Rock Creek Pharmaceuticals Announces First Study Using Anatabloc® Nutritional Supplementation in Alzheimer's Patients

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GLEN ALLEN, Va., PRNewswire via COMTEX/ -- Star Scientific, Inc. /quotes/zigman/80562/quotes/nls/cigx CIGX +5.90% through its wholly owned subsidiary, Rock Creek Pharmaceuticals, Inc., announces that it has received IRB approval of the first human clinical study of the safety and effects of nutritional supplementation with Anatabloc® in individuals with Alzheimer's disease. The study will be undertaken in conjunction with the Roskamp Institute of Sarasota, Florida, which has been acting as a research partner in assessing the impact of Anatabloc® on Alzheimer's

New development in Alzheimer's research

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ScienceDaily — Studying a mouse model of Alzheimer's disease, neuroscientists at the Technische Universitaet Muenchen have observed correlations between increases in both soluble and plaque-forming beta-amyloid -- a protein implicated in the disease process -- and dysfunctional developments on several levels: individual cortical neurons, neuronal circuits, sensory cognition, and behavior. Their results, published in Nature Communications, show that these changes progress in parallel and that, together, they reveal distinct stages in Alzheimer's disease with a specific order in time.


In addition to its well known, devastating effects on memory and learning, Alzheimer's disease can also impair a person's sense of smell or vision. Typically these changes in sensory cognition only show themselves behaviorally when the disease is more advanced. A new study sheds light on what is happening in the brain throughout the disease process, specifically with respect to the part of the cerebral cortex responsible for integrating visual information. A team led by Prof. Arthur Konnerth, a Carl von Linde Senior Fellow of the TUM Institute for Advanced Study, has observed Alzheimer's-related changes in the visual cortex at the single-cell level.


Using a technique called two-photon calcium imaging, the researchers recorded both spontaneous and stimulated signaling activity in cortical neurons of living mice: transgenic mice carrying mutations that cause Alzheimer's disease in humans, and wild-type mice as a control group. By observing how neuronal signaling responded to a special kind of vision test -- in which a simple grating pattern of light and dark bars moves in front of the mouse's eye -- the scientists could characterize the visual circuit as being more or less "tuned" to specific orientations and directions of movement.


Konnerth explains, "Like many Alzheimer's patients, the diseased mice have impairments in their ability to discriminate visual objects. Our results provide important new insights on the cause that may underlie the impaired behavior, by identifying in the visual cortex a fraction of neurons with a strongly disturbed function." And within this group, the researchers discovered, there are two subsets of neurons -- both dysfunctional, but in completely different ways. One subset, thought to be the first neurons to degenerate, showed no activity at all; the other showed a pathologically high level of activity, rendering these neurons incapable of properly sensing objects in the mouse's environment. "While around half of the neurons in the visual cortex were disturbed in one way or the other, roughly half responded normally," notes Christine Grienberger, a doctoral candidate in Konnerth's institute and first author of this paper. "That could have significant implications for future research in the field of Alzheimer's disease, as our findings raise the question of whether future work only needs to target this population of neurons that are
disturbed in their function."


The in vivo single-neuron experiments were carried out for three age groups, corresponding to different stages of this progressive, degenerative disease. The results were correlated with other measurements, including soluble beta-amyloid levels and the density of beta-amyloid plaques in the brain tissue. The researchers' findings show for the first time a progressive decline of function in cortical circuits. "An important conclusion from this study," Konnerth says, "is that the Alzheimer's disease-related changes on all levels -- including behavior, cortical circuit dysfunction, and the density of amyloid plaques in diseased brains -- progress in parallel in a distinct temporal order. In the future, the identification of such stages in patients may help researchers pinpoint stage-specific and effective therapies, with reduced levels of side effects."


This research was supported by the German Excellence Initiative (TUM-IAS, CIPSM); the German Research Foundation (DFG, IRTG 1373); ERAnet; and the Friedrich Schiedel Foundation

Research funding and recruitment for dementia

Health care professionals and others caring for folks with dementia. Here is some information of importance.


Often when you are working with people who have dementia, finances can be a concern. First of all research in this field is key and advances in treatment can not be made without adequate funding. Thus you or your group can be instrumental in funding. But what if you do not have the time is undertake this task? life science executive search firms can help you not only with fundraising but also with helping you to find people to work for you or your organization. They have helped to raise money for the March of Dimes.

You may need a top medical device executive search firm to help find the right people with the right funding using the right equipment. Biotechnology Executive Recruiters have a history of finding top persons to do important research in many areas including dementia. If we ever are going to find effective treatments for this and other diseases, we have to find trained dedicated intelligent people to do the job.

A New Take on What Causes Alzheimer's

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JohnsHopkins

More than a century after German psychiatrist Alois Alzheimer first lectured about the gooey mass of plaques and tangles he noted in a postmortem brain tissue sample, scientists are still debating what causes Alzheimer's disease. 

The majority of scientists have agreed that plaques result from overproduction of beta-amyloid -- a protein found in the cell membrane of neurons. In people with Alzheimer's, this protein accumulates in clumps between brain cells. 

But recently, researchers from Washington University in St. Louis arrived at a new theory: that rising brain levels of beta-amyloid do not mean that patients are making more of it but that they can no longer clear it from their brains as effectively. 

