Doctors criticize IViG therapy for dementis

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

ABC News

Doctors Criticize IViG Study Results

Still, treatment is not advised for patients who have had a major stroke or heart attack, because it can increase the risk of vascular events.

IVIG may not just be a therapy that treats symptoms, according to Dr. Richard Caselli, a neurologist at the Mayo Clinic. The drug seems to block the "destructive process" of inflammation mechanisms in the brain.

"Its strength and therefore importance is that it seems to show a stabilizing effect over a sustained period of time," he said. "Its weakness as the authors state is the small number of patients as well as its unblinded open label format."

But Dr. Normal Foster at the Center for Alzheimer's Care, Imaging and Research at the University of Utah, said the selective reporting of the study's results are "suspicious."

"Not everyone who received treatment was included in the analysis," he said. "The results are intriguing, and I can see why they might want to share them, but they can't be relied upon."

Dr. James E. Galvin, director of the the Pearl Barlow Center for Memory Evaluation and Treatment at New York University's Langone Medical Center, said there may be "technical and logistical limitations" in how many patients might obtain the drug.

Natural Alzheimer's Remedies?Watch Video

Getting Alzheimer's Candidate to Doctor? Watch Video

Welcome to OnCall+ Alzheimer'sWatch Video

But Dr. Sam Gandy, director of Mount Sinai Center for Cognitive Health, said the study, though small, is "still good news, indeed."

He, like other experts, said more studies were needed to prove the drug's promise.

Marder showed no symptoms of the disease in his speech, memory or mood when interviewed by ABCNews.com. He said he first began noticing he was having trouble with his memory a decade ago.

"I thought it was all part of aging," he said.

After a series of tests with a neurologist that were inconclusive, he was preventively put on the drug Aricept. But within a matter of months, an official diagnosis of Alzheimer's disease was made.

"I was devastated," he said. "It blows you away."

As his confusion and forgetfulness worsened, Marder was put on Namenda, as well as Aricept, both of which he has continued for nine years.

Every six months Relkin puts Marder through a series of cognitive tests and so far, the decline has been minimal.

But now, the Marders worry that they may not get the drug if it does not get FDA approval when phase III clinical trials end next year.

And it's expensive – estimated to cost a patient $2,000 to $5,000 every two weeks, including the drug, equipment and a nurse to administer it.

Relkin has told the Marders there were other drugs, but Marder said, "I just want them to keep going."

Marder continues to play tennis and can ride his bike up the 11-mile stretch from Battery Park to the George Washington Bridge -- and back.

"He still has memory issues, no question," said his wife. He tends to repeat himself, but the drug has kept him stable. "There's no doubt he has Alzheimer's, but we would have expected him to progress downward by now."

Luckily, Marder has the self-awareness to know what the drug has done for him.

"It's heaven," he said. "I don't know where I could have been without it.

IViG therapy shows some success for treating dementia

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

ABC News

By STACEY SCHOTT, M.D., and SUSAN DONALDSON JAMES

Jason Marder watched the inevitable decline of his younger brother, who died of Alzheimer's disease at the age of 50. Then, just after his 60th birthday, he too, began to exhibit subtle, early symptoms -- forgetfulness and difficulty focusing on conversations.

At his birthday party, "I noticed he had a hard time keeping track of the presents," said he wife, Karin Marder. "He would forget small things -- like saying he went to the movies when he didn't."

The memory loss progressed, and in 2004, Marder got the dreaded diagnosis: Alzheimer's, a disease that affects 5.1 million Americans.

"It was devastating," said his wife, who works in business apparel. "I thought our lives were going to end."

But today, eight years after his diagnosis, Marder isn't any worse off. He has shown no further memory loss and has remained stable.

The Marders credit intravenous immunoglobulin, or IViG, therapy and a clinical trial that is swirling in controversy this week after an announcement of study results by the Alzheimer's Association International Conference 2012 in Vancouver.

Some doctors hailed the therapy as "exciting," something that could potentially stabilize the disease, while others said the research is inconclusive and the study -- with only 16 subjects -- was too small.

Nonetheless, today Marder, now retired from working in apparel, continues his independent lifestyle, playing tennis and biking in his native New York City.

