Alzheimer's related Press Releases

Crossbeta Biosciences, Good Biomarker Sciences and U-Protein Express join forces to develop Alzheimer's disease biomarker

Jennifer Levin — Wed, 08 Feb 2012 06:30:25 -0500

Crossbeta Biosciences, Good Biomarker Sciences and U-Protein Express join forces to develop Alzheimer's disease biomarker with a grant from IPC-BioFarmind

January 27, 2012 - Utrecht & Leiden, The Netherlands

Three Dutch biotech companies with complementary activities and expertise announced today that they will collaborate to develop a biomarker assay for Alzheimer's disease. This initiative is awarded with a grant from IPC-BioFarmind.

Crossbeta Biosciences, a biotechnology company focused on the discovery and development of drug treatments for misfolded protein diseases and a lead program in Alzheimer's Disease, Good Biomarker Sciences, a contract research company developing and performing diagnostic assays and test strategies and U-Protein Express, a contract manufacturing organization developing and producing recombinant proteins and antibodies, join forces with the aim to develop a test that can provide a tool for Alzheimer's disease for early detection and monitoring effects of treatment.

Alzheimer's disease is the main cause of dementia and affects a large and rapidly growing number of primarily elderly people. Treating this highly debilitating disease by reversing the toxic effects in the brain is not possible yet. A diagnostic test would be a great aid to enable early treatment when damage is still limited, allowing evaluation of treatment strategies and thus helping to preserve quality of life.

"The grant from IPC-BioFarmind is exactly the trigger we needed to effectively kick our collaboration off and to initiate this joint project." "With our matching capabilities and the support from academic groups we give this biomarker development effort the best chance of success." "We are very excited about the joint development potential of our teams." "Combining protein production, protein misfolding technology and biomarker development expertise makes this Alzheimer biomarker program unique." are some of the comments made by the CEOs of Crossbeta Biosciences, Good Biomarker Biosciences and U-Protein Express.

About Crossbeta Biosciences:

Crossbeta Biosciences is a biotech company aimed at developing therapeutic applications of its crossbeta technology. This technology is based on crossbeta structures and specific epitopes in misfolded proteins. Misfolded proteins are associated with the progression of major diseases of today's Western world and aging population. This includes diseases such as Alzheimer's disease and type 2 diabetes. Crossbeta Biosciences

strives to build up a pipeline of drug candidates for misfolded protein diseases and to offer services based on its technology to identify new targets and leads for drug discovery and diagnostic (biomarker) purposes.

For further information on Crossbeta Biosciences:

Guus Scheefhals

Phone +31 (0)30 253 2668

g.scheefhals@crossbeta.com

www.crossbeta.com

About Good Biomarker Sciences:

Good Biomarker Sciences is a company with a mix of applications of biomarker assays primarily in drug intervention studies in humans, and developing new assays from scratch. In the present project the development of assays is central and focuses on oligomeric misfolded proteins relevant for Alzheimer's disease. This is made possible by the joint effort with Crossbeta Biosciences providing the oligomers and U-Protein Express providing specific ligands for the oligomers.

For further information on Good Biomarker Sciences:

Kees Kluft

Phone + 31 (0) 6 536 22221

Kluft@euronet.nl

www.gbsleiden.nl

About U-Protein Express:

U-Protein Express is a dedicated provider in the field of expression and purification of recombinant proteins. Fully post-translational modified mammalian proteins are produced via the proprietary r-PEx technology (patent pending) using HEK293EBNA1 cells. In addition the HEK293EBNA1 cell line and CHO cell lines are used in an efficient high throughput pipeline for the production of recombinant antibodies. Moreover, E. coli and P. pastoris expression platforms are available for the production of more simple proteins. Produced recombinant proteins are purified in house by state-of-the-art purification technology. Main customers are academia, biotech- and pharma companies.