The study. As reported in the journal Science, the investigators tested 24 people, average age 74, and separated them into a group composed of people with minor Alzheimer's disease and another whose members were cognitively normal. Special testing revealed that both groups produced beta-amyloid at the same average rate within the brain. 

The study subjects were then tested to see how the beta-amyloid was cleared from their brains. One of the ways the brain does this is by moving it to the spinal fluid for disposal. The researchers took samples of cerebrospinal fluid by inserting a needle into the subjects' backs and drawing off the fluid that normally surrounds the spinal cord. They found that those with Alzheimer's had decreased clearance of beta-amyloid from the brain to the cerebrospinal fluid -- about 30 percent less than those who were cognitively normal. This suggests that Alzheimer's is associated with disruption of the brain's ability to normally handle the beta-amyloid. 

What it means. Early diagnosis of Alzheimer's has been elusive. But because researchers have uncovered a possible mechanism of early disease development, it is possible that this discovery could lead to both a test for early detection and the development of effective therapies to stop or reverse Alzheimer's memory disruption. They calculate that it would take an adult 10 years to build up enough amyloid in his or her brain to reach the amount typically present in someone with Alzheimer's. 

This knowledge could offer doctors a window of opportunity to diagnose someone long before dementia symptoms develop. Once they learn they are at risk for dementia, people could make more concerted efforts to reduce their personal risk factors for Alzheimer’s. At the same time, pharmaceutical companies could work on targeted medications to halt brain damage before symptoms become irrevocable. 

---

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Genes that influence hippocampal volume identified

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ZeeNews
London: Researchers have uncovered four loci that seem to be associated with decreasing the volume of the hippocampus.

The hippocampus is the region of the brain that plays an important role in the formation of specific, new memories, which is an ability that patients with Alzheimer’s disease lose.

The findings by an international team of researchers led by Boston University School of Medicine (BUSM) may have broad implications in determining how age, Alzheimer’s disease and other diseases impact the function and integrity of the hippocampus.

Previous research has shown that the hippocampus is one of the brain regions involved with short and long-term memory processes and that it shrinks with age.

It also is one of the first regions to exhibit damage from Alzheimer’s disease, which can cause memory problems and disorientation.

“One of the problems with studying the genetics of a disease like Alzheimer’s, which becomes symptomatic later in life, is that many people die of other causes before they reach the age at which they might have manifested the clinical dementia associated with the disease,” said Sudha Seshadri, MD, professor of neurology at BUSM and a senior author of the study.

“To get around this issue, we have been studying the genetics of traits that we know are associated with a high future risk of Alzheimer’s disease but that can be measured in everyone, often 10 to 20 years before the age when most persons develop clinical symptoms.”

The potential genetic traits are called endophenotypes, and hippocampal volume is one such trait. The hippocampus shrinks before and during the progression of Alzheimer’s disease, but other factors, such as vascular risk factors and normal aging, also lead to the decrease in size.

“Our research team wanted to pinpoint the genetic causes of changes in the hippocampal volume in a sample of apparently normal older persons,” said Seshadri.

The Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium allowed the researchers to gather data on hippocampal volume from 9,232 people who did not have dementia. They identified four genetic loci, including seven genes in or near these loci that appear to determine hippocampal volume.

The results show that if one of the genes is altered, the hippocampus is, on average, the same size as that of a person four to five years older. These results were replicated in two large European samples that included a mixed-age sample that included some participants with cognitive impairment.

“The findings indicate that these loci may have broad implications for determining the integrity of the hippocampus across a range of ages and cognitive capacities,” said Seshadri.

One of the genes identified by the researchers was also shown to play a role in memory performance in a different data sample.

The identified genetic associations indicate that certain genes could influence cell death by apoptosis, brain development and neuronal movement during brain development, and oxidative stress.

Additionally, the researchers found that the genes play a role in ubiquitination, which is a process by which damaged proteins are removed, whereas other genes code for enzymes targeted by new diabetes medications.

“Future studies need to further explore these genetic regions in order to better understand the role of these genes in determining hippocampal volume,” added Seshadri.

The study will be published online in Nature Genetics.

ANI

Pain relief and muscle stimulation products

Here is a great resource for health care professionals, caregivers for those with dementia and others needing pain relief units.  


There are times that a person with dementia may be in pain and they have trouble expressing this or are resistive to taking medication. One way to relieve their pain is to use Ultrasound Units and TENS Units

Sometimes a person with dementia or another person in your care may need their muscles stimulated. LG Med Supply also has Muscle Stimulators .



LG Med Supply has these units that are priced so that you can have one for personal use or for use with a person you care for. 


If you or they need both, you can get the  LG-TEC Dual Combo TENS Unit and Muscle Stimulator 



If you want to know more you can visit LGMedSupply Online .


You can also go to their online customer blog. There you can ask questions and get all the information you need.

Prepare financially for risk of getting dementia

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Forbes

CBS newsman Mike Wallace, who died last night at the age of 93, was a journalist’s journalist. In a career that spanned 60 years, most of it at “60 Minutes,” he confronted Nixon aide John Ehrlichman about alleged Watergate crimes; interviewed Jack Kevorkian, the assisted suicide doctor; and reduced Barbra Streisand to tears.

