Friday, December 30, 2011

Small brain cortex may mean early dementia

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By RICK NAUERT PHD Senior News Editor
Reviewed by John M. Grohol, Psy.D.
Size may matter in predicting the chance for Alzheimer’s disease as new research suggests an association between the size of various brain regions and the risk for very early Alzheimer’s disease.

The study suggests people with smaller regions of the brain’s cortex may be at risk.

Researchers have published their findings in the online issue of Neurology®, the medical journal of the American Academy of Neurology.

“The ability to identify people who are not showing memory problems and other symptoms but may be at a higher risk for cognitive decline is a very important step toward developing new ways for doctors to detect Alzheimer’s disease,” said Susan Resnick, Ph.D.

For the study, researchers used brain scans to measure the thickness of regions of the brain’s cortex in 159 people free of dementia with an average age of 76.

The brain regions were chosen based on prior studies showing that they shrink in patients with Alzheimer’s dementia.

Of the 159 people, 19 were classified as at high risk for having early Alzheimer’s disease due to smaller size of particular regions known to be vulnerable to Alzheimer’s in the brain’s cortex, 116 were classified as average risk and 24 as low risk.

Investigators tested subjects at the beginning of the study and over the next three years. Researchers administered tests that measured memory, problem solving and ability to plan and pay attention.

The study found that 21 percent of those at high risk experienced cognitive decline during three years of follow-up after the MRI scan, compared to seven percent of those at average risk and none of those at low risk.

“Further research is needed on how using MRI scans to measure the size of different brain regions in combination with other tests may help identify people at the greatest risk of developing early Alzheimer’s as early as possible,” said study author Bradford Dickerson, MD.

Researchers also discovered that 60 percent of the group considered most at risk for early Alzheimer’s disease had abnormal levels of proteins associated with the disease in cerebrospinal fluid — which is another marker for the disease — compared to 36 percent of those at average risk and 19 percent of those at low risk.

Source: American Academy of Neurology

Wednesday, December 28, 2011

A New Way to Detect Alzheimer's Years Before Symptoms Appear

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The Atlantic

Afflicting millions of patients, Alzheimer's disease is becoming a growing burden to healthcare systems around the world. The condition is typically diagnosed after symptoms of mild cognitive impairment arise. Not all patients with mild cognitive impairment, however, develop Alzheimer's. To understand what sets Alzheimer's patients apart, scientists at the VTT Technical Research Centre (Espoo, Finland) set out to use biomarkers to look at the molecular changes behind the disease.

The new research indicates that a biochemical assay from a serum sample could be used to predict Alzheimer's disease months or years before symptoms begin to take a toll on a patient. Professor Matej Orešič from the VTT Technical Research Centre believes that the disease is preceded by a molecular signature indicating potential involvement of hypoxia and an up-regulated pentose phosphate pathway.

The research could lead to the development of a clinical test that could complement the neurocognitive assessment now used by physicians to help diagnose Alzheimer's.

As the announcement explains:

The team used metabolomics, a high-throughput method for detecting small metabolites, to produce profiles of the serum metabolites associated with progression to AD. Serum samples were collected at baseline when the patients were diagnosed with AD, MCI, or identified as healthy controls. 52 out of 143 MCI patients progressed to AD during the follow-up period of 27 months on average. A molecular signature comprising three metabolites measured at baseline was derived which was predictive of progression to AD. Furthermore, analysis of data in the context of metabolic pathways revealed that pentose phosphate pathway was associated with progression to AD, also implicating the role of hypoxia and oxidative stress as early disease processes.

The unique study setting allowed the researchers to identify the patients diagnosed with MCI at baseline who later progressed to AD and to derive the molecular signature which can identify such patients at baseline.

Though there is no current therapy to prevent AD, early disease detection is vital both for delaying the onset of the disease through pharmacological treatment and/or lifestyle changes and for assessing the efficacy of potential AD therapeutic agents. The elucidation of early metabolic pathways associated with progression to Alzheimer's disease may also help in identifying new therapeutic avenues

Monday, December 26, 2011

Dementia linked to body's clock in elderly women

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dailyRx)Dementia more often occurs in elderly women who are physically inactive, are active later in the day, or have abnormal sleep-wake schedules.

The group has an 80 percent higher chance of developing mild cognitive impairment (MCI) or dementia, says Greg Tranah, Ph.D., a scientist at the California Pacific Medical Center Research Institute in San Francisco. His team studied almost 1,300 women for five years.

Worried about memory loss? See a physician.
Most people's body clock, the circadian rhythm, helps wake them up between 6 a.m. and 8 a.m. They go to bed between 10 p.m. and 12 a.m. Normal rhythms vary for Individuals, but they are fairly regular.

In Dr. Tranah's study, women were less likely to develop dementia or MCI if they had strong circadian rhythm activity or were most physically active between 1:34 p.m. - 3:51 p.m..

The researchers collected data on activity and circadian rhythm from healthy women, all older than 75 (mean age 83). None lived in a nursing home or other group facility. No one had cognitive impairment or dementia when the study started.

After five years,15 percent of the women had developed dementia. MCI occurred in 24 percent. At highest risk were women with weaker circadian rhythm activity, lower levels of activity, or whose peak activity occurred after 3:50 p.m.

“We’ve known for some time that circadian rhythms can have an impact on the brain and the ability to function normally,” Dr. Tranah says. "This is the first study to show such a strong connection between circadian rhythm and the subsequent development of dementia or MCI."

No one knows why circadian rhythm and mental status are linked. A decrease in one might cause the other, says Dr. Tranah.

He says new research should study whether dementia and MCI rates improve after elderly women increase physical activity or use light to influence circadian rhythms.

Dr. Tranah and his team published their observational study in the Annals of Neurology.

Saturday, December 24, 2011

Can you deduct the cost of a caregiver?

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Michael Gilfix

Yes, assuming that they are "qualified long term care services." To satisfy the IRS, you have to verify, primarily by a carefully written letter from her personal physician, that states that a) she is chronically ill b) the services are provided in accordance with the physician's plan of care, and c) she required care and supervision to protect her from threats to her health and safety due, for example, to her diminished capacity. Her CPA will rely on Section 213 of the Internal Revenue Code in determining whether or not your mother's care qualifies.

Note: Physicians don't think about tax deductions when they care for their patients. Its OK to tell them about this opportunity and about the need for an appropriate letter or written plan.

Also, these expenses can only be itemized deductions if they exceed 7.5% of her adjusted gross income.

Remember to issue 1099s for each of the caregivers and submit to the IRS at year end.

Tuesday, December 20, 2011

Volunteers key to curing Alzheimer's disease

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NAPSI)—Although more than 5 million people age 65 and older in the U.S. are currently living with Alzheimer’s disease (AD), and while that number is expected to jump to 13.5 million by 2050, there is reason to hope. That’s good news for the almost 15 million more Americans—family members, friends, neighbors and volunteers—currently caring for their loved ones with AD without any real options to help them get better.

Alzheimer’s is the only disease in the top 10 causes of death without a way to prevent, cure or even slow the progression of the disease. In fact, between 2000 and 2008, deaths from AD increased by 66 percent, while deaths from HIV, stroke, heart disease and prostate cancer all declined significantly.

Scientists have learned a great deal about potential underlying causes of AD, and advancements in treatments have been accomplished in recent years. To spur more breakthroughs and speed discoveries, scientists are focusing on early detection through neuroimaging of the brain.

“We have to understand Alzheimer’s from its earliest signs in order to treat it effectively,” said Michael Weiner, M.D., principal investigator of the Alzheimer’s Disease Neuroimaging Initiative (ADNI). “If we can get a fuller picture of the brain and identify signs of the disease before someone gets ill, we can develop better treatment options, which could slow the progression and one day even prevent or cure Alzheimer’s.”