For more information on U-Protein Express:

Dr. Martin Hessing

M.Hessing@U-ProteinExpress.com

www.U-ProteinExpress.com

Phone: +31 30 253 8823 | Mail: info@crossbeta.com

Lifelong brain-stimulating habits linked to lower Alzheimer's protein levels

Jennifer Levin — Wed, 25 Jan 2012 08:19:50 -0500

Lifelong brain-stimulating habits linked to lower Alzheimer's protein levels

By Sarah Yang, Media Relations | January 23, 2012

BERKELEY - A new study led by researchers at the University of California, Berkeley, provides even more reason for people to read a book or do a puzzle, and to make such activities a lifetime habit.

PET scans reveal amyloid plaques, which appear as warm colors such as red and orange. The middle scan is from a person with no symptoms of cognitive problems, but with evident levels of amyloid plaque in the brain.

Brain scans revealed that people with no symptoms of Alzheimer's who engaged in cognitively stimulating activities throughout their lives had fewer deposits of beta-amyloid, a destructive protein that is the hallmark of the disease.

While previous research has suggested that engaging in mentally stimulating activities - such as reading, writing and playing games - may help stave off Alzheimer's later in life, this new study identifies the biological target at play. This discovery could guide future research into effective prevention strategies.

"These findings point to a new way of thinking about how cognitive engagement throughout life affects the brain," said study principal investigator Dr. William Jagust, a professor with joint appointments at UC Berkeley's Helen Wills Neuroscience Institute, the School of Public Health and Lawrence Berkeley National Laboratory. "Rather than simply providing resistance to Alzheimer's, brain-stimulating activities may affect a primary pathological process in the disease. This suggests that cognitive therapies could have significant disease-modifying treatment benefits if applied early enough, before symptoms appear."

An estimated 5.4 million Americans live with Alzheimer's disease, but the numbers are growing as baby boomers age. Between 2000 and 2008, deaths from Alzheimer's increased 66 percent, making it the sixth-leading killer in the country. There is currently no cure, but a draft of the first-ever National Alzheimer's Plan, released this week, revealed that the U.S. government is aiming for effective Alzheimer's treatments by 2025.

The new study, to be published Monday, Jan. 23, in the Archives of Neurology, puts the spotlight on amyloid - protein fibers folded into tangled plaques that accumulate in the brain. Beta-amyloid is considered the top suspect in the pathology of Alzheimer's disease, so finding a way to reduce its development has become a major new direction of research.

A molecular model of amyloid protein fibrils. Formed when mis-folded proteins self-assemble into fibrous sheet structures, they are found in the brains of sufferers of Alzheimer's disease.

The researchers note that the buildup of amyloid can also be influenced by genes and aging - one-third of people age 60 and over have some amyloid deposits in their brain - but how much reading and writing one does is under each individual's control.

"This is the first time cognitive activity level has been related to amyloid buildup in the brain," said study lead author Susan Landau, research scientist at the Helen Wills Neuroscience Institute and the Berkeley Lab. "Amyloid probably starts accumulating many years before symptoms appear. So it's possible that by the time you have symptoms of Alzheimer's, like memory problems, there is little that can be done to stop disease progression. The time for intervention may be much sooner, which is why we're trying to identify whether lifestyle factors might be related to the earliest possible changes."

The researchers asked 65 healthy, cognitively normal adults aged 60 and over (average age was 76) to rate how frequently they participated in such mentally engaging activities as going to the library, reading books or newspapers, and writing letters or email. The questions focused on various points in life from age 6 to the present.

The participants took part in extensive neuropsychological testing to assess memory and other cognitive functions, and received positron emission tomography (PET) scans at the Berkeley Lab using a new tracer called Pittsburgh Compound B that was developed to visualize amyloid. The results of the brain scans of healthy older individuals with various levels of lifetime cognitive activity were compared with those of 10 patients diagnosed with Alzheimer's disease and 11 healthy people in their 20s.

