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

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

You 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 Alzheimers1 on twitter

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