"Things are going really nicely. I can't complain," said Marder, now 70. "I don't feel any going backwards."

Natural Alzheimer's Remedies?Watch Video

Getting Alzheimer's Candidate to Doctor? Watch Video

Welcome to OnCall+ Alzheimer'sWatch Video

"This drug saved his life," said Karin Marder. "He's independent. He gets on the subways, bikes up and down the Hudson River, gets to go out with friends. He goes to the senior center twice a week. He does creative writing."

For the past five years, Marder has been part of a clinical trial with Dr. Norman R. Relkin, director of the Memory Disorders Program at New York-Presbyterian/Weill Cornell Medical Center.

Relkin presented data that found,overall, that 11 study participants who received the immunotherapy Gammagard (IViG) for three full years showed improvements in cognition, memory, daily functioning and mood.

"We are seeing encouraging results," Relkin told ABCNews.com. And despite negative publicity, "I don't want people to give up hope for symptomatic treatment of the disease".

Intravenous Immunoglobulin is a mixture that contains molecules pooled from plasma, a component of human blood. It is used to treat various autoimmune, infectious and idiopathic diseases, and its supply is therefore limited.

IViG works by using the body's natural defense or immune system and anti-amyloid antibodies. A protein called beta amyloid accumulates in the brain of those who have Alzheimer's.

"We don't know exactly what it targets, but we do know it contains all antibodies that the body produces," said Relkin. "It alters the function of the immune system and decreases inflammation in the brain".

He said that his research team found the rate of brain shrinkage had slowed and the study had "exceeded criteria" to go forward with a phase III trial.

"Typically, untreated Alzheimer's disease shows cognitive decline in three to six months," said Relkin. "Those treated with typical AD drugs show decline in six to nine months. Four out of four patients in the [phase IIB] extension trial were unchanged over a three-year period."

As for Marder, he still has some memory problems, but he can dress himself, cook, clean and walk around the neighborhood.

"I can be away from him for one to two nights," said his wife, Karin.

Every two weeks, a nurse comes to Marder's home and sets up the infusion, which takes about four hours.

"I am happy to spend the time," he said. "Then I walk out of my house and go bike riding."

Besides a minor rash that crops up three to five days after getting the drug, Marder has had no ill side effects with the treatment. "He hasn't even had a cold in five years," said Marder's wife.

Singing therapy for dementia

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

Alzheimer's Weekly

Using interviews with a group leader, volunteers, people with dementia and their partners, this film explains what Singing for the Brain is, as well as looking at the supportive and enjoyable atmosphere that makes it such a success.

'Singing for the Brain' is a service provided by Alzheimer's Society in approximately 30 locations, all of which use singing to bring people together in a friendly and stimulating social environment.

Singing is not only an enjoyable activity, it can also provide a way for people with dementia, along with their carers, to express themselves and socialise with others in a fun and supportive group.

For more information on Singing for the Brain, please go tohttp://alzheimers.org.uk/singingforthebrain

Alzheimer's drug fails in one study; second continues

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

USA Today

TRENTON, N.J. (AP) – Pfizer Inc. said Monday that a closely watched experimental Alzheimer's drug failed to slow the disease in one late-stage study, but the drug maker said it will continue to study the drug's effect on a different group of patients.

Pfizer, which is testing bapineuzumab with partner Johnson & Johnson, said the injected drug didn't slow mental or functional decline in patients with mild or moderate Alzheimer's disease. The study included patients who carry a gene called ApoE4, which gives people a higher risk of developing the memory-robbing disorder.

About half the population does not carry that gene, however, and Pfizer says a study of the drug in patients without the gene is continuing. Results of that study are expected to be announced later this summer.






Johnson & Johnson spokeswoman Ellen Rose said scientists who conducted mid-stage tests on bapineuzumab "saw a hint that the people who are carriers of the ApoE4 gene might not have as good a chance as people who are not carriers."


New York-based Pfizer and Johnson & Johnson, based in New Brunswick, N.J., are each running two studies of the experimental drug.


Current medicines for Alzheimer's disease temporarily control symptoms such as memory loss, confusion and agitation. But they do nothing to slow, stop or reverse mental decline, leaving patients and their loved ones desperate for a new treatment.