The researchers found a significant association between higher levels of cognitive activity over a lifetime and lower levels of beta-amyloid in the PET scans. They analyzed the impact of other factors such as memory function, physical activity, self-rated memory ability, level of education and gender, and found that lifelong cognitive engagement was independently linked to amyloid deposition.

Notably, the researchers did not find a strong connection between amyloid deposition and levels of current cognitive activity alone.

"What our data suggests is that a whole lifetime of engaging in these activities has a bigger effect than being cognitively active just in older age," said Landau.

The researchers are careful to point out that the study does not negate the benefits of kicking up brain activity in later years.

"There is no downside to cognitive activity. It can only be beneficial, even if for reasons other than reducing amyloid in the brain, including social stimulation and empowerment," said Jagust. "And actually, cognitive activity late in life may well turn out to be beneficial for reducing amyloid. We just haven't found that connection yet."

Other study authors include researchers from UC San Francisco's Memory and Aging Center and Department of Neurology, and Rush University Medical Center's Alzheimer's Disease Center in Chicago.

The National Institutes of Health and the Alzheimer's Association helped support this research.

Alzheimer's Drug Candidate May Be First to Prevent Disease Progression, Mouse Study Suggests

Maureen Martino — Thu, 15 Dec 2011 10:25:04 -0500

Alzheimer's Drug Candidate May Be First to Prevent Disease Progression, Mouse Study Suggests

ScienceDaily (Dec. 14, 2011) - A new drug candidate may be the first capable of halting the devastating mental decline of Alzheimer's disease, based on the findings of a study published in PLoS ONE.

When given to mice with Alzheimer's, the drug, known as J147, improved memory and prevented brain damage caused by the disease. The new compound, developed by scientists at the Salk Institute for Biological Studies, could be tested for treatment of the disease in humans in the near future.

"J147 enhances memory in both normal and Alzheimer's mice and also protects the brain from the loss of synaptic connections," says David Schubert, the head of Salk's Cellular Neurobiology Laboratory, whose team developed the new drug. "No drugs on the market for Alzheimer's have both of these properties."

Although it is yet unknown whether the compound will prove safe and effective in humans, the Salk researchers' say their results suggest the drug may hold potential for treatment of people with Alzheimer's.

As many as 5.4 million Americans suffer from Alzheimer's, according to the National Institutes of Health. More than 16 million will have the disease by 2050, according to Alzheimer's Association estimates, resulting in medical costs of over $1 trillion per year.

The disease causes a steady, irreversible decline in brain function, erasing a person's memory and ability to think clearly until they are unable to perform simple tasks such as eating and talking, and it is ultimately fatal. Alzheimer's is linked to aging and typically appears after age 60, although a small percentage of families carry a genetic risk for earlier onset. Among the top ten causes of death, Alzheimer's is the only one without a way to prevent, cure or slow down disease progression.

Scientists are unclear what causes Alzheimer's, which appears to emerge from a complex mix of genetics, environment and lifestyle factors. So far, the drugs developed to treat the disease, such as Aricept, Razadyne and Exelon, only produce fleeting memory improvements and do nothing to slow the overall course of the disease.

To find a new type of drug, Schubert and his colleagues bucked the trend within the pharmaceutical industry of focusing exclusively on the biological pathways involved in the formation of amyloid plaques, the dense deposits of protein that characterize the disease. To date, Schubert says, all amyloid-based drugs have failed in clinical trials.

Instead, the Salk team developed methods for using living neurons grown in laboratory dishes to test whether or not new synthetic compounds were effective at protecting the brain cells against several pathologies associated with brain aging. Based on the test results from each chemical iteration of the lead compound, which was originally developed for treatment of stroke and traumatic brain injury, they were able to alter its chemical structure to make a much more potent Alzheimer's drug.

