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Please Click on the Links Below to View Interesting Articles About Senior Care and Conditions


What to Ask About Alzheimer's Disease


Tracing the Path from DNA to Dementia


Zen and the Art of Coping With Alzheimer's


Preventing Falls in Older Adults


Success Through Teamwork in the Home Health Setting

 

 

Success Through Teamwork in the Home Health Setting

Success Through Teamwork in the Home Health Setting: The Role of Occupational Therapy

Pamela E. Toto, MS, OTR/L, BCG, FAOTA

Gerontology Special Interest Section for the American Occupational Therapy Association

Since 2002 and the introduction of outcome-based quality improvementreports by the Centers for Medicare and Medicaid Services, allhome health professionals have recognized a heightened importancein the measurement of change in the daily functioning of patientsfrom onset to discharge of the agency's service. As health careprofessionals whose expertise focuses on safe and meaningfulparticipation in occupations of daily living, occupational therapistscan play a key role on the inter-disciplinary team in a homehealth care agency. This article outlines the potential benefitsof expanding the role of the occupational therapist as an interdisciplinaryteam member and explores challenges and solutions to maximizecollaborative opportunities with the occupational therapy practitionerin home health.

 

Referenced from: Sage Journals Online

http://hhc.sagepub.com/cgi/content/short/19/1/31

 

Preventing Falls in Older Adults

Preventing Falls in Older Adults: A Multifactorial Approach

Marcie Weinstein, PhD, OT/L, FAOTA

College of Health Professions at Towson University in Baltimore, Maryland

Japhia Booth, OT/L

As people age they become increasingly at risk for falling withthe potential for serious injury. With the boom of individualsover age 65 enjoying an increasing life expectancy, falls willbe an increasingly important health care issue. Research intofall prevention and treatment emphasizes a multi-factorial approach.This approach involves carrying out a comprehensive assessmentof the whole person and surrounding environment, determiningfactors that create risk, and then treating all of these factors.The approach is effective because it specifically designs anintervention to target each of the factors that puts a personat risk for falling. To maximize that effectiveness, a multidisciplinaryteam is employed that draws on the expertise and specific skillsets of each team member. By making people aware of their increasedrisk for falling and providing strategies for prevention, theteam can help individuals more safely remain in their homesand communities.

Referenced From: Sage Journals Online

http://hhc.sagepub.com/cgi/content/short/19/1/45

 

Zen and the Art of Coping With Alzheimer's

August 29, 2007

The New York Times

Zen and the Art of Coping With Alzheimer's

By DENISE GRADY

IN BRIEF

The number of Alzheimer's patients is expected to increase dramatically in coming years, straining the health care system.
Scientists have not discovered the cause nor devised effective treatments. Even diagnosis is difficult.
In the absence of therapies, attention has turned to teaching the skills necessary to cope with demented patients.
Increasingly caregivers are encouraged to validate the feelings and perceptions of the person with Alzheimer's.

During the YouTube forum with the Democratic presidential candidates in July, the first question about health care came from two middle-age brothers in Iowa, who faced the camera with their elderly mother. Not everybody with Alzheimer's disease has two loving sons to take care of them, they said, adding that a boom in dementia is expected in the next few decades.

"What are you prepared to do to fight this disease now?" they asked.

The politicians mouthed generalities about health care, larded with poignant anecdotes. None of them answered the question about Alzheimer's.

Science hasn't done much better. There is no cure for Alzheimer's and no way to prevent it. Scientists haven't even stopped arguing about whether the gunk that builds up in the Alzheimer's brain is a cause or an effect of the disease. Alzheimer's is roaring down - a train wreck to come - on societies all over the world.

People in this country spend more than a $1 billion a year on prescription drugs marketed to treat it, but for most patients the pills have only marginal effects, if any, on symptoms and do nothing to stop the underlying disease process that eats away at the brain. Pressed for answers, most researchers say no breakthrough is around the corner, and it could easily be a decade or more before anything comes along that makes a real difference for patients.