Finding a drug that could at least slow the disease has become a sort of Holy Grail in the pharmaceutical industry. A successful medicine would be guaranteed to generate billions in annual sales, given the world's aging population.

New Model Of Alzheimer's Derived From Skin Cells Of People With The Disease

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

PR Newswire

VANCOUVER, British Columbia, July 16, 2012 /PRNewswire via COMTEX/ -- Researchers at the Alzheimer's Association International Conference® 2012 (AAIC® 2012) today reported the creation of a new model of Alzheimer's derived from the skin cells of people with the disease that were reprogramed into Alzheimer's brain cells.

This new Alzheimer's model may prove to be more accurate than current mouse models of the disease and therefore can be used (a) to generate important new insights into the biology of Alzheimer's and related disorders and (b) for early stage testing of new therapies.


"Current animal models of Alzheimer's are highly engineered to express elements of the disease, and, while valuable for research, incompletely represent how the disease forms and progresses in people," said William Thies, PhD, Alzheimer's Association® Chief Medical and Scientific Officer. "In order to develop better therapies and eventually prevent Alzheimer's, we need better, more accurate animal and cellular models of the disease. This newly reported research is a significant step forward in that direction."


Most of the current Alzheimer's mouse models incorporate genetic changes found in familial young-onset forms of Alzheimer's. Although these mice have taught us about many valuable aspects of the disease, the hallmark amyloid plaques found in the brains of people with Alzheimer's do not form in the same way as in the brains of mice expressing mutant forms of the most common young-onset Alzheimer's gene, and significant brain cell death does not occur. New approaches are needed.


Andrew Sproul, PhD, a postdoctoral associate, and colleagues working at The New York Stem Cell Foundation (NYSCF) in the laboratory of Scott Noggle, PhD, the NYSCF-Charles Evans Senior Research Fellow for Alzheimer's Disease, pursued an induced pluripotent stem cell (iPSC) approach to model Alzheimer's, and reported their results for the first time today at AAIC 2012. This involves taking cells from people with the disease and their unaffected family members, typically skin cells, and reprogramming them by adding genetic factors. The resulting iPSCs can be used to model Alzheimer's in a dish.


"One advantage of this technology is that we get a near infinite supply of disease and control patient stem cells," Sproul said. "Another is that we can then turn the iPSCs into any tissue in the body. This allows us to investigate the role of various cells in Alzheimer's disease progression by manipulating the iPSCs to form different types of brain cells (forebrain nerve cells, neural stem cells, glial cells) that we and others believe are involved in Alzheimer's."


The researchers generated iPSCs from a total of 12 people with Alzheimer's and healthy controls from two young-onset, genetic Alzheimer's families. The iPSC lines have been quality-controlled, including ensuring pluripotency, which is the ability to make all kinds of cells from the endoderm (interior stomach lining, gastrointestinal tract, lungs), mesoderm (muscle, bone, blood, urogenital), or ectoderm (skin and nervous system).


"We have made both the control and Alzheimer's iPSCs into brain cells and have demonstrated that they are electrically active. These new brain cells include forebrain cholinergic neurons, which are particularly vulnerable in Alzheimer's disease," Sproul said.


"We have also begun to use the iPSC-derived neurons and neural stem cells to compare differences in cellular function between people with Alzheimer's and their unaffected relatives. For example, we, in conjunction with Dr. Sam Gandy's group at Mount Sinai School of Medicine, have demonstrated that Alzheimer's neurons produce more of the toxic form of beta amyloid, the protein fragment that makes up amyloid plaques, though this aspect of the research is preliminary," Sproul added.


The research reported at AAIC 2012 focuses on people with presenilin-1 (PSEN1) mutations, which are responsible for the most common form of rare, inherited, young-onset Alzheimer's (estimated to be less than two percent of total cases). According to Sproul, this work may provide a platform to screen new drugs that could alleviate defects caused by the faulty gene.


However, because the overwhelming majority of people with Alzheimer's have the late onset "sporadic" form of the disease, the scientists say they plan to expand their research to include large-scale production of iPSCs from people with different types of Alzheimer's.