ADNI, the largest Alzheimer’s study of its kind, is now in its second phase (ADNI 2). Scientists are looking for volunteers ages 55−90 to participate in the study to allow them to continue their research at the pace needed to be successful against the disease. They are seeking healthy individuals, those with some memory concerns and people with diagnosed AD.

Participants will not only be contributing to the search for treatments and a cure for AD, they will also have the benefit of access to leading medical experts in the field. In many communities, it is difficult to find someone who knows specifically about Alzheimer’s disease, so clinical trials can be a great way to work with specialists.

“We cannot cure what we do not understand,” said Dr. Weiner. “But with the help of volunteers across the nation, we’re on the right path and making great strides to end the Alzheimer’s epidemic.”

To volunteer or learn more about the study, contact the National Institute on Aging’s Alzheimer’s Disease Education and Referral (ADEAR) Center at (800) 438-4380 or visit www.adni-info.org.

Sunday, December 18, 2011

IV treatment for dementia

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Globe

In this year’s blockbuster Rise of the Planet of the Apes, a scientist reverses his father’s Alzheimer’s disease with a simple shot in the arm. The cure was temporary. But not entirely far-fetched.

Canadian scientists are working on an intravenous treatment for Alzheimer’s that could halt the progression of the disease and improve cognitive functions – without the risk of a mass ape revolt.

Vancouver researcher Neil Cashman and colleagues have discovered a biomarker on toxic molecules called amyloid-beta (a-beta) oligomers, which are catalysts in the brain degeneration of Alzheimer’s.

Their industry partner, Cangene Corp., a Winnipeg-based biopharmaceutical company, is developing antibodies designed to attack the toxic molecules without harming healthy ones.

If their work is successful, the antibodies could be used as an immune therapy for Alzheimer’s, or as a preventive vaccine, says Dr. Cashman, scientific director of PrioNet Canada, a network of centres conducting research into neurodegenerative disorders.

“We believe that we’ve found a target – perhaps the target – for treatment of Alzheimer’s disease,” he says.

Alzheimer’s is a neurodegenerative disorder, not an immune disease. Nevertheless, the immune system can be harnessed to defend against the harmful molecules involved in Alzheimer’s, says Dr. Cashman, a specialist in neurological diseases at the University of British Columbia.

He and other researchers at UBC and the University of Sherbrooke have found that selected antibodies will attack a-beta oligomers in cultured nerve cells. “It renders them non-toxic,” he says.

The next step is to test the treatment on mice engineered to develop Alzheimer’s. Mice studies will be completed at UBC and a lab in Milan, Italy, likely within three months, Dr. Cashman says.

If the work goes as planned, Cangene will begin developing an experimental treatment for clinical trials in humans, he says. “Cangene thinks it’s four years away.”

Immunotherapy for Alzheimer’s is a “very promising approach,” says Paul Aisen, a professor of neurosciences at the University of California, San Diego. But because various types of molecules may be involved in causing the disease, he says, “it’s not clear which precise targets are going to prove most useful.”

Alzheimer’s researchers have been testing different forms of immune therapy for some time. About a decade ago, Elan, a biotechnology company headquartered in Dublin, conducted human trials in the San Francisco Bay area using a vaccine against a-beta molecules. The trials were cut short in 2002 because 6 per cent of the patients developed meningoencephalitis, an inflammation of the brain that resulted in several deaths.

At the time, researchers concluded that the vaccine activated the immune system’s T cells, which attacked a-beta molecules in healthy nerve tissue.

But Dr. Cashman and his colleagues are developing a treatment that will target only a-beta oligomers, using the marker he has found. A-beta oligomers are widely accepted as a main source of neuron-harming toxicity in Alzheimer’s disease, he says.

Recent findings by other researchers suggest that immunotherapy may be a viable treatment, Dr. Cashman says. He points to human trials funded by Baxter International at institutions including the New York-Presbyterian Hospital/Weill Cornell Medical Center. In the multiphase trials, researchers are testing antibodies prepared from the blood of healthy plasma donors, known as intravenous immunoglobulin (IVIG), on patients with mild to moderate Alzheimer’s. “They’re getting remarkable results,” Dr. Cashman says.

In April, 2010, Baxter released unpublished findings of a phase II study showing that patients with Alzheimer’s who received IVIG had less brain atrophy and better cognitive functioning after 18 months compared with patients in a control group.

The Baxter trials are taking what some researchers call a “kitchen sink” approach to immunotherapy, giving patients a blood product containing all available human antibodies in hopes that some will be of benefit.

Instead, Cangene will select specific antibodies to develop an IVIG product with a “more concentrated effect,” Dr. Cashman says. Given Baxter’s success using unselected IVIG, he adds, “I think it’s actually going to work.”

But others are skeptical, and several Canadian specialists declined to comment on such early research.

Dr. Aisen cautions against jumping to conclusions based on the success of Baxter’s phase II study. Since only 14 patients received the full course of IVIG, the evidence that immunotherapy can halt Alzheimer’s is “too preliminary,” he says.

Dr. Aisen was not involved in the phase II trial, but he and colleagues at Alzheimer’s Disease Co-operative Study are conducting Baxter’s phase III trials using IVIG. The team has recruited 380 patients with mild to moderate Alzheimer’s for the third study, which is set for completion in about a year. Although the phase II results are encouraging, he says, “we really want to see the results of the larger study.”

In the meantime, Dr. Aisen suggests that lab experiments on cultured nerve cells and mice provide little evidence that a cure for Alzheimer’s is on the horizon.

“It’s a long way from a cell culture study to a human treatment,” he says

Friday, December 16, 2011

Transcending Dementia through the TTAP Method

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The brain-stimulating approach known as Therapeutic Thematic Arts Programming (TTAP) has a proven record of improving the lives of people with dementia by increasing their engagement and functioning. In Transcending Dementia through the TTAP Method: A New Psychology of Art, the Brain, and Cognition you now have all the tools and instructions for putting this innovative and life-affirming approach to work in your own care setting. You too can successfully invigorate the minds and hearts of people living with this challenging cognitive disease.

Participation in the creative arts has been shown to promote cell growth that enhances the brain’s ability to learn and recall new information, create new ideas, and make new connections. Using 12 separate forms of creative expression — ranging from sculpture and painting to physical movement and mental imagery — TTAP builds on themes in an integrative way that helps each individual with dementia draw upon memories, feelings, and intellectual reserves that promote positive self-regard and active social participation. Sample activity protocols guide you through the process of engagement to help you quickly master the steps.

Activities using the TTAP method can provide

significant stimulation and integration of multiple brain regions
enjoyment, engagement, creativity, relaxation, and a sense of purpose for people with even advanced dementia
an easy-to-follow framework that allows infinite variations on themes and personal interests
complete documentation for tracking and evaluation
opportunities for one-on-one or group programming
By blending the principles of art and therapeutic recreation with the latest findings in brain research, Transforming Dementia through Therapeutic Thematic Arts Programming presents an exciting new psychological taxonomy that captures the dynamic interplay between brain functioning and expressive and emotional stimulation.

Wednesday, December 14, 2011

Simple way to fight Alzheimer's disease

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ANI

Washington, (ANI): Scientists have developed a surprisingly simple method to design antibodies aimed at combating disease.

Antibodies are large proteins produced by the immune system to combat infection and disease. They are comprised of a large Y-shaped protein topped with small peptide loops. These loops bind to harmful invaders in the body, such as a viruses or bacteria

Once an antibody is bound to its target, the immune system sends cells to destroy the invader. Finding the right antibody can determine the difference between death and recovery.

When trying to design an antibody, the arrangement and sequence of the antibody loops is of utmost importance. Only a very specific combination of antibody loops will bind to and neutralize each target.

With billions of different possible loop arrangements and sequences, it is seemingly impossible to predict which antibody loops will bind to a specific target molecule.

The new antibody design process was used to create antibodies that target a devastating molecule in the body - the Alzheimer's protein.

The research, led by Assistant Professor of Chemical and Biological Engineering Peter Tessier, uses the same molecular interactions that cause the Alzheimer's proteins to stick together and form the toxic particles that are a hallmark of the disease.