Meanwhile, the numbers are staggering: 4.5 million people in the United States have Alzheimer's, 1 in 10 over 65 and nearly half of those over 85. Taking care of them costs $100 billion a year, and the number of patients is expected to reach 11 million to 16 million by 2050. Experts say the disease will swamp the health system.

It's already swamping millions of families, who suffer the anguish of seeing a loved one's mind and personality disintegrate, and who struggle with caregiving and try to postpone the wrenching decision about whether they can keep the patient at home as helplessness increases, incontinence sets in and things are only going to get worse.

Drug companies are placing big bets on Alzheimer's. Wyeth, for instance, has 23 separate projects aimed at developing new treatments. Hundreds of theories are under study at other companies large and small. Why not? People with Alzheimer's and their families are so desperate that they will buy any drug that offers even a shred of hope, and many will keep using the drug even if the symptoms don't get better, because they can easily be convinced that the patient would be even worse off without it.

It is telling, maybe a tacit admission of defeat, that a caregiving industry has sprung up around Alzheimer's. Books, conferences and Web sites abound - how to deal with the anger, the wandering, the sleeping all day and staying up all night, the person who asks the same question 15 times in 15 minutes, wants to wear the same blouse every day and no longer recognizes her own children or knows what a toilet is for.

The advice is painfully and ironically reminiscent of the 1960s and '70s, the literal and figurative high point for many of the people who are now coping with demented parents. The theme is, essentially, go with the flow. People with Alzheimer's aren't being stubborn or nasty on purpose; they can't help it. Arguing and correcting will not only not help, but they will ratchet up the hostility level and make things worse. The person with dementia has been transported into a strange, confusing new world and the best other people can do is to try to imagine the view from there and get with the program.

If a patient asks for her mother, for instance, instead of pointing out that her mother has been dead for 40 years, it is better to say something like, "I wish your mother were here, too," and then maybe redirect the conversation to something else, like what's for lunch.

If Dad wants to polish off the duck sauce in a Chinese restaurant like it's a bowl of soup, why not? If Grandma wants to help out by washing the dishes but makes a mess of it, leave her to it and just rewash them later when she's not looking. Pull out old family pictures to give the patient something to talk about. Learn the art of fragmented, irrational conversation and follow the patient's lead instead of trying to control the dialogue.

Basically, just tango on. And hope somebody will do the same for you when your time comes. Unless the big breakthrough happens first.

Tracing the Path from DNA to Dementia

August 29, 2007

The New York Times

Tracing the Path from DNA to Dementia

By IRENE M. WIELAWSKI

Dr. Marcelle Morrison-Bogorad is director of the neuroscience and neuropsychology of aging program at the National Institute on Aging. In collaboration with the Alzheimer's Association, the institute runs the Alzheimer's Disease Genetics Initiative, which is collecting and banking genetic and cellular material from families in which multiple relatives have late-onset Alzheimer's, the most common form of the disease.

Q: How do researchers today differentiate between the brain effects of normal aging and Alzheimer's disease?

A: This is really fundamental to one of our major problems in Alzheimer's research.

We're used to saying that there is memory loss and a decline in brain function as we age. Things get a bit slower. You don't remember quite as readily. But laid on these are changes in cognition that aren't part of normal aging and that indicate that at some point later in time, the person is going to develop Alzheimer's disease.

As the brain ages, inflammation and oxidative damage caused by free radicals increase. Free radicals are very unstable molecules that attack different components of cells, like DNA and protein and lipids, and transform them into oxidized products that do not work as well. It is a sort of brain rusting, to give you an analogy.

There are also age-related changes in the activity of particular genes. When we are young, we have in every cell of our body a rate of production which is very specific for every single one of the 30,000 proteins that we need to keep life going. As aging progresses, the levels of certain of these proteins change, with biological consequences. Specifically, in the brain there are changes in the production of neurotransmitters, which are the molecules responsible for connecting neuronal circuits - the basis for memory. The connections between neurons, called synapses, get weaker in certain areas of the brain.

It turns out to be very tricky to differentiate between changes that are normal aging and changes that are due to Alzheimer's disease. Normal aging makes you even more susceptible to developing the pathology of Alzheimer's disease, such as amyloid plaques and neurofibrillary tangles, and dementia.

