Are Alzheimer's drugs good for other memory problems?

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

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UCLA School of Nursing

New insights in using Alzheimer's drugs for other memory problems shows why these medications are no simple memory patch. 

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When people experience memory loss that looks a little like Alzheimer's but isn't, doctors diagnose it as "Mild Cognitive Impairment (MCI)". Some prescribe the Alzheimer's drug donepezil (Aricept®). New research shows why it should not be prescribed for people with mild cognitive impairment (MCI) without a genetic test.

UCLA School of Nursing researchers discovered that for people who carry a specific genetic variation — the K-variant of butyrylcholinesterase, or BChE-K — donezpezil could accelerate cognitive decline.

When It Isn't Alzheimer's

Mild cognitive impairment is a transitional state between normal age-related changes in cognition and dementia. Because many people with the condition display symptoms similar to those caused by Alzheimer’s disease, some physicians prescribe donepezil, which is marketed under the brand name Aricept and is the most-prescribed medication for Alzheimer’s. Donepezil was tested as a possible treatment for mild cognitive impairment in a large, federally funded study published in 2005, but it was not approved by the FDA. Still, doctors have often prescribed the drug “off-label” — meaning that it is not approved for that specific disorder — for their patients with mild cognitive impairment.

Worse Instead of Better

From data collected during the 2005 trial, the researchers looked at the association between BChE-K and changes in cognitive function. Using two tests that measure cognitive impairment, the Mini-Mental State Examination and the Clinical Dementia Rating Sum of Boxes, they found that people with the genetic variation who were treated with donepezil had greater changes in their scores than those who took placebos. They also found that those who took donepezil had a faster cognitive decline than those who took the placebo.

Benefits versus Risks - Ask Your Doctor

Physicians are increasingly using personalized medicine, including pharmacogenetics — the study of how genetics affect a person’s response to a drug — to tailor their patients’ care. The findings reinforce the importance of physicians discussing the possible benefits and risks of this treatment with their patients. 

• SOURCE:
  UCLA School of Nursing
• AUTHORS:
  The study was led by Sophie Sokolow, an associate professor at the UCLA School of Nursing. Co-authors were Ziaohui Li, Lucia Chen, Kent Taylor and Jerome Rotter, all of UCLA.
• REFERENCE JOURNAL:
  The study was published in the Journal of Alzheimer’s Disease.
• FUNDING:
  The work was supported by the National Institute on Aging (grant 1K23AG05141601A1).

HiV drug may slow memory loss

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

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

WebMD

By Brenda Goodman, MA
WebMD Health News

A drug that's already been approved by the FDA for use in HIV patients may also help slow the decline of memory and mental function experienced by people who are in the early stages of Alzheimer's disease.

The drug, Egrifta, stimulates the release of human growth hormone from the brain's pituitary gland. It was approved by the FDA in 2010 to help correct the abnormal distribution of body fat that often occurs in patients who live with HIV.

A new study published in the Archives of Neurology suggests it may also slowmemory loss in people who have mild cognitive impairment (MCI), a condition that often precedes full-blown Alzheimer's disease.

For the study, researchers assigned adults between the ages of 55 and 87 to get either nightly injections of Egrifta or a placebo for five months. Some were healthy and showed no evidence of memory problems on a battery of mental function tests. Others showed MCI, or memory loss that was worse than expected for their age but was not yet severe enough to interfere with daily living.

A total of 137 patients -- 76 who were healthy and 61 with MCI -- finished the study. Researchers brought them back to the lab four times: at the start of the study, then at weeks 10, 20, and then another 10 weeks after the nightly shots stopped.

At each visit, their blood was drawn. In addition, they took a battery of tests that measured different skills used in mental processing and short-term recall of words, shapes, and facts. Researchers also asked them about their mood and sleeping patterns.

In both healthy adults and those with MCI, those taking Egrifta fared better than their counterparts who took placebo injections.

Healthy adults saw their executive function improve by about 200% over their peers who got a placebo. Executive function refers to the brain's ability to manage attention and concentration, to switch between thoughts, and use working memory to plan and strategize tasks.

