets such as an expensive home or stock portfolio.

To be competitive, nursing homes are trying to transform themselves into becoming more home-like and less like an institution; in short, more like assisted living facilities, he said.

Low savings rates and falling home equity raise the question of whether fewer baby boomers will be able to afford assisted living compared with their parents’ generation, Golant said. The average one-year base price is close to $36,000, not including the additional supervision required with Alzheimer’s disease and more serious medical conditions, he said.

“Assisted living is here to stay – and is now very much part of the ordinary consumer’s lexicon,” he said. “But its rate of growth and the number and share of older boomers who will choose this long-term care option in the future is very uncertain.”

Earlier Alzheimer’s Diagnosis With Automated MRI Technique

An automated system for measuring brain tissue with magnetic resonance imaging (MRI) can help physicians more accurately diagnose Alzheimer’s disease at an earlier stage according to a new study published in the July issue of the journal Radiology.

In Alzheimer’s disease, nerve cell death and tissue loss cause all areas of the brain, especially the hippocampus region, to shrink. MRI with high spatial resolution allows radiologists to visualize subtle anatomic changes in the brain that signal atrophy, or shrinkage. But the standard practice for measuring brain tissue volume with MRI, called segmentation, is a complicated, lengthy process.

“Visually evaluating the atrophy of the hippocampus is not only difficult and prone to subjectivity, it is time-consuming,” explained the study’s lead author, Olivier Colliot, Ph.D, from the Cognitive Neuroscience and Brain Imaging Laboratory in Paris, France. “As a result, it hasn’t become part of clinical routine.”

In the study, the researchers used an automated segmentation process with computer software developed in their laboratory by Marie Chupin, Ph.D., to measure the volume of the hippocampus in 25 patients with Alzheimer’s disease, 24 patients with mild cognitive impairment and 25 healthy older adults. The MRI volume measurements were then compared with those reported in studies of similar patient groups using the visual, or manual, segmentation method.

The researchers found a significant reduction in hippocampal volume in both the Alzheimer’s and cognitively impaired patients when compared to the healthy adults. Alzheimer’s patients and those with mild cognitive impairment had an average volume loss in the hippocampus of 32 percent and 19 percent, respectively. Studies using manual segmentation methods have reported similar results.

“The performance of automated segmentation is not only similar to that of the manual method, it is much faster,” Dr. Colliot said. “It can be performed within a few minutes versus an hour.”

According to the Alzheimer’s Association, more than five million Americans currently have Alzheimer’s disease. One of the goals of modern neuroimaging is to help in the early and accurate diagnosis of Alzheimer’s disease, which can be challenging. When the disease is diagnosed early, drug treatment can help improve or stabilize patient symptoms.

“Combined with other clinical and neurospychological evaluations, automated segmentation of the hippocampus on MR images can contribute to a more accurate diagnosis of Alzheimer’s disease,” Dr. Colliot said.

No Difference in NSAIDs for Alzheimer’s Risk Reduction

BALTIMORE, May 28 — Ibuprofen (Advil, Motrin) may be no better than other nonsteroidal anti-inflammatory drugs for Alzheimer’s disease prevention, researchers here said.

Patients who used NSAIDs had a 23% reduced the risk of developing Alzheimer’s disease compared with those who never used the drugs, regardless of the type taken, reported Peter P. Zandi, Ph.D., of Johns Hopkins, and colleagues in the May 28 online issue of Neurology.

 

Their meta-analysis of six prospective, observational trials argues against the hypothesized mechanism for the risk reduction seen with NSAIDs in other epidemiological studies, they said.

 

Ibuprofen selectively lowers the 42-residue form of amyloid beta (Aß₄₂), which was thought to target plaques found in the brain of Alzheimer’s patients, they said.

 

Earlier studies had found almost a two-fold greater benefit for Alzheimer’s prevention with this type of NSAID than with the group that includes naproxen (Aleve) and celecoxib (Celebrex) (See: NSAID Use Linked to Reduced Alzheimer’s Risk).

 

However, randomized clinical trials of primary prevention or of patients with established Alzheimer’s disease have shown no benefit.

 

Earlier this month, the randomized Alzheimer’s Disease Anti-inflammatory Prevention Trial (ADAPT) was reported to have shown no primary prevention benefit with naproxen and celecoxib for either cognitive decline or Alzheimer’s diagnosis (See: NSAIDS Don’t Keep the Brain Nimble).