"We are actually exploiting the same protein interactions that cause the disease in the brain to mediate binding of antibodies to toxic Alzheimer's protein particles," Tessier said.

Alzheimer's disease is due to a specific protein, the Alzheimer's protein, sticking together to form protein particles. These particles then damage the normal, healthy functions of the brain. The formation of similar toxic protein particles is central to diseases such as Parkinson's and mad cow disease.

Importantly, the new Alzheimer's antibodies developed by Tessier and his colleagues only latched on to the harmful clumped proteins and not the harmless monomers or single peptides that are not associated with disease.

The study has been published in the Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS). (ANI)

Monday, December 12, 2011

New Vaccine for Alzheimer's Disease

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CANBERRA, Dec. 10 (Xinhua) -- Australian scientists from University of Sydney on Saturday announced they have developed a vaccine to help halt the progression of Alzheimer's disease of humans in a joint race.

The vaccine, which targets a damaged protein inside brain's nerve cell known as tau, prevents the ongoing neurofibrillary tangles in the brain of a mouse with Alzheimer's disease. The progress of neurodegenerative condition affects more than 35 million people worldwide.

The research team at the University of Sydney's Brain and Mind Research Institute (BMRI) was led by Associate Professor Lars Ittner, from the Alzheimer's and Parkinson's disease Laboratory.

Professor Ittner said so far the vaccine was only tested in mice with Alzheimer's and results have shown it can stop the disease progressing.

"Our study is the first to show that a vaccine targeting the tau protein can be effective once the disease has already set in," he said in a statement.

"Most of the other vaccines targeting tau were tested only before or around the onset of the disease in animal models, but the vast majority of people with Alzheimer's disease are only diagnosed after the symptoms have appeared."

According to Ittner, his team are working with a major pharmaceutical company on developing the vaccine for human trials within five years.

While none of the vaccines is considered a cure, the team was collaborating with the U.S. pharmaceutical industry to develop this new vaccine and about 269,000 Australians suffering from dementia will therefore be benefited.

Currently, there are some existing drugs can help stop Alzheimer's and other forms of dementia from getting worse. However, they do not tackle the underlying causes and become less effective over time.

The scientists published details of study on the vaccine in scientific journal PLoS ONE this week.

Saturday, December 10, 2011

Dementia risk is higher if you have.....

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HealthDay News -- Patients with diabetes who have comorbid depression are at increased risk for developing dementia compared with those with diabetes alone, study results indicate.

"Given that depression is potentially modifiable, future studies are needed to further evaluate whether effective depression interventions reduce the risk of dementia and identify the mechanisms that may explain our observation," Wayne Katon, MD, from the University of Washington in Seattle, and colleagues wrote in the Archives of General Psychiatry.

They surveyed a random sample of 19,239 patients with type 2 diabetes, aged 30 to 75 years, from the Diabetes and Aging Study to identify prevalent cases of depression. Dementia diagnoses were identified based on International Classification of Diseases, Ninth Revision-clinical modification [ICD-9-CM] criteria three to five years post-baseline to ensure that depression was not a prodrome of dementia. The researchers then estimated dementia risk for patients with depression and diabetes relative to patients with diabetes alone using Cox proportional hazard regression models adjusted for sociodemographic, clinical, risk factors and healthcare use.

One or more dementia diagnosis occurred in 2.1% of 3,766 patients with diabetes and comorbid depression, and in 1% of the 15,473 patients with diabetes alone (incidence rate=5.5 and 2.6 per 1,000 person-years, respectively), the researchers found. A 100% increased risk of dementia was observed in patients with comorbid depression (adjusted HR=2.02).

Previous studies have associated depression with poorer adherence to diet and exercise regimens, increased rates of cigarette smoking and higher HbA1c levels, according to the researchers, which could "worsen the course of diabetes and increase the risk of dementia associated with depression."

However, controlling for these potential confounding factors did not significantly change the risk for dementia among these patients. "These data suggest that biologic factors associated with depression may be important risk factors for dementia in patients with type 2 diabetes," the researchers wrote. They called for more studies to further examine potential mechanisms of action.

One of the study researchers disclosed financial ties to the pharmaceutical industry.

Katon W et al. Arch Gen Psychiatry. 2011; doi:10.1001/archgenpsychiatry.2011.154.

Thursday, December 8, 2011

An apple a day should keep dementia at bay

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Eoxnews

Anew study finds that white fruit reduces your risk of having a stroke or getting vascular dementia

The old adage that "an apple a day keeps the doctor away" is a good one to follow, according to a new Dutch study. The researchers found that eating plenty of fruits and vegetables with white flesh, such as apples and pears, may protect you against stroke and vascular dementia.
"To prevent stroke and vascular dementia, it may be useful to consume considerable amounts of white fruits and vegetables," Linda M. Oude Griep, lead author of the study and a postdoctoral fellow in human nutrition at Wageningen University in the Netherlands, said in a statement. "For example, eating one apple a day is an easy way to increase white fruits and vegetable intake."

Although previous research has shown the positive health benefits of daily fruit intake, the new study suggests a link between stroke risk and fruits and vegetables of certain colors.
Orange, green and red

Researchers looked at the answers 20,000 adults gave to questions about what they ate over the previous year. The average age of the participants was 41, and all were free of cardiovascular diseases at the study's start.
Over the next 10 years, 233 suffered strokes. The researchers found that the risk of stroke was 52 percent lower for people with a high intake of white fruits and vegetables, compared with people who ate few foods in that color group.
The researchers classified fruits and vegetables into four color groups: orange/yellow, which contained mostly citrus fruits; green, which had dark leafy vegetables, cabbages and lettuce; red/purple, for mostly red vegetables; and white, of which 55 percent of the foods eaten were apples and pears.
The fruits were grouped based on the color of their flesh, not their skin. For example, a red apple belongs to the white group because although its skin is red, its flesh is white.
The color of the edible portion of fruits and vegetables reflects the presence of plant compounds such as carotenoids, which are organic pigments, and flavonoids.

Food color and stroke and vascular dementia risk
Apples and pears may lower stroke risk because they are high in dietary fiber and an antioxidant flavonoid called quercetin, the researchers said. Other foods classified in the white category were bananas, cauliflower and cucumbers. (Potatoes were classified as a starch.)
Green, orange/yellow and red/purple fruits and vegetables didn’t affect participants' stroke risk, according to the study, but the study authors said that people shouldn't dismiss them as less beneficial overall.

:Other fruits and vegetable color groups may protect against other chronic diseases," Oude Griep said.

The researchers also warned that the study findings should be interpreted with caution because food frequency questionnaires are subject to errors.
"The observed reduction in stroke risk might further be due to a generally healthier lifestyle of individuals consuming a diet rich in fruits and vegetables," according to Dr. Heike Wersching, of the Institute of Epidemiology and Social Medicine at the University of Münster in Germany, who was not involved in the study but wrote an editorial accompanying it in publication.

The study was recently published in Stroke: Journal of the American Heart Association.
Pass it on: Increasing your daily intake of "white fruits," such as apples, pears and bananas, may lower your risk of stroke, a new study shows.


Read more: http://www.foxnews.com/health/2011/09/16/try-upping-white-fruits-to-avoid-stroke/#ixzz1eODJF3tX

Tuesday, December 6, 2011

Top ten traveling tips when traveling with elderly family (part 4)

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AgingCare

By Leonard J. Hansen

8. Consider Destination and Travel Options
The world of travel is open to just about everyone, even those elderly parents receiving care. Start a discussion with Mom or Dad to learn her or his travel wishes. Determine if your parent can travel solo, or if you want or need to share in the adventure. Start with the mission of fulfilling a parent's dream; don't just go online to find cheap air tickets.