"We have begun to extend this work by collaborating with four different institutions in New York City - the Mount Sinai School of Medicine, Columbia University, New York University, and Rockefeller University. Over the next few years, we expect to provide substantial insight into Alzheimer's and valuable tools to help create the next generation of therapeutics," Sproul said.


About AAICThe Alzheimer's Association International Conference (AAIC) is the world's largest conference of its kind, bringing together researchers from around the world to report and discuss groundbreaking research and information on the cause, diagnosis, treatment and prevention of Alzheimer's disease and related disorders. As a part of the Alzheimer's Association's research program, AAIC serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community.


About the Alzheimer's Association The Alzheimer's Association is the world's leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research, to provide and enhance care and support for all affected, and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's. For more information, visit www.alz.org or call 800-272-3900.


\\\SOURCE Alzheimer's Association

Can walking predict Alzheimer's

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

isciencetimes

The way you walk could be a hint as to whether you will develop dementia or Alzheimer's disease, according to three new studies, presented at the annual meeting of the Alzheimer's Association in Vancouver. Researchers found that changes in walking patterns could be an early warning that cognitive decline is underway.

In one four-year study, researchers followed more than 1,200 elderly patients who went to a memory clinic and compared their walking speed to that of a mentally healthy person. They found that a slowing of walking pace and a change in gait was linked to mental decline, whether it was mild cognitive impairment (MCI) or Alzheimer's disease.

"Those with Alzheimer's dementia walked slower than those with MCI, who in turn walked slower than those who were cognitively healthy," Dr. Stephanie Bridenbaugh, study author and researcher with the Basel Mobility Center, told HealthDay.

A second study, which looked at 1,300 patients, found that a decline in mental skills, including memory and executive function loss, were linked to a slowed pace and a change in gait.

"These results support a possible role of gait changes as an early predictor of cognitive impairment," Dr. Rodolfo Savica, a researcher with the Mayo Clinic, said in a statement.

Kenichi Meguro, researcher of the third study and researcher with the Tohoku University Graduate School of Medicine in Sendai, had similar findings, and told HealthDay that gait velocity was significantly diminished in people with Alzheimer's, as compared to people with MCI's and mentally healthy people.

"Gait should no longer be considered a simple, automatic motor activity that is independent of cognition," he said. "They are linked."

Alzheimer's disease is the most common form of dementia in the United States, affecting more than 5 million people, according to the Centers for Disease Control and Prevention. The number of people who suffer from the disease is expected to double every 20 years as population increases and people live longer

Symptoms of Alzheimer's include memory loss, confusion, difficulty completing familiar tasks, decreased judgment and problems speaking or writing.

Healthcare costs related to Alzheimer's disease totaled almost $8 billion in 2010, according to the Alzheimer's Association, a nonprofit organization that advocates for Alzheimer's patients in the federal and state governments.

There is as yet no cure or successful treatment for Alzheimer's disease. The Obama administration set a goal of 2025 to find an effective treatment and pledged to spend an additional $50 million on dementia research on top of the $450 million the government spends annually until a treatment is found.

Gene mutation will help Alzheimer's treatment

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

Connie K. Ho for redOrbit.com – Your Universe Online

5 million. That’s the number of people in the U.S. suffering from Alzheimer’s disease, according to a recent CNN article. Scientists recently announced that they had discovered a gene that fights Alzheimer’s. This is a positive step forward as the gene could help develop treatments to fight the disorder.

In the journal Nature, researchers explained how the gene that caused an early form of Alzheimer’s could also be created to produce an office effect, prohibiting the development of the disorder. According to the Guardian, carriers of the mutation have a 47% greater likelihood of living until 85 years of age as compared to those who don’t have the mutation. The findings also discuss how new drugs could copy the effect of the mutation.

“Less than 1% of the population has these alleles,” explained Dr. William Thies, chief medical and scientific officer of research and advocacy group Alzheimer’s Association, in a Reuters Health article. “But many companies are working on compounds that target the mechanism they found and so might be encouraged by these results.”