 

“Some have proposed that the lack of benefit in NSAID clinical trials reflects their choice of the ‘wrong’ non- selective Aß₄₂-lowering agents,” Dr. Zandi and colleagues said.

 

But the meta-analysis results suggest the discrepancy “may instead be the result of other factors such as timing and duration of exposure, or in other systematic differences in participants of epidemiologic studies versus clinical trials,” they said.

 

To further explore the difference between these types of NSAIDs, Dr. Zandi’s group pooled patient-level data from six prospective cohort studies to obtain a sufficient sample to examine Alzheimer’s disease risk by type of NSAID used.

 

The analysis included 13,499 initially dementia-free participants from the Baltimore Longitudinal Study of Aging, the Cache County Study, the

Canadian Study of Health and Aging, the Cardiovascular Health Study, the Framingham Heart Study, and the Monongahela Valley Independent Elders Study.

 

During 70,863 person-years of follow-up in these studies, 29.6% of participants used an NSAID of any type at any time according to self-report or with validation by examining medicine bottles.

 

Ibuprofen was the most commonly used selective Aß₄₂-lowering agent, and accounted for 52.9% of total NSAID use.

 

Naproxen was the most commonly used non-selective agent (20.4% of total NSAID use).

 

Overall, 820 men and women were diagnosed with Alzheimer’s disease during the studies.

 

This risk of incident Alzheimer’s was reduced with any NSAID use compared with never use (hazard ratio 0.75, 95% confidence interval 0.64 to 0.89).

 

The association remained significant after adjustment for age, sex, and education (HR 0.77, 95% CI 0.65 to 0.91) and further control for arthritis status (HR 0.83, 95% CI 0.69 to 0.99).

 

NSAIDs that selectively lower Aß₄₂ did not show a greater benefit than nonselective agents (adjusted HR 0.87, 95% CI 0.72 to 1.04, versus adjusted HR 0.75, 95% CI 0.56 to 1.01).

 

Participants who took only NSAIDs that selectively lower Aß₄₂ did not benefit more than those who took only nonselective agents (P=0.32).

 

Aspirin also appeared to reduce risk of Alzheimer’s disease for the 40.7% of participants who used it, even when they used no other NSAIDs (adjusted HR 0.78, 95% CI 0.66 to 0.92).

 

Acetaminophen, however, was not significantly linked to decreasing the Alzheimer’s risk (adjusted HR 0.93, 95% CI 0.76 to 1.13).

 

The researchers cautioned that their analysis could have been affected by recall bias and incomplete adjustment for confounding factors, such as socioeconomic status.

 

Although concerns about potential cardiotoxicity and other side effects of NSAIDs, as well as discouraging clinical trial results, dampen enthusiasm for these agents in Alzheimer’s prevention, the researchers concluded that “a better understanding of these effects will be important, even if the current generation of drugs has limitations.”

Source:  http://www.medpagetoday.com/Neurology/AlzheimersDisease/tb/9632

Celery May Help Lessen Brain Inflammation Associated With Alzheimer’s Disease

Jupiter Kalambakal – AHN News Writer

Chicago, IL (AHN) – A recent study showed celery can help lessen the inflammation of the brain associated with Alzheimer’s Disease (AD).

The study, published by the Proceedings of the National Academy of Sciences in its May 27 issue, involved mice made to drink water with luteolin, an antioxidant. The study showed the rodents had reduced inflammation compared with other mice similarly tested with bacteria, Bloomberg reported.

The author of the study Rodney W. Johnson told Bloomberg that about 47 human servings of celery daily were given the mice. Johnson is an associate professor at the University of Illinois at Urbana-Champaign’s department of animal sciences.

The result of the experiment suggested plants such as celery are beneficial to the brain in terms of the protection they give.

A first, the study showed the luteolin regulates the inflammation of the brain as a result of certain diseases, such as AD and schelosis.

AD leads to memory loss, among other progressive and irreversible brain disorders, including deterioration in one’s ability to think. The death of brain cells and the losing of connections between such cells are said to be connected to these losses.

Research suggested that nutritional deficiencies may possibly be related to AD.

Recommended daily vegetable serving is 2  cups, advised the US Department of Agriculture.