"Alzheimer's is a complex disease, but most drug development in the pharmaceutical world has focused on a single aspect of the disease--the amyloid pathway," says Marguerite Prior, a research associate in Schubert's lab, who led the project along with Qi Chen, a former Salk postdoctoral researcher. "In contrast, by testing these compounds in living cell cultures, we can determine what they do against a range of age-related problems and select the best candidate that addresses multiple aspects of the disease, not just one."

With a promising compound in hand, the researchers shifted to testing J147 as an oral medication in mice. Working with Amanda Roberts, a professor of molecular neurosciences at The Scripps Research Institute, they conducted a range of behavioral tests that showed that the drug improved memory in normal rodents.

The Salk researchers went on to show that it prevented cognitive decline in animals with Alzheimer's and that mice and rats treated with the drug produced more of a protein called brain-derived neurotrophic factor (BDNF), a molecule that protects neurons from toxic insults, helps new neurons grow and connect with other brain cells, and is involved in memory formation.

Because of the broad ability of J147 to protect nerve cells, the researchers believe that it may also be effective for treating other neurological disorders, such as Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis (ALS), as well as stroke.

The research was funded by the Fritz B. Burns Foundation, the National Institutes of Health, the Bundy Foundation and the Alzheimer's Association.

Researchers design Alzheimer's antibodies

Mark Hollmer — Fri, 09 Dec 2011 12:11:59 -0500

Researchers design Alzheimer's antibodies
A surprisingly simple method to target harmful proteins

Troy, N.Y. - Researchers at Rensselaer Polytechnic Institute have developed a new method to design antibodies aimed at combating disease. The surprisingly simple process was used to make antibodies that neutralize the harmful protein particles that lead to Alzheimer's disease.

The process is reported in the Dec. 5 Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS). The process, outlined in the paper, titled "Structure-based design of conformation- and sequence-specific antibodies against amyloid β," could be used as a tool to understand complex disease pathology and develop new antibody-based drugs in the future.

Antibodies are large proteins produced by the immune system to combat infection and disease. They are comprised of a large Y-shaped protein topped with small peptide loops. These loops bind to harmful invaders in the body, such as a viruses or bacteria. Once an antibody is bound to its target, the immune system sends cells to destroy the invader. Finding the right antibody can determine the difference between death and recovery.

Scientists have long sought methods for designing antibodies to combat specific ailments. However, the incredible complexity of designing antibodies that only attached to a target molecule of interest has prevented scientists from realizing this ambitious goal.

When trying to design an antibody, the arrangement and sequence of the antibody loops is of utmost importance. Only a very specific combination of antibody loops will bind to and neutralize each target. And with billions of different possible loop arrangements and sequences, it is seemingly impossible to predict which antibody loops will bind to a specific target molecule.

The new antibody design process was used to create antibodies that target a devastating molecule in the body: the Alzheimer's protein. The research, which was led by Assistant Professor of Chemical and Biological Engineering Peter Tessier, uses the same molecular interactions that cause the Alzheimer's proteins to stick together and form the toxic particles that are a hallmark of the disease.

"We are actually exploiting the same protein interactions that cause the disease in the brain to mediate binding of antibodies to toxic Alzheimer's protein particles," Tessier said.

Alzheimer's disease is due to a specific protein - the Alzheimer's protein - sticking together to form protein particles. These particles then damage the normal, healthy functions of the brain. The formation of similar toxic protein particles is central to diseases such as Parkinson's and mad cow disease.

Importantly, the new Alzheimer's antibodies developed by Tessier and his colleagues only latched on to the harmful clumped proteins and not the harmless monomers or single peptides that are not associated with disease.

Tessier and his colleagues see the potential for their technique being used to target and better understand similar types of protein particles in disorders such as Parkinson's disease.

"By binding to specific portions of the toxic protein, we could test hypotheses about how to prevent or reverse cellular toxicity linked to Alzheimer's disease," Tessier said.