9. Consider Tours and Cruises
There are thousands of tour and cruise possibilities. Tours and cruises offer a unique service, in that they are totally planned, operated and staffed to deliver the promised program and destination discovery. Several tours operators, including Accessible Journeys and Flying Wheels, specialize in "accessible lifestyle vacations," which cater to those with special needs and disabilities.
Cruise and tour accommodations are priced on a per-person basis based on double-occupancy. Therefore, if choosing a tour or cruise, travel with your Mom or Dad to provide caregiving assistance while in the room and during non-programmed times. A cruise or tour may be the ultimate escape and very civilized adventure.

10. Ensure Those at The Destination are Prepared
If your parent is flying solo to visit other family, schedule a telephone conference with your relatives to go over the caregiving support your elder needs. Advise of your approach in assisting Mom or Dad, so that they do not assume to take the domineering and dictating role. Advise of your parent's favorite foods and activities so that they can try to be accommodating during the visit, making it all the more "like home" for Mom or Dad. And, importantly, advise of the medical and medication regimen that must be followed. Also make sure that they have all important legal documents with them should an emergency arise (for example, if you are listed as their agent for the Advance Directive, be certain this information is with them should something happen).
On the day of travel, arrive at the airport or other transportation two hours early, to visit with your parent without pressure, share a meal or snack, review the travel plan and itinerary and, importantly, to use the wheelchair-capable restroom shortly before heading to the gate. The latter should reduce the need for your parent to access the small restroom during travel.

In Summary
Travel with Mom or Dad. You may find it to be one of the best experiences of your life. Yes, you continue to be a caregiver, but your travel and destination will probably prove to be an escape, a freedom because of the new setting, environment and opportunity.
Travel safely and well.

Sunday, December 4, 2011

Top ten traveling tips when traveling with elderly family (part 3)

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AgingCare

By Leonard J. Hansen


5. Think about Safety, Security and Comfort
There are thieves everywhere and, particularly, in high-traffic travel centers. Don't give the scalawags any opportunity to steal from your parent.
Mom should not carry a purse but, instead a money belt worn under a blouse or a neat Passage Wallet hidden under her coat by a neck cord. Dad should not carry a wallet in his back pocket but, instead, the same Passage Wallet from the neck cord or as a hidden wallet tucked into his pants and secured by a cord to his belt.
Advise Mom or Dad, if traveling alone, always to keep their carry-on between their feet when standing, or with the shoulder strap looped around the leg of a chair when seated.
For comfort, consider the purchase of a travel pillow, a c-shaped balloon that supports the neck and head when resting aboard transportation.
6. Arrange Medication Management
Most mature adults take five or more medications once or even several times a day. The transportation staff has no obligation regarding the medical dosing of your parent. But you can ask in advance that at a specified time (stated in local time), the staff remind Mom or Dad to take the medication. The alternative is to provide your parent with an alarm watch.

7. Plan for Security Checkpoints
If Mom or Dad is in a wheelchair at transportation centers, access to and through TSA (transportation security administration) security may actually be quicker than through the long line of other travelers.
Brief your parent (or state to the TSA, if you are traveling together) about any medical condition that would set off alarms, such as surgical hip and knee implants. To avoid unwanted delays, get a physician's statement about the implanted steel and make sure the senior has that documentation with them. Oftentimes, personnel will ask the elder to step aside and perform a wand screening, rather than passing through the sensors. If your parent is in a wheelchair, security will use a wand while he or she is seated.
Dress your parent in easily-removed (but safe) walking shoes. Security will probably want them removed. Present, if pertinent, any physician statement regarding your Mom or Dad's medical condition or limitation.
Before traveling, explain to Mom or Dad that the security process is vital to her or his safety.

8. Consider

Friday, December 2, 2011

Top ten traveling tips when traveling with elderly family (part 2)

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AgingCare

By Leonard J. Hansen


3. Prepare Documentation
A government passport is accepted as the highest level of identification by federal TSA security officers. If you or your parent do not already have a passport, consider applying for such months prior to your travel. Your local post office will have the application forms; or you can go online to access the information and forms. Official photographs are available at AAA offices and at many large drug and department stores. Personal photos are not acceptable. Two copies of the photograph must be sent with your application.
Request copies of prescriptions and/or statements of medical conditions from each physician and medical treatment center.
Make at least four photocopy sets of the passport, driver's license, Medicare and insurance cards, travel tickets and itinerary, boarding pass (if secured in advance online), plus any physician prescriptions and/or statements. One complete set is placed in your parent's hand-carry bag, another in his or her roll-aboard luggage. One set is forwarded to family at the arrival destination, and one is left at home.
Provide a telephone calling card so that he or she can maintain contact. An alternative is to provide a cell phone, perhaps one with a predetermined number of minutes. Program in your telephone number as the first emergency number.

4. Be Practical When Packing
Pack light. For a person traveling with at least some limitation, aim to pack everything necessary in a roll-aboard suitcase plus a medium-size over-the-shoulder carry-on. Do not check the roll-aboard as luggage, as in-cabin flight staff will gladly stash it in the overhead rack. Such will save a lot of time at the final destination airport.
All prescription and over-the-counter medications should be placed in a one quart zip-lock freezer bag, including also copies of any prescriptions and/or physician statements in the hand-carry bag. Do not place the pill combinations separately into a separate plastic box as "the next combined dosage." Such will never get through security. Enclose also any medical appliances such as extra braces or first-aid needs.
If Mom or Dad is toting gifts to relatives, do not wrap them. Place the items in the roll-aboard luggage.
If your parent is traveling alone, before you close up her or his carry-aboard bag, prepare and slip in at the top a note stating "I love you" and "I delight in your new adventure."

5. Think about

Wednesday, November 30, 2011

Top ten traveling tips when traveling with elderly family

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AgingCare

By Leonard J. Hansen

Travel may be one of the greatest gifts you can give Mom or Dad.
The trip may be to visit other family and, particularly, grandkids and great grandchildren. It may be an adventure to a destination, aboard a cruise ship or even a return to a home of long ago.
You may accompany your parent; or, if he or she can maintain some independence, the trip may be solo. Either way, there are 10 important steps to take:
1. Research and Plan Ahead
Whether you will travel together or your parent will be solo, planning, reserving and confirming must be accomplished sooner rather than later. When the destination is resolved with target dates, research airlines, Amtrak, buses, cruise lines. For air and land transportation, seek the most direct and shortest travel times.
If there is a choice of three airlines, for example, enroll your parent in the no-cost frequent flier program for each. This should give you access to the lowest fares and possible benefits at the airport and aboard the flight, as well as for requesting special services.
Know that once very common, most senior discount fares are history except for Southwest Airlines and Amtrak. To find other senior-special offers, go online to SmarterTravel.com.

2. Request and Reserve Special Services
Request seat assignment in the rows designated for disabled travelers. And, importantly, request cost-free wheelchair service at every airport origination, connection and arrival location. If there is meal service aboard, advise the reservation system of any dietary needs.
If traveling alone, ensure your parent will have human assistance from the counter, through security, to the gate and then to aboard the aircraft. If staffed by an airline employee, there is no cost for wheelchair or assistance. If staffed by Red Cap-type personnel, you or your parent will be expected to tip for that assist. If you are traveling together, you can offer to handle the wheelchair.
If you don't make and confirm all of these requests at the time of reservation, the airline, train or bus line has no obligation to make them available on check-in or while en route.

3. Prepare

Monday, November 28, 2011

Scientists discover additional Alzheimer's proteins in the tangles

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Medicine Net

New research in the FASEB Journal suggests that tangles, 1 of the 2 main Alzheimer's markers, consist of proteins called neurofilaments and vimentin as well as the tau protein
Scientists from the National Institutes of Health in the United States have made an important discovery that should forever change the scope and direction of Alzheimer's research. Specifically, they have discovered that the protein tangles which are a hallmark of the disease involve at least three different proteins rather than just one. The discovery of these additional proteins, called neurofilaments and vimentin, should help scientists better understand the biology and progression of the disease as well as provide additional drug discovery targets. This discovery was published in the November 2011 issue of the FASEB Journal .