Source:  http://www.allheadlinenews.com/articles/7011006504

How One Mutation Tips Biochemistry To Cause Alzheimer’s Disease

ScienceDaily (May 12, 2008) — Your fate can be determined by tiny events. Imagine you live in the city and you walk everywhere to get exercise — you are healthy and not afraid of getting mugged. You almost never eat breakfast so you don’t stop at the donut shop on the way to work, until one day the manager replaces the girl at the counter with her pretty red-haired younger sister. This seemingly unimportant change in your world is just enough to overcome your ability to resist high-fat temptation. A million donuts later, your cholesterol level surges and then your heart gives out. Curse you, little red-haired girl!

Like staff change at the donut shop, subtle, seemingly inconsequential differences in human genetic design can lead to some unexpected tipping points in cellular chemistry that can lead to disaster. Cellular processes, like all the routines of life, are unfathomably complex, constantly evolving, and are sometimes dramatically sensitive to the smallest of changes. Consider the case of Alzheimer’s disease…

Alzheimer’s is a terrifying brain-destroying disease whose causes have proven very difficult to pin down. In recent years, science has been closing in on solving the puzzle, particularly regarding some of the hereditary, “early onset” forms of the illness. Unusual by-products of cell metabolism, clumps of protein aggregates, have been shown to have a toxic effect on brain cells and certain gene mutations have been shown to be associated with increasing production of these by-products, though the evidence for an exact mechanism has remained hidden.

Now, using sophisticated computer simulations, a team of physical chemists have shown precisely how a minor, seemingly inconsequential mutation results in unexpected changes in a very delicate chemical balance, creating build-up of the toxic by-products.

The mutation, the substitution of a single base among the 3 billion found in human DNA, seems to have the greatest effect on a fragment of a specific protein that is abundantly present in living cells. The difference causes a subtle change in the shape of the fragment at a critical point, which can slightly shift the odds towards an inappropriate biochemical reaction that sidetracks the metabolic path. The increase in the reaction simply tips the balance of chemical processes, causing the build-up of a substance that kills brain cells, leading to the early deterioration of mental capacity and, eventually, death.

“It is a really tiny change but it has tremendous consequences,” said Andrij Baumketner, lead author on the study and a faculty member in the department of physics and optical science at the University of North Carolina at Charlotte. The finding, published in the April 7 issue of the Publication of the National Academy of Sciences, was co-authored by Mary Griffin Krone and Joan-Emma Shea, both from the department of chemistry and biochemistry at the University of California at Santa Barbara.

The group studied the effects caused by the Dutch Mutation, a mutation that has been discovered to be associated with a specific, hereditary form of Alzheimer’s disease. The mutation is small, the simple substitution of one DNA base for another, resulting in the change of only one amino acid residue — glutamic acid changing to the very similar glutamine — among hundreds of amino acids that form a protein known as the amyloid precursor protein (APP). The greatest effect of the Dutch-type mutation on APP, whose primary biological function is unknown, seems to be through a fragment known as amyloid-beta peptide that is created when cells break down the protein. Studies have shown that mutated forms of the fragment have greater tendency to stick to bond together and form protein clumps or aggregates. Some forms of the amyloid-beta clumps have been shown to be toxic to brain cells.

Why the change in one amino acid would cause this peptide to form clumps more readily has, until now, been unclear. Amyloid-beta peptide, unlike most other proteins present in the cell, is largely lacking in specific shape (conformation), the characteristic that usually controls how proteins interact with each other. However the fragment does have two places in its sequence of amino acids — a section known as the “bend” and an area known as the “central hydrophobic cluster” where the polypeptide chain does conform to a more-or-less fixed shape. These areas, in fact, seem to be involved when the fragments bond together into clumps.

The researchers created complex computer models of the two structured areas of the fragment and found that the single amino acid change caused by the mutation had a subtle effect on their properties. In order for fragments to bond together, the structured areas must first undergo a “conformational change” (a change in structural shape) from the conformations they normally have as single, water-soluble amyloid-beta peptides into a “transition state” conformation that leads up to forming clumps. The researchers found that mutation increased the likelihood that the structures would be in a form similar to the transition state before the reaction occurred. When the structured areas were already in the required transition state, bonding was encouraged because less energy was required for the bonding reaction to take place.

