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

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

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.”

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.

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.

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.

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

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.

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.

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.

Abnormal Protein May Explain Loss of Smell With Alzheimer’s

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Doctor's Lounge

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

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.