Q: What do we know about the genetic risk of Alzheimer's disease?

A: We know most about early-onset Alzheimer's disease, which you can get as early as age 30, ranging up to age 65. That's because about 10 percent of early-onset disease is inherited in an autosomal dominant fashion, which means that if your mother or father has the disease, you have a 50 percent chance of getting it, too. The rest of early-onset disease is not inherited in such an all-or-nothing fashion, but certainly the disease tends to run in families.

As for late-onset disease, it looks like quite a large percentage runs in families as well. It therefore has a genetic component, but it is more like having a risk factor gene for heart disease. Having a family where Alzheimer's occurs certainly increases your chances of developing it, perhaps about threefold in some estimates, although that is a very soft number. But it certainly doesn't mean that you yourself will get it.

Q: What gene mutations are involved in Alzheimer's disease?

A: Three autosomal dominant genes have been identified for early-onset disease. The first one is the amyloid precursor protein (APP) gene, located on chromosome 21. Mutations in the APP gene lead to an increase in the production of amyloid, which is the major component of the plaques that develop in the brains of Alzheimer's patients. The mutation also results in a more sticky form of amyloid.

The other two genes in early-onset disease are called presenilin 1 (PS1) and presenilin 2 (PS2). Mutations in these genes cause them to act as molecular scissors that help cut the amyloid out of the precursor protein. They cut it more rapidly, and they cut it in a form which is more toxic. These mutations account for only perhaps 1 percent of the total number of Alzheimer's cases, but they gave us very important clues as to where to focus our research.

For late-onset Alzheimer's, the only risk factor gene known right now is ApoE-4. You can have one or two copies, or no copies, of the gene. According to how many copies you have, your risk of getting Alzheimer's increases. If you have one copy, you usually get the disease earlier. If you have two copies, then perhaps much earlier.

Q: Is it useful for someone who, say, has older relatives with late-onset Alzheimer's to seek genetic testing?

A: There is a great difference in the value of genetic testing between early-onset and late-onset disease. In genetic tests of people with a family history of early-onset disease, testing can determine pretty much for sure that they will or will not get it. In terms of late-onset disease, it is much trickier. All the genetic tests can tell patients is that their risk of getting Alzheimer's is increased, nothing more.

Perhaps when we find a few more late-onset genes and you can do a mix of them, then the predictive value might be higher, but we are not at that stage yet. We don't know for sure any other late-onset genes, although there are several promising candidates. That's why we have the Alzheimer's Disease Genetics Initiative: to try to find other late-onset genes that are risk factors for Alzheimer's.

Q: Why are biological markers, whether gene mutations or pathological brain changes, important to the development of effective treatments for Alzheimer's disease?

A: At the moment, all that we have to measure efficacy in clinical trials are psychological tests: how well you are doing compared to how well you did a year ago. There is quite a lot of variability in Alzheimer's patients as to how they are doing mentally. You can do a test one day and get one result, and the next day you might get a different result. In order to account for these differences, you have to do the trial for quite a long period - years. We're hoping that one or two of the biomarkers, whether through imaging or biochemical studies, will give better, more accurate indications whether a drug has an effect or not.

Q: What do scientists hope to learn from the Alzheimer's Disease Genetics Initiative?

A: Just as the genes for early-onset disease gave us clues about how important amyloid is, identifying those for late-onset Alzheimer's will give us clues about other pathways which are important. That will give us new avenues for potential therapies, so that when a patient comes to a doctor's office, the doctor can do a test and say, "Well, you've got the ApoE-4 gene, so you are at risk. But you don't have any of the other risk factor genes, so you aren't very much at risk."

The ApoE-4 gene turns out to be a very strong risk factor for late-onset Alzheimer's. Other risk factor genes that we don't know about yet probably have much smaller effects, but there might be quite a few of them. In order to find genes with much smaller effects, we have to analyze many thousands of cases. Our genetics initiative in large part is a way of collecting enough DNA samples from controls and diseased individuals that geneticists can find the remaining risk factor genes.