Announcing his retirement as a regular correspondent in March 2006, he said, “my eyes and ears, among other appurtenances, aren’t quite what they used to be.”

Wallace had also been public about his battle with depression. In 1996, appearing before the Senate’s Special Committee on Aging to urge more federal funds for depression research, he described feeling “lower, lower, lower than a snake’s belly,” and his recovery through psychiatric treatment and antidepressant drugs. Later, he disclosed that he once tried to commit suicide during that spell.

Perhaps that inspired his son, “Fox News Sunday” host Chris Wallace, to reveal in a recent interview with The New York Times, that his father suffered from dementia. “Physically, he’s okay. Mentally, he’s not,” Wallace said. “He still recognizes me and knows who I am, but he’s uneven.”

Advancements in medical science and care may enable us to live fuller, longer lives. The flip side is that more of us, like Mike Wallace, are likely to suffer from a diminished mental state–a harsh reality that’s difficult to accept. Here’s a scary statistic: One in eight baby boomers will get Alzheimer’s after they turn 65. Sure, you hope you won’t be one of them. But the risk of a slow decline and incapacity, meaning that you don’t know what assets you have, what you want to do with them and who your family members are, lurks for us all.

Once you do become incapacitated, it is generally too late legally to make changes in your estate planning documents. And unless you have made other, binding arrangements, your family may need to ask a court to appoint a conservator (also called a guardian) to oversee your finances. This can be an expensive and an embarrassing ordeal, and for many families involves unpleasant, even acrimonious, exchanges.

Maybe you figure you’ll have time to plan after the onset of symptoms. But you could instead suffer a stroke, or get hit by a bus and immediately need someone else to make medical decisions for you. The bottom line is that regardless of your current age or health, it’s crucial to anticipate that at some point you might become physically or mentally unable to manage your finances or make medical choices.

Here are issues to consider.

Who Will Make Health Care Decisions?

Someone needs to be able to make medical decisions if you no longer can. To appoint this person, you will need a health care proxy – known in some states as a health care agent or health care power of attorney. Legally, the health care proxy also automatically gives the agent access to your medical records. (Some states have surrogate decision-making laws that give specific family members the right to make certain medical decisions for others.) Sign four copies of both this document and your living will. Keep one and give one each to your health care agent, your primary physician and a trusted advisor.

What Are Your Final Wishes?

If you have preferences about end-of-life care, you should create a living will (also called an advance directive) – a written statement that anced directives,expresses your wishes. Although it is difficult to address every contingency, living wills typically cover pain relief and whether you would want treatments such as surgery, a ventilator, a feeding tube or resuscitation that might prolong your life but without necessarily ensuring your return to a functional state.

More on preparing for the financial risk of getting dementia

Diabetics are fifty percent more likely to develop dementia

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Philly.com

Several large studies have shown that people with diabetes are at especially high risk for Alzheimer's disease.

Steven Arnold, director of the University of Pennsylvania's Memory Center, said diabetics are 50 to 100 percent more likely to get the fatal, memory-destroying disease.

This has made researchers increasingly interested in the role that insulin, the hormone that's out of whack in diabetes, might play in Alzheimer's.
In the brain, Arnold said, insulin is important for cell growth and releasing neurotransmitters that allow cells to communicate. It enhances learning and memory.

Arnold is the senior author of a new study in the Journal of Clinical Investigation that looked at the brains of people with Alzheimer's disease and mild cognitive impairment, often a precursor to dementia. He found insulin resistance in their brains, even though the people did not have diabetes. Arnold said the chemical differences between those who did and did not have memory problems were striking. "I've never seen a difference this large," he said.

When cells are insulin resistant, insulin is present but the cells don't respond as much as they normally would. Insulin resistance is the hallmark of Type 2 diabetes, the kind that 90 percent of American diabetics have. Untreated, it leads to high blood sugar.

Arnold's team studied brain samples taken from people who had died. Even in dead cells, several steps of chemical reactions could be seen. The study found "tremendous abnormalities pretty much all the way down the line" in people with Alzheimer's.

There's no easy way to test brain insulin resistance in the living. Arnold said it's likely that people with diabetes have brain insulin resistance, but others could have it, too.

Many diabetes drugs are designed to lower blood sugar, but some act as insulin sensitizers. Arnold is now seeking funding to test whether one such drug, metformin, can help people with dementia or mild cognitive impairment.

- Stacey Burling

Fighting dementia

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Alzheimer's Association

It’s a sad fact that 1 out of 7 people who have Alzheimer’s or dementia live alone.

Living alone with dementia increases the risk of missed diagnosis, injuries and even death, as well as the likelihood of being placed into a nursing home earlier, increasing overall health care costs.
But they don’t have to fight this disease alone. Act Now!