Alzheimer’s is a common form of dementia and early signs include memory loss, mood swings, as well as feelings of isolation and withdrawal. The illness is progressive and those who are diagnosed with the disorder become dependent on others to help them with daily tasks. With Alzheimer’s disease, the brain is plagued with sticky plaques made of amyloid beta, a peptide. The amyloid beta is from the amyloid precursor protein (APP), which is a larger protein. Scientists have discovered about two dozen mutations in the APP genes that lead to early-onset Alzheimer’s within the last twenty years. Early-onset Alzheimer’s is normally diagnosed in people who are a bit younger than 65.

However, researchers from deCODE genetics in Iceland found that a new mutation in the APP gene does the opposite and has certain benefits. In the project, scientists sequenced the genomes of 1,795 Icelanders. It led to the discovery that participants of 85 years of age and older who had the beneficial mutation had a 81 percent less likelihood to develop Alzheimer’s when compared to others in the same group. In all age groups, those who had the variant genes were four times less likely to develop the neurogenerative disease.

“It confers extraordinarily strong protection,” noted lead scientist Dr. Kari Stefansson. “We found only five Alzheimer’s cases (out of thousands of people) with it.”

As well, the mutation is so rare that its discovery will help scientist in creating drugs that can prevent or treat Alzheimer’s. The mutation influences how APP is broken up and, after the brain produces the protein, the enzymes are broken into pieces. The enzymes are listed as alpha, beta, and gamma. The break up of APP by Alpha-secretase makes it so amyloid beta and plaques cannot be produced. As such, the fragment allows for growth and survival of the neurons.

On the other hand, the beta-secretase (BACE) works with the gamma-secretase to cut APP, so it can produce amyloid beta. The BACE then adheres to other amyloid beta fragments and forms plaques. Luckily, the beneficial mutation can stop the BACE’s ability to cut the APP and reduces the creation of amyloid beta by 40 to 50%t. Overall, it slows down the production of BACE, which hinders Alzheimer’s from developing.

A number of follow-up studies also showed that the DNA sequence with the mutation shielded the participants from decline in brain performance that is normally related old age. It proves that Alzheimer’s and other age-related neural problems are connected to a cycle of disorders and have the same basic cause.

“This gives you a proof of concept that if you inhibit BACE it will protect against Alzheimer’s,” remarked Stefansson in the Reuters Health article. “Big pharma has been working on inhibitors for beta-secretase for 15 to 20 years, and this offers greater confidence” that those efforts will pan out.”

According to Reuters Health, many companies are working on creating commands that can stop BACE actions.  For example, Merck presented early-stage human trails of MK-8931 last April. Vitae Pharmaceuticals and Boehringers Ingelheim are also working together to create a BACE inhibitor. Likewise, Eli Lilly and Co’s BACE inhibits is already in mid-stage human trials. However, it’ll mostly take at least four to five years or longer until the drugs become successful treatments.

“We know that the development of Alzheimer’s can be linked to a combination of genetic and lifestyle factors. We still have a lot to learn about what happens in the brain but this research offers new insight into a gene we already know is linked to the disease,” Anne Corbette of the Alzheimer’s Society told  HYPERLINK “http://www.guardian.co.uk/science/2012/jul/11/rare-genetic-mutation-alzheimers” the Guardian. “One in three people over 65 will develop dementia. This development offers interesting new information about how our genes might affect our chances of developing Alzheimer’s disease. It could also provide a new target for future investigations to find treatments to help people live well with dementia, or even find a cure.”

Source: Connie K. Ho for redOrbit.com - Your Universe Online

Source: redOrbit (http://s.tt/1hLVD)

Will the new Alzheimer's drugs work

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

Forbes


Michael Waldholz, 

In the coming months researchers will release results of several drug studies that will impact millions of Alzheimer’s victims and their families, as well as the fortunes of drugmakers,  Merck, Pfizer, Lilly and Johnson & Johnson  among others. Just as important, maybe even more so, the studies may finally provide evidence to support a controversial 20-year old theory of how the mind-robbing and lethal illness works.