“We knew quite a bit about what these peptides are from experimental studies, but we didn’t know the microscopic details,” noted Baumketner. “An experiment never gives you atomic resolution — you always have to guess what is actually going on with the molecules. But with a computer simulation you start with atoms and how they interact and you end with atoms, so there is no question with missing any details.”

The detail of the simulations showed that, because the mutation made the protein fragments more likely to be in a transition state for bonding, bonds between fragments were more likely to be formed than broken (in the reverse reaction), so clumps of fragments accumulated. The end result of the subtle, mutation-driven change in the protein fragment’s shape was the tipping the reaction’s balance enough to allow clumps composed of multiple fragments to occur and to build up –with a disastrous effect on brain tissue.

“The barrier between the reactants and the products is the conformational difference between the peptide and its transition state,” Baumketner said. “The fewer changes the peptide needs to undergo, the easier it is for it to change. The mutation predisposes the single amyloid-beta peptide to jump onto the barrier that keeps the reaction from happening.”

The ultimate problem responsible for Alzheimer’s Disease, Baumketner notes, is that the design of the protein affected is so “close to the edge” in the reactions it must undergo that extremely small changes can cause problems, like the formation of toxic by-products.

“It looks like whoever designed the proteins in our bodies only made the beta peptides to be right on the edge of where they have to be for us to be alive,” he said facetiously. “You make a small push and you push it over the edge and then there is no return. If you were farther from the edge, that would be fine, and you could tolerate one mutation.

“There is lots of discussion about why this happens — is it the failure of evolution? Maybe evolution never has had a chance to optimize us against this. Humans now live to be much older, but evolution never has had a chance before to detect and avoid these problems through natural selection. When the lifespan was 35 years, you didn’t have a large problem with Alzheimer’s. Now you do.”

Obesity can increase dementia risk by up to 80%

Obesity can increase dementia risk by up to 80 per cent – people who are underweight also face an elevated risk

But it’s not just weight gain that poses a risk. People who are underweight also have an elevated risk of dementia, unlike people who are normal weight or overweight.

US researchers carried out a detailed review of 10 international studies published since 1995, covering just over 37,000 people, including 2,534 with various forms of dementia. Subjects were aged between 40 and 80 years when the studies started, with follow-up periods ranging from three to 36 years.

The review, which included studies from the USA, France, Finland, Sweden and Japan, also included a sophisticated meta-analysis of seven of the studies, published between 2003 and 2007 with a follow-up period of at least five years.

All kinds of dementia were included, with specific reference to Alzheimer’s Disease and to vascular dementia – where areas of the brain stop functioning because the blood vessels that supply them are damaged by conditions such as high blood pressure or heart disease.

“Our meta-analysis showed that obesity increased the relative risk of dementia, for both sexes, by an average of 42 per cent when compared with normal weight” says Dr Youfa Wang, Associate Professor of International Health and Epidemiology at Johns Hopkins Bloomberg School of Public Health, Baltimore.

“And being underweight increased the risk by 36 per cent.

“But when we looked specifically at Alzheimer’s Disease, the increased risk posed by obesity was 80 per cent. The increased risk for people with vascular dementia was 73 per cent.

“The risks were greater in studies where sufferers developed Alzheimer’s Disease or vascular dementia before the age of 60 or in studies with follow-up periods of more than 10 years.

“We also found that obesity was more likely to be a risk factor for women when it came to developing Alzheimer’s Disease and for men when it came to vascular dementia.”

The authors estimate that 12 per cent of the dementia risk in the study population could be attributed to obesity, with this rising to just over 21 per cent in patients with Alzheimer’s Disease.

It’s estimated that up to 10 per cent of people aged 65 or more suffer from some form of dementia and two-thirds of those have Alzheimer’s Disease.

“There has been controversy about the links between obesity and dementia for a number of years, but previous findings have been mixed and inconclusive” says Dr Wang.

“The advantage of carrying out a meta-analysis is that it provides researchers with access to a large number of study subjects and it is possible to iron out the inconsistencies and come to overarching conclusions.

“Our detailed analysis clearly shows a U-shaped relationship between weight and dementia, with people who are obese or underweight facing a greater risk.

“We believe that our results show that reducing the prevalence of obesity is a promising strategy for preventing the progression of normal ageing into Alzheimer’s Disease.”