As the number of people with the disease grows and the cost of providing care skyrockets, our nation can take steps to support Alzheimer’s research, public awareness and education, health provider training, and family caregiver support. The Obama Administration has put forth a draft National Alzheimer's Plan, which is an important step forward for our nation. However, there is still time to strengthen the plan in areas like research, clinical care and community services. So urge the President to take the next bold step forward in the fight against Alzheimer’s by issuing a strong National Alzheimer's Plan.
Update: Funding for Alzheimer’s

In 2010, Congress unanimously passed the bipartisan National Alzheimer's Project Act (NAPA) , which requires the Secretary of Health and Human Services to develop a National Alzheimer's Plan. The Plan must include recommendations to reduce the financial impact of Alzheimer's on families and federally funded programs, and to improve health outcomes and care quality for people living with Alzheimer's and their caregivers.
In anticipation of the first-ever National Alzheimer’s Plan, the President’s Fiscal Year 2013 Budget request to Congress included $100 million to address Alzheimer’s disease. These resources are sorely needed in order to accelerate the development of breakthrough treatments that would prevent, halt, or reverse the course of Alzheimer’s, help the increasing number of families living with Alzheimer’s and address Alzheimer’s steadily mounting impact on our healthcare system and economy.
However, these funds depend on Congressional action. Over the coming weeks we will be asking Alzheimer’s Association advocates like you to reach out to your members of Congress, urging them to provide these necessary resources.

Dementia therapy-patch or pill (part 2)

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Family Practice News

The NMDA (N-methyl-d-aspartate) receptor antagonist memantine is also approved for patients with mild to moderate Alzheimer’s, with optimal dosing titration to 10 mg b.i.d. "Side effects are quite rare, but can include somnolence, headache, and dizziness," said Dr. Cummings, who is also chair of neurotherapeutics at the Cleveland Clinic’s Neurological Institute. "Most patients, by the time they reach mid-disease, are on both a cholinesterase inhibitor and memantine."

Other treatment options include the medical foods CerefolinNAC and Axona, which are generally recognized as safe by the Food and Drug Administration and are available by prescription. "No demonstration of clinical benefit is required for these agents," Dr. Cummings said. "The data set supporting medical foods is not as robust as the data set supporting cholinesterase inhibitors."

CerefolinNAC is a combination of vitamin B6, vitamin B12, and folate that Dr. Cummings uses for hyperhomocysteinemia. "I know that high levels of homocysteine are correlated with cognitive impairment, so I try to reduce that by giving CerefolinNAC," he said. "However, there are no data which prove that lowering will necessarily improve the prognosis of the patient. What you are doing is piecing together various types of data to support that use, but it’s not as strong as a double-blind, placebo-controlled trial showing a direct benefit."

Axona is a proprietary formulation of medium-chain triglycerides that increase plasma concentrations of ketone bodies. "This is considered an energy source for neurons," Dr. Cummings said.

Dr. Cummings disclosed that he has provided consultation to the following pharmaceutical companies: Abbott, Acadia, Adamas, Anavex, Astellas, Avanir, Bayer, BMS, Eisai, EnVivo, ExonHit, Janssen, Forest, Genentech, GSK, Lundbeck, Merck, Neurokos, Novartis, Otsuka, Pfizer, Prana, QR Pharma, Sanofi-Aventis, and Takeda.

Dementia therapy-:patch or pill

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Family Practice News

If you’re stumped about which cholinesterase inhibitor to prescribe for your patients with newly diagnosed Alzheimer’s disease, rest assured that the clinical effects are similar with all such agents.

"There is no substantive scientific evidence that says one of the cholinesterase inhibitors is better than another, so get comfortable with one or two of them," Dr. Jeffrey L. Cummings advised during a psychopharmacology conference sponsored by the Nevada Psychiatric Association. "The effect is demonstrable late in the disease, so if you take patients with Mini-Mental State Exam scores of less than 10, you still get the same response that you do in somebody whose Mini-Mental State Exam score is 20. There’s no proven effect on the underlying disease state."

Clinical evidence from nearly 20 years of cholinesterase inhibitor use suggests that 25% of patients who take them will experience modest cognitive improvements, defined as a 2-4 point increase on the Alzheimer’s Disease Assessment Scale-cognitive subscale or a 1-2 point increase on the Mini-Mental State Exam. This "makes it very difficult to see a response if it’s not on the upper end of that [response]," Dr. Cummings said. "But about 80% of patients on cholinesterase inhibitors have a delay in decline of 6-9 months. That’s worthwhile, because patients are usually only on therapy for about 5 or 6 years over the course of their disease. So if you can delay almost 20% of that, that’s fantastic."

Dr. Cummings, director of the Cleveland Clinic’s Lou Ruvo Center for Brain Health, lets convenience drive the choice of which cholinesterase inhibitor to prescribe. "I sit with the patient and the caregiver and I ask: ‘Do you want a pill or a transdermal patch?’ If they say, ‘I want a pill,’ I give them donepezil. If they say, ‘I want a patch,’ I give them the rivastigmine transdermal patch," he said.

"I’m trying to respond to the perceived convenience of the caregiver. That’s the question I pose, and those are the two drugs I use."

He went on to note that donepezil "is more likely to give you diarrhea than rivastigmine is, and the rivastigmine patch will give you a rash in 5-10% of patients. Bradycardia is a contraindication for all cholinesterase inhibitors."

Donepezil is available in 5-mg, 10-mg, and 23-mg formulations. The 23-mg form is approved only for patients with moderate to severe disease. "There is more diarrhea with the 23-mg dose; maybe 15% of patients will get diarrhea with that higher dose," he said. "To ameliorate this, for 1 month I have patients go from 10 mg to 15 mg before jumping to the 23-mg dose. I think that helps rather than going directly from 10 mg to 23 mg."