"Since neurofilaments are the predominant protein in nerve cells, our study suggests that we should refocus our research on the biology of these filamentous proteins in an effort to understand how they are normally regulated and deregulated in response to human aging," said Harish C. Pant, Ph.D., a senior researcher involved in the work from the Cytoskeletal Regulatory Protein Section of the Laboratory of Neurochemistry at the National Institute of Neurological Disorders and Stroke at the National Institutes of Health in Bethesda, Maryland.

To make their discovery, Pant and colleagues identified normal and abnormal proteins present in autopsy samples of the brains of Alzheimer's disease victims. Then they isolated and purified the tangles (which are knots of abnormally aggregated filaments that fill and compromise nerve cells) from the autopsy samples and compared their protein composition to age- and post mortem-matched samples of brains from patients who died of other causes, such as accidents. Through a combination of improved instrumentation and informatics, it was possible to resolve the mixture of proteins successfully and identify the novel Alzheimer's disease proteins. Previous research suggested that only one protein, called "tau," is present in these tangles.

"This is a breakthrough of great importance: tau is not the only target," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "Before this discovery, we approached these tangles as if they were woven of one piece of string. Now we know that there are at least three proteins involved, we're much closer to untangling the Alzheimer's web. Without question, discoveries like this bring us closer than ever to advanced Alzheimer's treatments, and it is a good example of why NIH funding is among the best investments our nation can make toward improving health and well being."

Source: Federation of American Societies for Experimental Biology

Saturday, November 26, 2011

New Study Challenges Accepted Approaches to Research in Senile Dementia

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Health canal

Amsterdam, NL – Impacting millions of families and devouring billions of dollars globally, Alzheimer’s disease is the focus of exhaustive research to find a cure.

Although intensely investigated over the last three decades using cutting-edge technologies, the “pathogenic cause” of Alzheimer’s disease has not been found. While many research “breakthroughs” have been claimed and high-profile drugs trials carried out, why does the promised “cure” still seem to elude scientists?

In an effort to address this question, Ming Chen, PhD, Huey T. Nguyen, BS, and Darrell R. Sawmiller, PhD, Aging Research Laboratory, R&D Service, Bay Pines VA Healthcare System and University of South Florida, undertook an independent and systematic analysis of the underlying research assumptions against the established scientific principles. This analysis led them to hypothesize that perhaps the main problem is the research community’s perception of the disease.

In an article scheduled for publication in the December issue of the Journal of Alzheimer’s Disease the authors suggest that when the National Institutes of Health separated out dementia from other senile conditions and redefined it as a distinct and “curable” disease — Alzheimer’s – in the 1970s, it opened a Pandora’s box and may have misdirected research for decades. It triggered the search for pathogenic factors and cures, and disregarded the role of demographic change and its diverse end results in the elderly.

The authors argue that senile disorders – diseases occurring after age 60 and eventually affecting the majority of the elderly, such as tooth, hearing or memory loss – are caused by aging, thus differ fundamentally from distinct diseases by origin, study paradigm and intervention strategy.

Moreover, the authors contend that a central regulator in cognition − the Ca2+ signaling system − has been misconceived by institutional thinking that favors a “cure” for senile dementia. The dominant hypothesis, although unproven, is that Ca2+ levels rise throughout the aging process, leading to cell death, and thus research has focused on calcium antagonists to lower those levels. This viewpoint has been promoted by policy makers, and the subject of a number of high profile clinical trials, but to date no positive results have emerged.

In contrast, the authors propose that declining functionality of Ca2+ signaling as a result of the aging process, among a myriad of other age-related changes, leads to cognitive decline. Therefore interventions for senile dementia could activate Ca2+ function by promoting energy metabolism and also by Ca2+ agonists such as caffeine and nicotine. At the same time, risk factors play a key role. “Aging and Ca2+ deficits set the stage for senile dementia, but do not always lead to senile dementia in real life,” explains Dr. Chen. “Lifestyles and other risk factors are the key. So we think that senile dementia may be explained by ‘advanced aging plus risk factors.’ This model points to a new direction for prevention. This means we must support the elderly in healthy lifestyles. And we should develop medications to extend the lifespan of old neurons, rather than looking for ways to inhibit far-fetched ‘pathogenic’ factors.”

“The model implies that senile dementia is, by and large, a lifestyle disease,” says Dr. Chen. “This view, in fact, has been shared by many in the medical and clinical community, but contrasts sharply with current dominant theories in the Alzheimer research field, which assume a linear and ‘cause and effect’ mechanism. Since they have not taken into account the fundamental roles of aging and risk factors, it is clear that these theories, though highly appealing to the public and researchers alike, are of little relevance to the scientific nature of senile dementia.”

“The two overwhelming concepts, senile dementia as a distinct disease and the Ca2+ overload hypothesis, have effectively blocked any meaningful progress in senile dementia research, and have inhibited the self-correcting mechanism of science,” concludes Dr. Chen. “An independent scrutiny on the field may be helpful.”

“Although incurable”, Dr. Chen is optimistic. “Our research, if guided by correct theories, will produce medications to help delay dementia to a certain extent − similar to the drugs that delay or ameliorate atherosclerosis and osteoporosis today.”

Sunday, November 20, 2011

Facing the Key Challenges for Fighting Alzheimer's Disease

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WebMD

The Alzheimer's Association in a new report has identified 10 "critical challenges" that need to be addressed by the nation to combat the growth and devastating impact of Alzheimer's disease.

The challenges include lack of funding and problems with diagnosing Alzheimer's.

An estimated 5.4 million Americans are living with Alzheimer's now, and that number is expected to grow to 16 million by the year 2050, according to the Alzheimer's Association.

Because of this looming health crisis, President Obama signed into law the National Alzheimer's Project Act on Jan. 4, with the aim of creating a national strategic plan to address what the Alzheimer's Association described as an "escalating crisis."

The Alzheimer's Association's report, "Alzheimer's from the Frontlines: Challenges a National Alzheimer's Plan Must Address," was produced to help the government develop its strategy.

Findings of the report were based on input from 43,000 people in all 50 states, Puerto Rico, and Washington, D.C.

In all, the Alzheimer's Association hosted 132 public input sessions nationwide, involving people with Alzheimer's, caregivers, researchers, community leaders, and health care professionals.

"We want to make sure the administration is aware of the challenges that emerged, that we heard frequently, during the public input process," Alzheimer's Association spokeswoman Toni Williams tells WebMD. "We thought it would be a good idea to open it up to the public. We are hoping this helps to inform the advisory council and Secretary [Kathleen] Sebelius [of the U.S. Department of Health and Human Services] in formulating a plan."

When a Loved One Has Alzheimer's
Top Challenges in Fighting Alzheimer's

The 10 challenges highlighted by the Alzheimer's Association are:

Lack of public knowledge and awareness of the disease
Insufficient funding
Problems in detecting and diagnosing the disease
Poor dementia care
Inadequate treatments
Specific challenges faced by diverse communities
Specific challenges faced by those with younger-onset Alzheimer's
Unprepared caregivers
Ill-equipped communities
Mounting costs of care
The new report shows that costs relating to Alzheimer's care and treatment will surpass $1 trillion by mid-century unless the current trajectory of the disease changes.

"Individuals, families and communities are at the center of the escalating Alzheimer's crisis," Harry Johns, president and CEO of the Alzheimer's Association, says in a news release.

Call to Action

Americans who participated in the sessions aimed at identifying challenges want the nation's leaders to know that the disease changes lives, and that "they want and deserve a transformational plan that urgently addresses their needs," Johns says.

Robert Egge, vice president of the Alzheimer's Association, says the input sessions made it clear that people are not looking for symbolic acts but the start of "real, transformational action."

He says, "we hope those developing the National Alzheimer's Plan will be inspired and guided by the challenges, experiences and needs echoed throughout this report."