But there’s plenty of reason to believe these studies tests will be inconclusive. The biggest worry is that even if the drugs work, the studies may show that to be effective, the medicines must be used much like anti-cholesterol pills, well  before the disease begins to show debilitating symptoms. If that’s true it will mean years of uncertainty about an effective treatment or cure. Alternately, the 

drugs may turn out to be complete busts, or only improve memory and thinking in a statistically negligible manner that will spark conflicting interpretations. And since there is nothing in drugmakers’ pipeline to replace the drugs being tested, negative results will force Alzheimer’s research back to square one for a disease that is already costing untold suffering and adding hundreds of millions of dollars a year in health costs that will explode as the population ages.

What follows is a review, a scorecard of sorts, of what is at stake. Much of this conversation will be front and center at an international research meeting beginning this weekend in Vancouver.

A primer: The experimental medicines all focus on attacking beta amyloid, a protein autopsies show masses in the brains of Alzheimer’s victims. According to the amyloid theory, these packets of plaque destroy brain cells over time, though exactly how they do this is still unknown. One school of scientists believes the plaques, which collect in small amounts in nearly all people as they reach old age, arise earlier and in much larger amounts in people with a predisposing genetic makeup. Another group argues that the clumping is merely the residue of some other unknown chain of events, so drugs designed to prevent or destroy amyloid will provide little if any benefit.

Alzheimer’s researchers, doctors and victims are literally holding their collective breath, hoping the studies will not only provide relief, but give scientists the kind of clear roadmap needed to fuel future investigations

A gene discovery backing the amyloid theory:  Just this week, a well-regarded research team in Icelandreported in the journal Nature that they had identified a gene that, when mutated, slows the body’s production an enzyme called beta secretase. This is a valuable discovery because beta secretase appears to play an important role in amyloid formation. Merck, Lilly and Esai are in advanced clinical studies of drugs that mimic the protective action of the gene by blocking the action of the enzyme. The Iceland group, under the direction of the gene-hunting company DeCode and its charismatic founder, Kari Stefansson, found that people with an unusual variant of the gene either don’t have the disease or don’t amass plaque in large amounts. Because the study involved a small number of people in Iceland, there is reason to be cautious about broader application.

• The garbage collectors:  Perhaps the most important advanced study, whose results will be reported in October, involves the drug bapineuzumab, being developed by Pfizer and Johnson & Johnson and a similar drug called solanezumab from Lilly. These medicines are laboratory produced antibodies that, given through infusions, have been shown to attack and clear amyloid from the brain. Early results of another drug, Gammagard from Baxter, a combination of plaque-clearing antibodies, will also be released at the week the Alzheimer’s Association International Conference. Even a slight increase in cognition from these drugs will likely result in FDA approval and annual sales of billions of dollars. The worry is that even there though the drugs can sterilize amyloid clumps from the brain, the patient population studied may be too far advanced in their disease to be helped, or the study not be sensitive enough to detect benefits.

Still another antibody, crenezumab, being developed by Roche’s Genentech unit, is being tested in a $100 million trial in a family in Colombia where an early-onset form of the disease is common. That trial, involving about 300 relatives, won’t be completed for years.

• The gatekeepers: Merck and Lilly are in the second of three phases of clinical trials of drugs called beta-secretase inhibitors, also referred to as BACE drugs. Unlike the antibody medicines, these drugs are being tested in pill form. The science underlying these drugs got a boost from the Iceland gene study. The idea behind these medicines is to inhibit the formation of amyloid plaque before it can cause havoc. As with the amyloid clearing drugs, there is concern that the studies underway involve patients too far into their disease.

• The takeaway: It is clear that all the drugs in development will be most effective if used early in the disease, meaning the ability to identify those at risk is critical. Even then, the health profession and policymakers will face a dilemma. Conducting population-wide screening will be enormously expensive. Giving these medicines as long-term preventive treatments will cost many billions of dollars more. This is just one of many example of why the nation’s health bill will continue to rise sharply, with or without success in battling Alzheimer’s disease.

Easy to use medical billing forms

As a healthcare provider or a caregiver, you will have to fill out medical insurance form. Wouldn't it be nice to be able to use software that makes this task easier. I have found such a medical billing forms software company.

UB-04 Software is a medical insurance form filling software company. They create software that almost anyone can use to assist them in filling out medical insurance forms.