Rivastigmine is approved for mild to moderate Alzheimer’s and for patients with mild to moderate Parkinson’s disease dementia. It’s available in 1.5-mg, 3-mg, 4.5-mg, and 6-mg capsules, or as a 4.6-mg or 9.5-mg transdermal patch.

Galantamine is another cholinesterase inhibitor approved for patients with mild to moderate Alzheimer’s disease, and it has dosing options of 6 mg, 8 mg, or 12 mg b.i.d. Extended formulations are available in 12-mg and 24-mg doses.

Eli Lilly Says FDA Approved Alzheimer's Diagnostic Agent Amyvid

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RTT News

Eli Lilly and Company (LLY: News ) on Friday said the Food and Drug Administration (FDA) has approved Amyvid, a radioactive diagnostic agent for use in patients being evaluated for Alzheimer's Disease and other causes of cognitive decline.

Amyvid or florbetapir F 18 injection is a molecular imaging agent under investigation for the Positron Emission Tomography imaging of beta-amyloid plaque in the brains of Alzheimer's disease patients.

A negative Amyvid scan indicates sparse-to-no amyloid plaques are present, which is inconsistent with a neuropathological diagnosis of Alzheimer's Disease and reduces the likelihood that a patient's cognitive impairment is due to Alzheimer's Disease.

A positive scan indicates moderate to frequent amyloid plaques are present. This amount of amyloid plaque is present in patients with Alzheimer's Disease, but may also be present in patients with other types of neurologic conditions and in older people with normal cognition.

Amyvid was a lead candidate of Avid Radiopharmaceuticals, which became a wholly owned subsidiary of Lilly through its acquisition by the Indianapolis, Indiana-based health care giant in December 2010.

Alzheimer's Biomarker Linked to Major Depression

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Medscape Today

Deborah Brauser

disorder (MDD) may have low levels of amyloid beta 42 (Aß-42), a biomarker that has been implicated in Alzheimer's disease (AD), new research suggests.

In a small study of older adult volunteers who had no mild cognitive impairment (MCI), those with MDD had significantly lower cerebrospinal fluid (CSF) levels of Aß-42 than those without depression.

In addition, levels of F2-isoprostane, considered a biomarker of oxidative stress, were higher for the participants with MDD.

"Current treatments for depression are not very satisfactory," lead author Nunzio Pomara, MD, director of the Geriatric Psychiatry Division of the Nathan S. Kline Institute for Psychiatric Research in Orangeburg, New York, and professor of psychiatry at the New York University School of Medicine, told Medscape Medical News.

"That's why, in my opinion, it's important to explore novel mechanisms which would underlie the development of depression in humans," said Dr. Pomara.

He noted that this study was an "interesting first step" and that if its findings bear out in further research, it may lead to the development of better therapeutic interventions.

"One must be very cautious because this was a small study. But I believe its importance lies not so much in finding a final truth about pathogenesis of depression but really in setting the stage for future studies of this molecule as a possible factor in both the development of depression and in shaping Alzheimer's disease."

The study was published online March 28 in the American Journal of Psychiatry.

Proteome Sciences Completes 1,000-Patient Validation Study of Alzheimer's Plasma Protein Markers

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Proteomesciences

By Adam Bonislawski

Researchers from Proteome Sciences, the UK's National Institute for Health Research, and Millipore have completed a 1,000-sample validation study of blood-based protein biomarkers for Alzheimer's disease.

Preliminary results from the study identified three biomarker panels – each containing between 11 and 16 proteins – that can distinguish between controls, mild cognitive impairment, and Alzheimer's disease, Ian Pike, Proteome Sciences' chief operational officer, told ProteoMonitor.

The data were presented this week at the Research & Standardization in Alzheimer's Disease 2012 meeting in Melbourne, Australia, by Simon Lovestone, director of the NIHR's Biomedical Research Centre for Mental Health and of the Research King’s Health Partners Academic Health Sciences Centre, London.

According to Pike, Proteome Sciences and Kings College London jointly own intellectual property for the panels, and Proteome Sciences has an exclusive license to commercialization rights.

Proteome Sciences also has an exclusive licensing deal with Millipore for research use of the markers on that company's Milliplex MAP platform, which is based on Luminex's xMAP technology.

The validation study, Pike said, follows on discovery work done several years ago by Proteome Sciences and researchers, including Lovestone, at King's College London. Some of that discovery work was published in a 2006 Brain paper.

In that work the researchers "analyzed a cohort of Alzheimer's patients and a cohort of age- and sex-matched controls using a range of techniques including two-dimensional gels" and an earlier iteration of Proteome Sciences' Tandem Mass Tag isobaric tagging reagents, Pike said.

"That [research] identified an original panel of 30 or 35 [plasma] proteins," linked to Alzheimer's, which the company and its Kings College partners also jointly patented, Pike said.

In the recently completed study the team measured these markers and combinations thereof in 1,000 randomized, blinded samples comprising age- and sex-matched Alzheimer's cases, MCI cases, and controls, using both the Milliplex MAP platform and selected-reaction monitoring mass spectrometry.