Egge says many Americans know little about the disease, and education is needed about warning signs of the disease and incorrect perceptions about it. Also, though the goal is a cure, better treatments are needed, he says, and more funding for research.

Currently, caregivers are isolated and uninformed about the disease. He says African-Americans and Hispanics are more likely to develop Alzheimer's, and less likely to be diagnosed.

The new plan, he says, "must address disparities in diverse and underserved communities.

Friday, November 18, 2011

Drink away Alzheimer's disease

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TheDenverChannel.com

TAMPA, Fla. -- Imagine slowly losing the sense of who you are and not being able to stop it. Millions of people in the U.S. live with Alzheimer's disease or watch a loved one suffers from it.

Now, researchers are looking at a high-powered prescription shake to ease the symptoms.

At 93, Teresa Alfonzo has seen and done a lot. But because of a devastating diagnosis 10 years ago, she's now fighting to keep her most precious "We started noticing she couldn't take care of herself," Rafael Alfonzo, Teresa's son, said.

The Alfonzo family is one of 35 million families dealing with the devastating effects of Alzheimer's disease. A few months ago, Teresa's ability to remember the most basic skills started to go. She couldn't even draw a clock.

"There was a lot of resistance. I don't understand," Margaret Alfonzo, Teresa's daughter, said.

That's when they decided to try something new. Teresa started on Axona, a medical shake regulated by the FDA. It's like an energy drink for the brain.

"It basically gives the brain an alternative food source," Richard S. Isaacson, M.D., an associate professor of clinical neurology at the University of Miami Miller School of Medicine

"It's a powder, so they mix it with usually a high protein drink, usually a milkshake or Boost, and they drink it right after breakfast," Susan Steen, M.D., a neurologist at South Tampa Memory center, said.

Alzheimer's patients lose the ability to use glucose in the blood. Two hours after drinking Axona, it's converted into ketone bodies that circulate to the brain and produce energy.

"Ketone bodies are the only things aside from sugar your brain can use as food." Dr. Richard S. Isaacson said.

In a 90-day, double blind study of 152 Alzheimer's patients, 77 took Axona. 45 percent of them showed signs of improvement after 45 days. While it doesn't work for everyone, Isaacson says it's worth a shot.

"You have at least a 40 to 45 percent chance of having this medical food work, in my opinion, 40 percent is a lot higher than zero," Isaacson said.

After three months on Axona, Teresa wa able to draw a clock.

"It's a blessing really. It's a huge progress," Margaret said.

Axona is a prescription medical food. The FDA does not approve medical foods, but they do regulate them. It costs $70 to $90 for a 30-day supply.

Isaacson says a genetic test can actually help figure out if Axona will work on patients. Axona's website says the side effects include mild stomach aches and diarrhea.

Wednesday, November 16, 2011

Yeast model connects Alzheimer's disease risk and amyloid beta toxicity

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EurekAlert

In a development that sheds new light on the pathology of Alzheimer's disease (AD), a team of Whitehead Institute scientists has identified connections between genetic risk factors for the disease and the effects of a peptide toxic to nerve cells in the brains of AD patients.

The scientists, working in and in collaboration with the lab of Whitehead Member Susan Lindquist, established these previously unknown links in an unexpected way. They used a very simple cell type—yeast cells—to investigate the harmful effects of amyloid beta (Aβ), a peptide whose accumulation in amyloid plaques is a hallmark of AD. This new yeast model of Aβ toxicity, which they further validated in the worm C. elegans and in rat neurons, enables researchers to identify and test potential genetic modifiers of this toxicity.

"As we tackle other diseases and extend our lifetimes, Alzheimer's and related diseases will be the most devastating personal challenge for our families and one the most crushing burdens on our economy," says Lindquist, who is also a professor of biology at Massachusetts Institute of Technology and an investigator of the Howard Hughes Medical Institute. "We have to try new approaches and find out-of the-box solutions."

In a multi-step process, the researchers were able to introduce the form of Aβ most closely associated with AD into yeast in a manner that mimics its presence in human cells. The resulting toxicity in yeast reflects aspects of the mechanism by which this protein damages neurons. This became clear when a screen of the yeast genome for genes that affect Aβ toxicity identified a dozen genes that have clear human homologs, including several that have previously been linked to AD risk by genome-wide association studies (GWAS) but with no known mechanistic connection.

With these genetic candidates in hand, the team set out to answer two key questions: Would the genes identified in yeast actually affect Aβ toxicity in neurons? And if so, how?

To address the first issue, in a collaboration with Guy Caldwell's lab at the University of Alabama, researchers created lines of C. elegans worms expressing the toxic form of Aβ specifically in a subset of neurons particularly vulnerable in AD. This resulted in an age-dependent loss of these neurons. Introducing the genes identified in the yeast that suppressed Aβ toxicity into the worms counteracted this toxicity. One of these modifiers is the homolog of PICALM, one of the most highly validated human AD risk factors. To address whether PICALM could also suppress Aβ toxicity in mammalian neurons, the group exposed cultured rat neurons to toxic Aβ species. Expressing PICALM in these neurons increased their survival.

The question of how these AD risk genes were actually impacting Aβ toxicity in neurons remained. The researchers had noted that many of the genes were associated with a key cellular protein-trafficking process known as endocytosis. This is the pathway that nerve cells use to move around the vital signaling molecules with which they connect circuits in the brain. They theorized that perhaps Aβ was doing its damage by disrupting this process. Returning to yeast, they discovered that, in fact, the trafficking of signaling molecules in yeast was adversely affected by Aβ. Here again, introducing genes identified as suppressors of Aβ toxicity helped restore proper functioning.

Much remains to be learned, but the work provides a new and promising avenue to explore the mechanisms of genes identified in studies of disease susceptibility.

"We now have the sequencing power to detect all these important disease risk alleles, but that doesn't tell us what they're actually doing, how they lead to disease," says Sebastian Treusch, a former graduate student in the Lindquist lab and now a postdoctoral research associate at Princeton University.
Jessica Goodman, a postdoctoral fellow in the Lindquist lab, says the yeast model provides a link between genetic data and efforts to understand AD from the biochemical and neurological perspectives.

"Our yeast model bridges the gap between these two fields," Goodman adds. "It enables us to figure out the mechanisms of these risk factors which were previously unknown."

Members of the Lindquist lab intend to fully exploit the yeast model, using it to identify novel AD risk genes, perhaps in a first step to determining if identified genes have mutations in AD patient samples. The work will undoubtedly take the lab into uncharted territory.

###
Notes staff scientist Kent Matlack: "We know that Aβ is toxic, and so far, the majority of efforts in the area of Aβ have been focused on ways to prevent it from forming in the first place. But we need to look at everything, including ways to reduce or prevent its toxicity. That's the focus of the model. Any genes that we find that we can connect to humans will go into an area of research that has been less explored so far."

This work was supported by an HHMI Collaborative Innovation Award, an NRSA fellowship, the Cure Alzheimer's Fund, the National Institutes of Health, the Kempe foundation, and Alzheimerfonden.

Susan Lindquist's primary affiliation is with Whitehead Institute for Biomedical Research, where her laboratory is located and all her research is conducted. She is also a Howard Hughes Medical Institute investigator and a professor of biology at Massachusetts Institute of Technology.