Source:  http://www.news-medical.net/?id=38144

Book Lays Out ‘Action Plan’ for Alzheimer’s Patients

Durham, N.C.  A pair of Duke University experts hope that a new book will be able to help Alzheimer’s sufferers and their families find good information early the progress of the disease.

Psychiatrist Dr. Murali Doraiswamy and Lisa Gwyther, with Duke Family Support Program, teamed up to author The Alzheimer’s Action Plan.

They wanted to create an alternate source of information to the often-bewildering facts on the Internet.

“We wrote this book in order to provide an action plan so that people can get the best possible diagnosis and care at the earliest stages of Alzheimer’s,” Doraiswamy said.

“People can go the Internet, and they can be overwhelmed by information that isn’t relevant to their first source,” Gwyther said.

Mary Davis turned to the Internet’s multiplicity of sources when her husband, Bob, was diagnosed with the early stages of Alzheimer’s. The couple was in their early retirement years.

“You know, there’s a lot of frustration in the beginning,” Mary Davis said.

The Alzheimer’s Action Plan includes information about reliable Web sites, how to get an accurate diagnosis and the latest research.

The book is geared toward early-stage patients, the authors said, because new research shows certain practices can slow the progression of the disease.

“There are many things that you can influence through diet, through exercise and through healthy eating habits,” Doraiswamy.

Bob Davis said doing math puzzles helps him keep an active mind. “I eat them up, which is kind of amazing,” he said.

“He has problems with memories, but as far as being himself, he’s still himself,” Mary Davis said.

The Alzheimer’s Action Plan is widely available in most bookstores.

More information about the disease is available from the Alzheimer’s Association.

Source:  http://www.wral.com/lifestyles/healthteam/story/2768264/

Diabetes in Mid-life Linked To Increased Risk Of Alzheimer’s Disease

ScienceDaily (Apr. 10, 2008) Men who develop diabetes in mid-life appear to significantly increase their risk of developing Alzheimer’s disease, according to a long-term study published in the April 9, 2008, online issue of Neurology.

“Our results have important public health implications given the increasing numbers of people developing diabetes and the need for more powerful interventions,” said study author Elina RÃnnemaa, MD, with Uppsala University in Uppsala, Sweden.

The study involved 2,269 men in Sweden who underwent glucose testing at age 50 to test for diabetes, which is caused by abnormal insulin levels. During an average follow up of 32 years, 102 participants were diagnosed with Alzheimer’s disease, 57 with vascular dementia and 235 with other types of dementia or cognitive impairment.

The study found that the men with low insulin secretion capacity at age 50 were nearly one-and-a-half times more likely to develop Alzheimer’s disease than people without insulin problems. The risk remained significant regardless of blood pressure, cholesterol, body mass index and education.

“Our results suggest a link between insulin problems and the origins of Alzheimer’s disease and emphasize the importance of insulin in normal brain function,” said Rönnemaa. “It’s possible that insulin problems damage blood vessels in the brain, which leads to memory problems and Alzheimer’s disease, but more research is needed to identify the exact mechanisms.”

The study also found the association between diabetes and risk of Alzheimer’s disease was strongest in people who did not have the APOE4 gene, which is known to increase the risk of Alzheimer’s disease. Rönnemaa says this shows that insulin problems are an important risk factor for Alzheimer’s disease when the high risk gene is missing.

The study was supported by grants from Uppsala University Hospital and the Swedish Research Council.

Adapted from materials provided by American Academy of Neurology.

Cup Of Coffee A Day Could Help Protect Against Alzheimer’s Disease, Study Suggests

ScienceDaily (Apr. 2, 2008) A daily dose of caffeine blocks the disruptive effects of high cholesterol that scientists have linked to Alzheimer’s disease. A study in the open access publication, Journal of Neuroinflammation revealed that caffeine equivalent to just one cup of coffee a day could protect the blood-brain barrier (BBB) from damage that occurred with a high-fat diet.

The BBB protects the central nervous system from the rest of the body’s circulation, providing the brain with its own regulated microenvironment. Previous studies have shown that high levels of cholesterol break down the BBB which can then no longer protect the central nervous system from the damage caused by blood borne contamination. BBB leakage occurs in a variety of neurological disorders such as Alzheimer’s disease.

In this study, researchers from the University of North Dakota School of Medicine and Health Sciences gave rabbits 3 mg caffeine each day — the equivalent of a daily cup of coffee for an average-sized person. The rabbits were fed a cholesterol-enriched diet during this time.