The researchers then assimilated the mass spec data and the immunoassay data with about 250 clinical measures they had for each patient into a unified database, which they then submitted to univariate and multivariate analyses, Pike said. "And by doing that we identified between 11 and 16 proteins in each [of three panels] that differentiate between Alzheimer's and controls, Alzhiemer's and MCI, and MCI and controls," he said.

In addition to providing validation data on the markers, the study offered a good test of the robustness of Proteome Sciences SRM-MS platform, Pike said. He noted that at 2,000 measurements from 1,000 samples, it represented one of the larger multiplexed SRM-MS-based protein biomarkers studies to date.

"We had very robust measurements with good reproducibility across the sample cohort," he said. "The mass spec platform held up extremely well in terms of being able to handle that many samples."

Alzheimer's biomarkers have of late been a significant area of focus for Proteome Sciences, and, in fact, last year the company released a report it had commissioned that estimated that protein biomarkers for Alzheimer's disease would represent a cumulative $9 billion market over the next ten years (PM 6/3/2011). In addition to their promise for diagnosis and predicting progression of the Alzheimer's, early detection and progression biomarkers are seen as key to pharmaceutical research into drugs for the disease.

Proteome Sciences currently offers an SRM-MS assay for measuring nine plasma proteins linked to Alzheimer's disease as well as a mass spec-based assay for measuring phosphorylated tau in cell culture and tissue samples. It introduced the plasma protein panel in July of 2010 (PM 7/16/2010) and inked a contract with pharmaceutical company Eisai in February 2011 to use it in that company's drug-development work (PM 2/4/2011). The nine proteins in the panel were included as part of the validation study presented this week, Pike said.

Much Alzheimer's biomarker work has focused on proteins in cerebrospinal fluid. Sample collection for CSF studies and clinical applications, however, requires patients to undergo a lumbar puncture. Plasma proteins like those investigated in the Proteome Sciences-NIHR validation study, on the other hand, are desirable because they can be sampled via a blood draw, making them more useful for purposes like regular monitoring.

Alzheimer's markers have typically been more difficult to detect in plasma than CSF, however, and some high-profile Alzheimer's plasma biomarker research has shown poor reproducibility.

In particular, a team of Lund University researchers published a study in January in PLoS One in which they evaluated a panel of 18 plasma proteins previously identified as Alzheimer's biomarkers in a 2007 Nature Medicine study produced by a Stanford University team headed by Tony Wyss-Coray (PM 1/30/2012).

The Lund researchers were unable to reproduce the original study's results and found that, according to its new analysis, none of the 18 proteins could identify Alzheimer's patients with high diagnostic precision.

Based on the results of the Nature Medicine paper, Wyss-Coray founded the biotech firm Satoris, which aimed to commercialize the markers. However, in an interview with ProteoMonitor following the release of the Lund group's PLoS One paper, he said that he and his collaborators had been "probably a bit naïve and too enthusiastic" about the markers they identified.

Rules-Based Medicine – now Myriad RBM – acquired Satoris in May of last year. The proteins have made it into research panels now owned by Myriad RBM, but not into an US Food and Drug Administration-approved diagnostic, and, Wyss-Coray said, he believes work on the markers is "on the backburner."

"I think there are differences [in the plasma proteome of Alzheimer's patients], and actually we continue to see differences, but I think there are a lot of issues," he said, adding that that his lab has since moved away from blind biomarker discovery work and is focusing on identifying signaling pathways linked to Alzheimer's with the aim of better understanding mechanisms of the disease.

"Measuring plasma proteins is a huge challenge, and I think most people who have experience in the field recognize that," Wyss-Coray said. He added that many such efforts have been plagued by small sample sizes, noting that his team's original Alzheimer's work looked at roughly 100 patients and controls.

"Just measuring proteins in cases and controls and then thinking you have a biomarker for the disease isn't going to work unless you have the luxury of measuring 10,000 samples," he said.

Pike noted, however, that both the discovery and validation cohorts used in Proteome Sciences' Alzheimer's biomarker researcher were considerably larger than the sets used by either the Stanford or Lund teams. He added that a number of their markers – including proteins like clusterin, alpha-2-macroglobulin, and complement factor H – have been identified as Alzheimer's markers in independent studies.

Proteome Sciences has no plans to develop the markers as an in vitro diagnostic itself, Pike said, but, rather, it intends to license them out to interested diagnostic companies.

"We've been marketing [the markers] based on the preliminary data to a number of diagnostic companies, and I would anticipate that this data, when it is fully processed, will add to the weight behind these markers and generate a lot more interest," he said. The researchers, Pike added, are currently preparing their results for submission to a peer-reviewed publication.

The company is now focusing on analyzing the mild cognitive impairment data, "to better understand the drivers of cognitive dysfunction at early timepoints that best correlate with progression to Alzheimer's type dementia and other types of dementia," he said.

Proteome Sciences is also offering SRM-MS analysis of the proteins from the three panels out of its ISO 9001-accredited facility in Frankfurt, Germany. It might add certain of the proteins to its existing nine-protein SRM-MS Alzheimer's assay, as well.

"We already offer the nine-plex plasma assay, and we will certainly look at the various data going forward to see if it justified producing a new SRM multiplex [assay] covering more of these proteins," Pike said.