Q: How close are scientists to finding effective treatments for Alzheimer's disease?

A: Not as far along as we would like. Unfortunately, there are no clinical trials whose results say this drug stops the disease or this drug will prevent it. But there are drugs which are being tested in the preclinical phases, some being developed from basic science findings and some being tested in humans right now. These include drugs that attack different parts of the process of plaque formation, including blunting the scissors that cut the amyloid and preventing amyloid aggregation. Another approach currently being tested is immunotherapy, which is like giving a vaccine to protect against infection. The idea is to induce the body to develop antibodies against amyloid. Clinical trials are underway, but there are no results yet. If we're lucky we could have something in five years. If we're unlucky, who knows?

One of the reasons it is hard to develop drugs for Alzheimer's is that the brain is the most complicated organ in the body by many, many fold. Because Alzheimer's pathology begins to develop before the patient shows any signs, drugs for prevention would need to be taken for many years. So these drugs need to be targeted very specifically, and they need to be very safe with minimal side effects. It's going to take a lot of work to get it just right.

What to Ask About Alzheimer's Disease

August 29, 2007

The New York Times

What to Ask About Alzheimer's Disease

BY IRENE M. WIELAWSKI

Confronting a new diagnosis can be frightening - and because research changes so often, confusing. Here are some questions you may not think to ask your doctor, along with notes on why they're important.

How can we be sure my symptoms aren't the result of a stroke, mental illness or another treatable condition?

There is no definitive test for Alzheimer's disease, and it can be misdiagnosed in patients suffering depression, memory deficits because of normal aging, arterial blockages or even certain vitamin deficiencies. Doctors generally rule out other possibilities, then apply criteria developed by various medical organizations to arrive at the diagnosis.

What stage of Alzheimer's disease am I in? What comes next?

Clinicians classify the progressive deterioration of brain function in Alzheimer's disease into seven stages. By the last stage, patients require round-the-clock care. In the first, second and third stages of this slow moving illness, symptoms are minimal, and many patients work and live independently.

What can I do to preserve my health and mental abilities for as long as possible?

Although there are no treatments to halt or cure Alzheimer's disease, recent studies have suggested that exercise, a healthy diet and mental stimulation may delay the onset of disabling symptoms.

What physical symptoms should I anticipate?

Patients typically complain of problems with memory and organizational ability, but Alzheimer's disease also attacks the brain's motor centers, resulting in problems with balance, coordination, bladder and bowel control, and certain reflexes, including the ability to swallow. Patients and their caregivers should prepare for mental and physical disabilities.

Should I undergo brain neuroimaging?

Imaging of the brain occasionally can help differentiate Alzheimer's disease from other potential causes of dementia in new patients; however, imaging is rarely useful for determining the severity of the disease.

My children are worried about inheriting this illness. Would it be useful for our family to undergo genetic testing?

Scientists have identified several gene mutations associated with an increased risk of developing Alzheimer's disease, but the predictive value of each mutation is low. As a result, genetic testing is useful only for individuals who have several close relatives suffering from early-onset forms of the disease.

What drugs are currently available for Alzheimer's disease, and how well do they work?

Two types of drugs are currently prescribed for treatment of Alzheimer's disease. Cholinesterase inhibitors, such as donepezil and galantamine, regulate acetylcholine, a neurotransmitter influential in learning and memory. The only NMDA receptor antagonist on the market, memantine, tamps down excessive brain activity. Both types have been shown to delay brain deterioration for a brief period (6 to 12 months) in about half the people treated.

My family is afraid to let me drive. Would you refer me for a driving evaluation so we can have an objective opinion of my ability?

Driving is often a focal point of familial controversy. Diagnosis of Alzheimer's disease doesn't always require that a patient immediately stop driving. An objective medical evaluation can be helpful in clarifying the extent of a new patient's disability.

What can I do to make things easier on my family?

Because Alzheimer's erodes cognitive ability, it's important for patients to plan for a day when they can no longer take care of their affairs. Newly diagnosed patients should execute medical and durable powers of attorney that authorize spouses or other family members to deal with banks, insurance companies, doctors and others on their behalf.

 

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