Adults with MCI still saw their executive function slip over the five months of the study, but their declines were not as large as those in the placebo group.

"Their expected decline was cut in half," says researcher Laura D. Baker, PhD, apsychiatrist at the University of Washington School of Medicine in Seattle.

By the end of the study, people on the drug were also better able to recall words and details of stories a bit better than people on the placebo, though the differences between the groups were not significant.

How Egrifta Works

Egrifta is a close copy of a chemical that's already made by the body called growth-hormone-releasing hormone. As the name implies, it stimulates the production of human growth hormone (HGH). Human growth hormone, in turn, triggers the release of a whole cascade of other hormones including insulin and its close cousin, insulin-like growth factor.

How Egrifta Works continued..

Insulin is probably best known for its role in regulating blood sugar, but it also has important work in the brain. In the brain, insulin stimulates the growth of new nerves and protects existing nerves from damage. Insulin levels in the brain fall with age, and previous studies have found that they're especially low in the brains of patients with Alzheimer's and other kinds of dementia.

The same group of researchers involved in the study has been testing whether inhaled insulin can reverse memory loss in Alzheimer's patients.

Egrifta may boost insulin in the brain less directly, and that could be a good thing, Baker says.

"What's so nice about this particular strategy is that it stimulates a whole cascade of hormone activities. Once this whole cascade is stimulated, it behaves normally, as it does when we're younger adults. So all we're kind of doing is boosting the system and letting it do what it does best," she says.

"It also shuts itself off when levels of one hormone or another get too high," Baker tells WebMD, so the levels always stay within a more normal range.

Risk, Side Effects, and Cost to Be Considered

Should a larger, longer study confirm the benefits of the medication for patients with early memory loss, it wouldn't come cheap.

Baker says that given at the dosages used in the study, the drug costs about $750 a day, or more than $22,500 for a 30-day supply.

"Of course that's not feasible," she says. "No health plan would ever pay for this."

She says drug companies are hard at work trying to find a way to make a less expensive version.

Side effects were reported by 68% of people on Egrifta -- twice the rate of adverse events experienced by those on the placebo injections. Side effects were mostly mild. They included skin reactions like itching, redness, and stinging around the injection site. It was also common for people to report increased joint pain and stomach upset.

There are already products at vitamin and health foods stores that claim to boost growth-hormone-releasing hormone, but Baker cautions that they could do so dangerously.

But, she says, there is a far less expensive and less risky way to get virtually the same degree of benefit as was seen with this pricey drug: Exercise.

"We completed a study last year testing exercise for brain function in people with mild cognitive impairment," Baker says. "We had the same improvements in executive function. We used the same tests in both studies, and we saw the same benefits."

How much exercise is needed to get the benefit? In her previous study, which was published in 2010 in the Archives of Neurology, people engaged in aerobic exercisefor 45 to 60 minutes at least four days of the week for six months.

"Up to this point, this is the most potent way to slow things down or improve cognition," she says.

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.

Daffodil Drug Improves Dementia

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Here are more interesting dementia brain boosting activities



Worldhealth.net |

A new drug designed to treat Alzheimer's disease looks set to be an effective treatment for vascular dementia. A recent 12-month clinical trial of the drug Galantamine (Reminyl), which is derived from the daffodil, revealed that the drug improved cognitive function, delayed the effects of dementia, and prevented behavioral decline.

SOURCE/REFERENCE: Reported by www.health-news.co.uk

Alzheimer's Disease Screening Breakthrough Will Help Identify Potential Treatment Drugs

ScienceDaily (Dec. 12, 2008) — CSIRO scientists have developed a new system to screen for compounds that can inhibit one of the processes that takes place during the progression of Alzheimer’s disease. Certain yeast species could be used to develop this rapid screening process. Folate has been shown to be beneficial in the screening system
Lead author, CSIRO’s Dr Ian Macreadie says folate is already well known to have a protective effect against Alzheimer’s disease which is believed to be caused by the loss of neurons in the brain due to a process whereby toxic multimers of a small protein called Aβ are formed.

“However, a team of scientists working within CSIRO’s Preventative Health Flagship has discovered a....read the whole article

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