Recent Study Reveals Two Natural Ways to Protect Brain Cells

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The Doctors Health Press, a publisher of various natural health newsletters books and reports, including the popular online Doctors Health Press e-Bulletin, is reporting on a study that finds evidence that two natural substances -- a mineral and a fatty acid -- can protect against both cancer and Alzheimer's disease.
As reported in the Doctors Health Press e-Bulletin on Friday, March 30, 2012 (http://www.doctorshealthpress.com/two-natural-ways-to-protect-your-brain-cells), researchers have found that zinc and DHA exert very different -- but beneficial -- effects when it comes to protecting your good health. They prefaced their study by noting that dietary intake of zinc and DHA have health benefits for a number of human diseases.
The Doctors Health Press e-Bulletin reports that after conducting extensive tests, the research team discovered that zinc and DHA affect expression levels of histones H3 and H4 in human neuronal M17 cells. Histones are small proteins that help build DNA. Building healthy DNA, especially in nerve cells, helps keep diseases like cancer and Alzheimer's at bay.
Specifically, zinc helps to reduce the levels of the anti- apoptotic marker Bcl-2, while increasing the apoptotic marker caspase-3 levels. Sounds complicated, but basically, this means that zinc is protecting your cells: it helps the cells that should die do so and prevents substances that halt death in proliferating cells (such as cancer cells) from performing this task. As for DHA, it promotes gene expression (the building of proteins) and neuroprotection, aiding in staving off Alzheimer's.
The Doctors Health Press e-Bulletin also revealed the food sources of zinc include liver, beef, lamb, scallops, sesame seeds, and pumpkin seeds. Food sources of DHA include flaxseeds, salmon, walnuts and sardines.
(SOURCE: "Effects of Zinc and DHA on the Epigenetic Regulation of Human Neuronal Cells," Cell Physiol. Biochem., 2012; 29(1-2):.87-98.)
Doctors Health Press e-Bulletin is a daily e-letter providing natural health news with a focus on natural healing through foods, herbs and other breakthrough health alternative treatments. For more information on the Doctors Health Press, visit http://www.doctorshealthpress.com.
David Juan, MD, is the editor of The Vitamin Doctor newsletter that reveals some of the inside facts, including potential hazards, of today's popular world of vitamins and supplements. The Vitamin Doctor has released a new video revealing the foods that can have negative consequences when mixed with popular supplements. To see the video, visit http://www.doctorshealthpress.com/foods-never-to-mix.

Quercetin can prevent cancer and dementia

Healthcare professionals, here is some information you will find useful.

Have you ever heard of a substance called quercetin. It is a strong antioxidant found in many fruits like blueberries, strawberries and grapes. It has been known for many years that people who eat a lot of fruits and vegetables live longer and are healthier. It is most likely because of the strong flavanoid called quercetin. Quecetin helps protect the body against cancer because it is a cytotoxin. It is felt that it is an alternative cancer treatment

Quercetin has been studied by the Cleveland Clinic and many other reputable clinics, hospitals, universities, and labs. Quercetin is chemically attracted to damaged cells, attaching to them and making them harmless and stopping the damaged cells from reproducing.thereby inhibiting the replication of damaged, diseased cells.

Quercetin helps to prevent dementia Quercetin does this by preventing cholesterol from oxidizing, thereby rendering the cholesterol harmless and unable to cause arterial damage and hardening.

If you or your loved ones or clients are having trouble eating enough fruits and vegetables, you can buy quercetin capsules.. which are most effective in conjunction with vitamin C.

Quercetin has also been shown to fight other diseases such as heart disease, kidney disease, osteoporosis, prostrate disease, and bacterial and viral infections.

When should you give nutritional drinks or shakes to those with dementia

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Aging care

Dr Amy Erlich

Under-nutrition due to lack of eating is a common problem among elderly people. It is also dangerous. Under-nutrition and extreme thinness can lead to higher mortality rates, according to a study published in the American Journal of Clinical Nutrition. It is a problem that can't be ignored.
Geriatricians (specialists in treating the elderly) take weight loss among the elderly very seriously and caregivers should, too. However, some caregivers feel that feeding their parent a nutrition supplement drink, such as Boost, in lieu of meals ensures the elderly loved one is getting the nutrition they need. This isn't the case, according to Dr. Amy Ehrlich, Associate Professor of Clinical Medicine and Interim Division Head of Montefiore Medical Center's Geriatrics Division.
"Just giving them a can of Ensure for dinner isn't enough," she says. "It is always better to try to use regular food to maintain a person's weight." If a caregiver wants to use nutrition drinks, they should be used between meals, as a snack or supplement to add calories to the senior's diet – not as a meal replacement.
Work with a doctor to determine elder's nutrition needs
Weight loss is a marker of frailty. However, it is not a normal part of aging. Dr. Ehrlich stresses that it is critical to find out what is causing the senior's loss of interest in food. A doctor should conduct a detailed medical evaluation to determine the cause of loss in appetite and weight loss. "There are a variety of treatable conditions that could be the culprit: ulcers, thyroid disease, dementia, depression, even ill-fitting dentures. All are treatable, so rather than immediately turning to a supplement, work with your doctor to address the cause of the problem," Dr Ehrlich says.
If a caregiver does decide a nutrition drink is right for their elderly loved one, a doctor should still be consulted to determine the type of supplement to use. For example, diabetics must choose a low-sugar product.
Frail elderly have different nutrition requirements
There is a misperception that frail elderly people should adhere to the same low-fat, low-calorie diet that is recommended for the general population. However, Dr. Ehrlich says that for frail elderly who have substantial weight loss, the opposite is true. "I'll see a 94-year-old person who is losing weight and he is restricting everything, eating a low-calorie, low-fat diet. It would be better to eat a bowl of ice cream, for the caloric intake!"
Elders who have experienced weight loss should eat what they like. And don't be afraid to incorporate eggs, cheese, peanut butter…even ice cream into the diet. There is no need for low-fat milk or cheese.
Elders often can't (or don't want to) eat three large meals a day. Rather, encourage them to have smaller, more frequent meals, including snacks, even before bed.
Nutrition drinks and supplements can interact with medications
Supplements, including nutrition drinks, can cause dangerous drug interactions in the same way prescription medications do.
If an elder is taking prescription and over-the-counter drugs and supplements, the drugs may conflict and, basically, go to war against each other, while also damaging otherwise functioning body organs and systems. Check with your doctor to avoid interactions. "I encourage my patients to bring in all their medications, supplements and vitamins, so I can check for possible interactions. I call it the 'brown bag visit,' " Dr. Ehrlich says. As an example, vitamin supplements may negatively interact with blood thinners like Coumadin.
The bottom line is that nutrition drinks are a not a magic fix for lack of eating or under-nutrition. These products are not bad when used as a dietary aid and supplement to regular meals. However, they should not be used as a meal replacement for elders – especially those who are frail or thin.