Full Citation:

"Functional Links Between Aβ Toxicity, Endocytic Trafficking and Alzheimer's Disease Risk Factors in Yeast"


Sebastian Treusch (1,2), Shusei Hamamichi (1,3), Jessica L. Goodman (1), Kent E.S. Matlack (1,2), Chee Yeun Chung (1), Valeriya Baru (1,2), Joshua M. Shulman (4,5), Antonio Parrado (6), Brooke J. Bevis (1), Julie S. Valastyan (1,2), Haesun Han (1), Malin Lindhagen-Persson (7), Eric M. Reiman (8,9), Denis A. Evans (10), David A. Bennett (11), Anders Olofsson (7), Philip L. DeJager (4,5), Rudolph E. Tanzi (6), Kim A. Caldwell (3), Guy A. Caldwell (3) and Susan Lindquist (1,2)

Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.
Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
Department of Biological Sciences, The University of Alabama, Tuscaloosa, AL 35487.
Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Departments of Neurology & Psychiatry, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115.
Program in Medical and Population Genetics, Broad Institute, Cambridge, MA 02142.
Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129.
Department of Medical Biochemistry and Biophysics, Umea University, Umea, Sweden.
Neurogenomics Division, Translational Genomics Research Institute and Arizona Alzheimer's Consortium, Phoenix, AZ 85004.
Banner Alzheimer's Institute and Department of Psychiatry, University of Arizona, Phoenix, AZ 85006.
Rush Institute for Healthy Aging, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612.
Rush Alzheimer's Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612.

Monday, November 14, 2011

Eye Surgery Improves Mood of Alzheimer's Patients(part 2)

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Eye Surgery Improves Mood of Alzheimer's Patients
Study Shows Alzheimer's Patients May Sleep Better, Be Less Depressed After Cataract Surgery (continued)
Benefits for Caregivers continued...

Thies points out that the study was small and there was no comparison group that did not get surgery to compare the results to.

Still, he tells WebMD, there are a lot of things that can contribute to a person's sensory deprivation. "If you can improve those things," he says, "you will improve their ability to perform."

AAO spokesman Jeffrey Whitman, MD, of the Key-Whitman Eye Center in Dallas, says, "I find this study to be a proof of what we may have already suspected -- that poor vision, in an already compromised patient, is a burden to both the patient and the patient's caretaker."

In an email, Whitman, who is the son of an Alzheimer's patient, told WebMD: "I have found that anything that can help mobility, the ability to feed oneself, or ambulate from room to room, is a great boon."

He adds that better vision leads to better nighttime behavior. A person with Alzheimer's often displays what's known as sun-downing behavior, in which forgetfulness and other symptoms worsen at dusk.

In addition, better vision can lead to less depression among people that uniformly become more depressed as the disease advances. "The continued evaluation and surgical management of cataracts should be pursued in these often forgotten patients," Whitman says.

These findings were presented at a medical conference. They should be considered preliminary as they have not yet undergone the "peer review" process, in which outside experts scrutinize the data prior to publication in a medical journal

Saturday, November 12, 2011

Eye Surgery Improves Mood of Alzheimer's Patients

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WebMD

Study Shows Alzheimer's Patients May Sleep Better, Be Less Depressed After Cataract Surgery
By Charlene Laino
WebMD Health News Reviewed by Laura J. Martin, MD

People with Alzheimer's disease should have regular eye tests to screen for vision problems.

That's the recommendation of researchers who found that people with mild Alzheimer's disease who have cataracts may benefit from vision-correcting surgery. The benefits include improved sight, better sleep, and less depressed mood.

Also, people with Alzheimer's often had better communication and interaction with others after the surgery.

According to Brigitte Girard, MD, a professor of ophthalmology at Tenon Hospital in Paris, treatment improved the patients' lives and also the lives of some caregivers.

Girard reported the researchers' findings at the annual meeting of the American Academy of Ophthalmology (AAO) at the end of October.

Despite fears to the contrary, Girard says, surgery did not worsen patients' general condition or dementia.

William Thies, PhD, scientific director of the Alzheimer's Association, reviewed the findings for WebMD. He says that general medical care, including vision problems, are often overlooked in people with Alzheimer's.

"The assumption is made they won't benefit," Thies says. The assumption, he adds, is wrong. "The fact that they do benefit is very much the message from this study."

Improvements in Mood and Sleep

More than 1.5 million cataract surgeries are performed annually in the U.S. One in three Americans, most of them older people, will have the surgery at some point in their life.

The surgery is performed to remove the natural lens of the eye, which sometimes becomes clouded over time. A permanent artificial lens is then implanted to replace the natural lens.

The study involved 38 people with mild Alzheimer's disease who underwent cataract surgery. The average age was 86; nine were 90 or older. The majority (82%) were women.

Three months after surgery, all but one patient could see better. Three in four patients had improved or unchanged scores on tests of mood, memory, and their ability to wash, dress, and otherwise function independently. Sleep, in particular, improved, Girard says.

Six of the seven people with depression before surgery were less depressed afterward. The other person's depression was about the same as before.

As rated by the patients and their caregivers, social lives improved or were unchanged in two out of every three people studied.

Girard says "unchanged" scores were considered a mark of success. "As one neurologist told me," she says, "if people with Alzheimer's disease don't get worse over three months, it's a win."

The researchers did find that some people were more agitated after the surgery.

Benefits for Caregivers

The study also found that the surgery eased the burden for one in four caregivers. For another one in four, though, caring for their loved one was harder. The main reason cited was an increased level of agitation.

Thursday, November 10, 2011

Sleep Disorders Lead To Increased Dementia Risk

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openPR

Older women with sleep-disordered breathing are more likely to develop cognitive impairment or dementia than women without this disorder according to a new study.

According to medical researchers, sleep-disordered breathing is a condition where the person has recurrent arousals from sleep and intermittent hypoxemia. "This condition can be common among older people and affects up to 60 percent of the elderly population," explains Jesse Slome, director of the American Association for Long Term Care Insurance.

Health experts report that the condition has been linked to various adverse health problems including hypertension, cardiovascular disease and diabetes. Researchers at the University of California, San Francisco, investigated the link between prevalent sleep-disordered breathing measured and the subsequent diagnoses of mild cognitive impairment and dementia.

The study tested nearly 300 women who were the average age of 82.3 years. The participants were without dementia at the start of the study. The participants' cognitive status was ranked as normal, dementia, or mild cognitive impairment. The study examined measures of hypoxia, sleep fragmentation and sleep duration as underlying mechanisms for any link between sleep-disordered breathing and cognitive impairment.

According to the study, some 35.2 percent of the tested women met the criteria for sleep-disordered breathing. Nearly an equal amount, some 35.9 percent of the women, developed mild cognitive impairment (20.1 percent) or dementia (15.8 percent) after an average follow up of 4.7 years. The study revealed, 47 of women (44.8 percent) with sleep-disordered breathing acquired mild cognitive impairment or dementia in comparison with 31.1 percent of those without sleep-disordered breathing.

Cognitive decline and dementia is a leading reason that aging senior women ultimately require costly long term care, Slome acknowledges. "Long term care insurance can pay for qualifying care at home or in a skilled nursing home but you must apply well before a decline in mental ability or physical health takes place," he notes.

Tuesday, November 8, 2011

The dangers of your aging parent covering up dementia (part 3)

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Forbes

Carolyn Rosenblatt

TO DO LIST
1. Persuade Dad to get a checkup from a reliable MD, preferably a neurologist who deals with aging patients.

You need information. If there are symptoms of dementia, you need to find out what’s going on. If other conditions are in play, appropriate care may make a difference. If you have to conspire with the doc in advance, do it.

2. Locate and update all estate planning documents. Work with your parents on this. Trusts, wills, durable powers of attorney and health care directives are the most important ones you need to review. It might have been years since anyone looked them over. Urge your parent to see an estate planning attorney. Tax laws change, state laws can vary. Some aging parents have never actually gotten the necessary legal papers together. The time may come when Dad is no longer competent to sign anything. Waiting until “the right time” is not good strategy. It can be too late before you know it.

3. Plan ahead for Dad’s possible care needs. Who would look after him if Mom could no longer do this? He may go downhill in the future. If he does have dementia, it won’t remain the same over time. People get more dependent on help with their daily needs. Help is not free. Some source of payment for help with daily care should be in the plan.

4. Discuss Dad’s situation with all family members. Call a family meeting. If Dad has memory problems now, everyone in the family will eventually be involved in the situation. Siblings may need to share caregiving duties. Some may need to make financial contributions. Taking care of both parents as they age is no longer rare. An honest conversation about who can do what, and who is willing to help aging parents can go a long way toward avoiding resentment and conflict later on. Take the first step. Be the leader. Someone has to do this, and it isn’t always an aging parent.