After 12 weeks a number of laboratory tests showed that the BBB was significantly more intact in rabbits receiving a daily dose of caffeine.

“Caffeine appears to block several of the disruptive effects of cholesterol that make the blood-brain barrier leaky,” says Jonathan Geiger, University of North Dakota School of Medicine and Health Sciences. “High levels of cholesterol are a risk factor for Alzheimer’s disease, perhaps by compromising the protective nature of the blood-brain barrier. For the first time we have shown that chronic ingestion of caffeine protects the BBB from cholesterol-induced leakage.”

Caffeine appears to protect BBB breakdown by maintaining the expression levels of tight junction proteins. These proteins bind the cells of the BBB tightly to each other to stop unwanted molecules crossing into the central nervous system.

The findings confirm and extend results from other studies showing that caffeine intake protects against memory loss in aging and in Alzheimer’s disease.

“Caffeine is a safe and readily available drug and its ability to stabilise the blood-brain barrier means it could have an important part to play in therapies against neurological disorders,” says Geiger.

Journal reference: Caffeine blocks disruption of blood brain barrier in a rabbit model of Alzheimer’s disease Xuesong Chen, Jeremy W. Gawryluk, John F. Wagener, Othman Ghribi and Jonathan D. Geiger Journal of Neuroinflammation (in press)

Adapted from materials provided by BioMed Central/Journal of Neuroinflammation, via EurekAlert!, a service of AAAS.

Alzheimer’s Progression Indicators

Alzheimer’s disease may progress more rapidly in people with high blood pressure or a form of irregular heartbeat, atrial fibrillation, according to results of a recent study from Johns Hopkins University School of Medicine inBaltimore (Neurology, Nov. 6, 2007).The findings suggest that treating these conditions may also slow memory loss in people with the disease. While current medications for Alzheimer’s disease are effective for some patients in slowing the rate of progression, many patients do not benefit from the treatments or cannot tolerate them, said lead researcher Michelle M. Mielke, PhD, of the Department of Psychiatry and Behavioral Sciences at Johns Hopkins. “The possibility that specific vascular conditions may affect how fast a person with AD declines provides new opportunities for slowing the rate of Alzheimer’s disease progression,” Dr. Mielke said. “Treatments for atrial fibrillation and high blood pressure are relatively inexpensive and safe and may reduce memory decline in patients with these conditions.” The study examined 135 men and women over 65 who were newly diagnosed with Alzheimer’s. All had undergone annual memory tests for an average of three years. Results showed that 10 patients with high blood pressure (systolic pressure over 160) at the time of the Alzheimer’s diagnosis showed a rate of memory loss roughly 100 percent faster than those with normal blood pressure. In addition, 10 patients with atrial fibrillation at the time of the diagnosis showed a rate of memory decline that was 75 percent faster than those with normal heartbeats. The study participants were part of the Cache County Study on Memory Health and Aging, which has been following a group of 5,092 people 65 or older living in Cache County, Utah, since 1995.”What makes this group and study unique is that we have been following these participants in the community for over a decade, even before they were first diagnosed with Alzheimer’s disease, so we know a good deal about their medical history,” said Dr. Mielke. “Studies that enroll patients [with Alzheimer's] only from clinics may miss key factors, such as date of onset and history of cardiovascular disease and treatment.” Dr. Mielke currently is working on similar studies using larger sample sizes to better understand the potential role that vascular factors play before Alzheimer’s diagnosis and their role over the course of the disease’s progression. Constantine Lyketsos, MD, Paul Rosenberg, MD, and Peter Rabins, MD, MPH, of the Department of Psychiatry and Behavioral Sciences at Johns Hopkins also contributed to the study. Additional researchers include JoAnn Tschanz, PhD, Maria Norton, PhD, Ron Munger, PhD, Larry Cook, and Chris Corcoran, PhD, of Utah State University in Logan, Utah; Kathleen Hayden, PhD, and Kathleen Welsh-Bohmer, PhD, ofDuke University in Durham, NC; Robert Green, MD, ofBoston University; and John Brietner, MD, of theUniversity ofWashington in Seattle.The study was supported by grants from the National Institute on Aging. Source:  http://speech-language-pathology-audiology.advanceweb.com/editorial/content/editorial.aspx?cc=110769