Fill out medical billing forms easily

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 touse. 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 Ihate to soundlikea 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

Relieving pain in those with dementia

LGMedSupplyers offers TENS Units, Muscle Stimulators, and Ultrasound Units for Pain Relief and Rehabilitation. You may need to use these with your loved one with dementia with the guidance of a therapist. It may improve his or her quality of life. They are extremely effective inrelieving pain without having to take any medication.

The LG-TEC Dual Combo TENS Unit and Muscle Stimulator is a combination unit that enables the dementia recipient to receive benefit from the TENS Pain Relief and the Muscle Stimulator for increased muscle tone and muscle pain rehabilition.

LGMedSupply's Pain Relief Products are used by thousands of satisfied patients worldwide. Visit LGMedSupply Online. All items are in-stock. Also get additional information on us at ouronline customer blog.

I recommend using these units because I have seen improvement in function and relief of pain in people who have dementia with no discomfort when using these machines.

The TENS Unit uses electrical energy on to a patient in order to quickly allowing recovery from most types of long term or short term problems. The electrotherapy equipment creates electric pulses within the specialized machine and then the appropriate kind of electric flow or present is passed throughout the chief power device into the particular affected portion of a person's body.

The National Institute of Neurological Disorders and Stroke which is a division of the National Institute of Health. They stated that these machines are really effective for lower back and other musculoskeletal pain,

What is sneekpeeq all about

Sneekqpeek might be for you

As a person who does shopping for you and persons with dementia, you should check out Sneekpeeq because you want a place that is convenient and easy to use

At sneakpeeq, you'll aways 'Find What You Love!' We bring you new discoveries every day, from gourmet foods to home products to accessories and apparel at prices so low we have to keep them private.

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Elevated SAP in Alzheimer’s disease

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

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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

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Healthcanal

The deposition of amyloid beta in the brain of individuals with Alzheimer’s disease is the focus of much research into both its cause and treatment.

While there may not be a consensus as to whether the deposition contributes to the disease or is a consequence of the disease, there is agreement that it is not favoured thermodynamically, meaning that something else is promoting the process.

Other proteins are often co-deposited in vivo with amyloid beta and one such protein is serum amyloid P component (or SAP). Recent evidence has suggested that SAP is elevated in Alzheimer’s disease and a team of researchers from Keele University in Staffordshire, led by Professor Chris Exley, has shown that physiologically-significant concentrations of SAP promote the deposition of amyloid beta under conditions approaching those found in vivo.

Professor Exley said: “We have shown that SAP is bound by fibrils of amyloid beta and that this interaction stabilises the fibrils over timescales which are physiologically significant. This is the first example of a physiologically significant biomolecule promoting and stabilising the formation of amyloid fibrils of amyloid beta 42 under near-physiological conditions.”

The group also found that this property of SAP was enhanced in the presence of aluminium, a metal which has also been shown to be co-deposited with amyloid beta in Alzheimer’s disease. There have been recent efforts to reduce the plasma concentration of SAP as a therapy for Alzheimer’s disease and the research provides strong evidence that SAP is involved in the deposition of amyloid beta 42 in Alzheimer’s disease and that by reducing the plasma concentration of SAP it might also reduce the deposition of amyloid beta. Their observations support serum amyloid P component as a therapeutic target in Alzheimer’s disease.

Serum Amyloid P Component Accelerates the Formation and Enhances the Stability of Amyloid Fibrils in a Physiologically Significant Under-Saturated Solution of Amyloid-β42 by Matthew Mold, Annette K Shrive, Christopher Exley will be published in the Journal of Alzheimer's Disease Volume 29, issue 4 (April 2012); DOI: 10.3233/JAD-2012-120076