You don’t want to be the one lulled into a false sense of security because no one has officially diagnosed your aging parent with a specific kind of dementia. It doesn’t matter. Trust your own eyes and ears. If your gut tells you there’s something wrong here with your loved one, there probably is something wrong. Jaclyn already knows something is brewing with her Dad. She’s being proactive and I applaud her.

You’re not alone if you have a parent with memory loss. Millions of people are facing this every day. They find a way to manage it, and survive and you will too. Be smart. Look down the road. Stand tall and do this last part of being a grown child of your parent. Take the basic steps to protect your aging parent and yourself and you will get through it without unnecessary stress.

Friday, November 4, 2011

Abnormal Protein May Explain Loss of Smell With Alzheimer’s

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The protein kills nerve cells in the nose, animal study finds.

(HealthDay News) -- A loss of a sense of smell can be one of the earliest signs of Alzheimer's disease.

New research suggests that an abnormal form of a protein -- amyloid precursor protein, or APP -- which has been previously associated with the Alzheimer's disease may be to blame.

A study in mice found that animals genetically engineered to produce high levels of the abnormal protein experienced high levels of death in nerve cells in their nose compared to normal mice.

Researchers say the findings may explain why people suffering from the progressive illness often lose their sense of smell while the disease is still in its initial stages. They added this new insight might help doctors detect the condition early on.

"Deficits in odor detection and discrimination are among the earliest symptoms of Alzheimer's disease, suggesting that the sense of smell can potentially serve as a canary in the coal mine for early diagnosis of the disease," study leader Leonardo Belluscio of the U.S. National Institute of Neurological Disorders and Stroke, said in a news release.

"The changes taking place in the olfactory system as a result of Alzheimer's disease may be similar to those in other regions of the brain but appear more rapidly," he added.

APP has been detected in the nose nerve cells of some people with early onset Alzheimer's, a rare form of the disease that runs in families and strikes before age 65.

The researchers found mice making the mutated form of APP had four times as much olfactory nerve cell death at three weeks of age than normal mice.

When researchers blocked the production of high levels of the mutated protein, more olfactory nerve cells survived.

"Reducing APP production suppressed the widespread loss of nerve cells, suggesting that such disease-related death of nerve cells could potentially be stopped," explained Belluscio.

The study, published in the Sept. 28 issue of The Journal of Neuroscience, also found that the cells that died in the nose did not contain amyloid plaques, which are derived from APP. Plaques have long been believed to contribute to the death of nerve cells in the brains of people with Alzheimer's, leading to memory loss.

The researchers say the findings suggest that APP itself may be responsible for the death of nerve cells.

"Together, these results support the hypothesis that amyloid proteins are involved in the degeneration of the brain that occurs with Alzheimer's disease," Donald Wilson of New York University School of Medicine and the Nathan Kline Institute for Psychiatric Research, said in a news release from the journal.

"Further, they provide an exciting opportunity to explore how to prevent or reverse the events that lead to cell death and, ultimately, dementia," added Wilson, an olfactory system expert who was not involved in the study.

While more research is needed, it should be noted that studies involving animals often fail to produce similar results with humans.

More information

The National Institutes of Health provides more information on Alzheimer's disease.

SOURCE: Society for Neuroscience, news release, Sept. 27, 2011

Wednesday, November 2, 2011

New research targets treatment for dementia

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From Surabhi Gupta(PTI)

People suffering from dementia can heave a sigh of relief as neuroscientists in Australia have discovered a fundamental component of the process that regulates memory formation.

Neuroscientists at the Queensland Brain Institute (QBI) of The University of Queensland discovered the component in the hippocampus � a part of the brain commonly associated with memory function.

The discovery explains, for the first time, how new nerve cells form in this area of the brain associated with learning and memory � which deteriorate in people with stroke and dementia, QBI Director Professor Perry Bartlett told PTI.

"The hippocampus is the region of the brain involved in important functions such as learning and memory, and loss of neuronal production in the hippocampus is associated with a range of neurodegenerative conditions. It is particularly evident in ageing dementia," Bartlett said.

"Surprisingly, however, studies so far have failed to identify a resident stem cell population in the hippocampus that''s capable of providing the renewable source of these essential nerve cells."
Research by Professor Bartlett and his QBI colleagues, Dr Tara Walker and Dr Dhanisha Jhaveri (a recipient of the Indian National Science Academy''s award for Young Scientist of the Year 2003), has identified the resident populations of stem cells in the hippocampus.

Even more importantly, this research has discovered how it can be activated to produce new neurons.

The discovery of the presence of precursors in the adult brain which have the potential to produce neurons via a process called neurogenesis, will help immensely in the case of dementia patients, Bartlett said.

"For the first time, we''ve been able to identify a mechanism that''s able to regulate production of nerve cells, a step that''s crucial to our understanding of memory and learning," Professor Bartlett said.

"The same mechanism helps regulate growth of healthy brain tissue, so identifying this process is essential for the development of therapeutics to treat conditions such as dementia and depression."
A detailed understanding of the activation process should enable the development of therapeutics that can stimulate the production of new neurons and reverse or prevent the cognitive decline that occurs during ageing dementia, he said.

"These significant advances in determining the molecular regulation of nerve production will also have a major impact on our understanding of more complex areas such as behavior, cognition, neurological disease and mental illness," he added.

He said that the latest research provides further evidence that the mammalian central nervous system has the potential capacity to respond to its outside environment by generating new nerve cells.

The QBI research augments ongoing efforts to identify cellular and molecular mechanisms that can repair compromised brain tissue, and represents another milestone in understanding the fundamental workings of the brain.

Monday, October 31, 2011

Alzheimer's may originate in a form similar to that of infectious prion diseases

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news-medical.net

The brain damage that characterizes Alzheimer's disease may originate in a form similar to that of infectious prion diseases such as bovine spongiform encephalopathy (mad cow) and Creutzfeldt-Jakob, according to newly published research by The University of Texas Health Science Center at Houston (UTHealth).

"Our findings open the possibility that some of the sporadic Alzheimer's cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease," said Claudio Soto, Ph.D., professor of neurology at The University of Texas Medical School at Houston, part of UTHealth. "The underlying mechanism of Alzheimer's disease is very similar to the prion diseases. It involves a normal protein that becomes misshapen and is able to spread by transforming good proteins to bad ones. The bad proteins accumulate in the brain, forming plaque deposits that are believed to kill neuron cells in Alzheimer's."

The results showing a potentially infectious spreading of Alzheimer's disease in animal models were published in the Oct. 4, 2011 online issue of Molecular Psychiatry, part of the Nature Publishing Group. The research was funded by The George P. and Cynthia W. Mitchell Center for Research in Alzheimer's Disease and Related Brain Disorders at UTHealth.

Alzheimer's disease is a form of progressive dementia that affects memory, thinking and behavior. Of the estimated 5.5 million cases of Alzheimer's in the United States, 90 percent are sporadic. The plaques caused by misshapen aggregates of beta amyloid protein, along with twisted fibers of the protein tau, are the two major hallmarks associated with the disease. Alzheimer's is the sixth leading cause of death in the United States, according to the Alzheimer's Association.

Researchers injected the brain tissue of a confirmed Alzheimer's patient into mice and compared the results to those from injected tissue of a control without the disease. None of the mice injected with the control showed signs of Alzheimer's, whereas all of those injected with Alzheimer's brain extracts developed plaques and other brain alterations typical of the disease.

"We took a normal mouse model that spontaneously does not develop any brain damage and injected a small amount of Alzheimer's human brain tissue into the animal's brain," said Soto, who is director of the Mitchell Center. "The mouse developed Alzheimer's over time and it spread to other portions of the brain. We are currently working on whether disease transmission can happen in real life under more natural routes of exposure."

Source: University of Texas Health Science Center at Houston
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