The ub04 claim form is the best in the business in my opinion

They offer 5 products

The first product is HCFA-1500 EDI Clearinghouse Software

This software has many options that make it ideal to use. You can even get a free trial No need to go anywhere else. You can download the software and easy to follow instructions are included. There is also free technical support and software updates.

The second product is UB-04 EDI Clearinghouse Software This software has the same advantages and a free trial

The third product is HCFA-1500 Fill & Print NPI Software Again this software has easy to follow instructions and someone to help you every step of the way should you need it. Check out the free trial

This software has won awards. There is even live chat to help you.

The fourth product is UB-04 Fill & Print NPI Software I hate to sound like a broken record but this software has won multiple awards and allows you to use a free trial

Another one of their award winning software is Dental Association Fill & Print EDI Software. This software as well as the others allows you to submit forms electronically. if you are unsure, try the free version

As you can see there are many benefits to using this software.

If you are a MAC user, there are programs for you as well.

Why not see these products at Utube Medical Billing Service

Tips for Older Adults with Dementia to Avoid Heat-Related Illness

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

SeniorAdvisor.com

Summertime, and the living is...hot -- TOO HOT. Alas, we are less able to handle hot days as we age. The wonderful summertime of youth can become a serious problem for a Senior. Heat-related illnesses, known as hyperthermia, can include heat stroke, heat fatigue, heat syncope (sudden dizziness after exercising in the heat), heat cramps and heat exhaustion, says the National Institute on Aging (NIA), part of the National Institutes of Health. NIH has some advice to help older people avoid these problems. A person's risk for hyperthermia is a combination of the outside temperature along with general health and lifestyle. These health-related factors can increase risk:

• Age-related changes to the skin such as poor blood circulation and inefficient sweat glands
• Heart, lung and kidney diseases, and any illness that causes general weakness or fever
• High blood pressure or other conditions that require changes in diet. For example, a salt-restricted diet may increase, but salt pills should not be used without consulting a doctor.
• The inability to perspire, caused by medications such as diuretics, sedatives, tranquilizers, and certain heart and blood pressure drugs
• Taking several drugs for various conditions. However, prescribed medication should not be stopped, so discuss possible problems with a physician.
• Being substantially overweight or underweight
• Drinking alcoholic beverages
• Being dehydrated

Lifestyle factors can also increase risk, including:

• extremely hot living quarters
• lack of transportation
• overdressing
• visiting overcrowded places
• not understanding how to respond to weather conditions

Older people, particularly those at special risk, should stay indoors on hot and humid days, especially when there is an air pollution alert in effect. People without fans or air conditioners should go to cool places such as shopping malls, movie theaters, libraries, or cooling centers which are provided by government agencies, religious groups, and social service organizations in many communities. Heat stroke is an advanced form of hyperthermia that occurs when the body is overwhelmed by heat and unable to control its temperature. Someone with a body temperature above 104 degrees is likely suffering from heat stroke and may have symptoms of confusion, combativeness, strong rapid pulse, lack of sweating, dry flushed skin, faintness, staggering, possible delirium, or coma. Seek immediate medical attention for a person with any of these symptoms, especially an older adult. If you suspect that someone is suffering from a heat-related illness:

• Get the person out of the sun and into an air-conditioned or other cool place.
• Offer fluids such as water, fruit and vegetable juices, but avoid alcohol and caffeine.
• Encourage the individual to shower, bathe or sponge off with cool water.
• Apply a cold, wet cloth to the wrists, neck, armpits, and/or groin, places where blood passes close to the surface and the cold cloths can help cool the blood.
• Urge the person to lie down and rest, preferably in a cool place.

For a free copy of NIA's Age Page on hyperthermia in English or in Spanish, call 1-800-222-2225 or go to http://www.niapublications.org/agepages/hyperther.asp (orwww.niapublications.org/agepages/hyperther-sp.asp for the Spanish-language version). NIA leads the U.S. federal effort supporting and conducting research on aging and the medical, social and behavioral issues of older people. For more information on research and the aging, go to http://www.nia.nih.gov. As the nation’s medical research agency, NIH includes 27 institutes and centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visithttp://www.nih.gov.