In the long term, as scientists learn more about methods to deliver drugs into the extremely well-protected brain tissue, the new antibody research may also help to develop new drugs to combat disorders such as Alzheimer's disease.
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The research was funded by the Alzheimer's Association, the National Science Foundation (NSF), and the Pew Charitable Trust.

Tessier was joined in the research by Rensselaer graduate students Joseph Perchiacca (co-first author), Ali Reza Ladiwala (co-first author), and Moumita Bhattacharya.

Diametric shift in 2 protein levels spurs Alzheimer's plaque accumulation

Mark Hollmer — Fri, 02 Dec 2011 18:06:58 -0500

Diametric shift in 2 protein levels spurs Alzheimer's plaque accumulation

AUGUSTA, Ga. - A diametric shift in the levels of two proteins involved in folding, moving and cutting other proteins enables accumulation of the destructive brain plaque found in Alzheimer's disease, researchers report.

VPS35 is a protein that folds others into specific positions to unleash their functions. When levels are reduced as they are in aging, it unleashes the normally dormant BACE1, a protein responsible for beta amyloid plaque production, Georgia Health Sciences University researchers report in The Journal of Cell Biology.

When researchers modified a mouse model of Alzheimer's so that VPS35 production was essentially cut in half, BACE1 activity was increased, accelerating aging and development of related problems such as memory deficits and poor communication between brain cells as well as beta amyloid accumulation, said Dr. Wen-Cheng Xiong, developmental neurobiologist and Weiss Research Professor at GHSU and the study's corresponding author.

It was known that expression of VPS35 was down and BACE1 was up in Alzheimer's but the direct relationship was unknown, Xiong said. "We believe impaired function of VPS35 could be a risk factor for Alzheimer's and Parkinson's diseases," Xiong said. Discovering the relationship makes VPS35 a potential biomarker for the diseases as well as a target for new therapies to keep VPS35 elevated. The accelerated aging model Xiong developed and patented will enable these future drug studies.

This unhealthy balance causes cells to accumulate more waste than their recycling systems can handle. Additionally misfolded proteins end up in the wrong cell compartment where they form aggregates that eventually kill the cell. Being in the wrong place is what enables BACE1 activity to increase: it ends up stuck in a cell compartment called the endosome where high acidity levels activate the protein. As BACE1 becomes more numerous and active, it chops up more potentially productive proteins, turning them into garbage.

"Each protein knows its destination, lifespan and when it should be degraded; everything is controlled. With aging, their trafficking, their control system is disrupted," Xiong said.

Future questions include what reduces VPS35 levels, such as increased levels of reactive oxygen species that come with age, and whether exercise can help keep them up. 'We think VPS35 will be a new, hot and hopefully productive area for Alzheimer's and Parkinson's research," Xiong said.

The protein is classified a retromer. Retromers are important to recycling inside cells. While silent in healthy adults, BACE1 plays an important role in brain development.

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Xiong is a faculty member in GHSU's Medical College of Georgia and College of Graduate Studies.

Early sign of Alzheimer's reversed in lab

Mark Hollmer — Thu, 01 Dec 2011 11:33:56 -0500

Early sign of Alzheimer's reversed in lab

One of the earliest known impairments caused by Alzheimer's disease - loss of sense of smell - can be restored by removing a plaque-forming protein in a mouse model of the disease, a study led by a Case Western Reserve University School of Medicine researcher finds.

The study confirms that the protein, called amyloid beta, causes the loss.

"The evidence indicates we can use the sense of smell to determine if someone may get Alzheimer's disease, and use changes in sense of smell to begin treatments, instead of waiting until someone has issues learning and remembering," said Daniel Wesson, assistant professor of neuroscience at Case Western Reserve and lead investigator. "We can also use smell to see if therapies are working."

A description of the research is published in the Nov. 2 issue of The Journal of Neuroscience.

Smell loss can be caused by a number of ailments, exposures and injuries; but since the 1970s, it has been identified as an early sign of this disease. The new research shows how and where in the brain this happens, and that the impairment it can be treated.

"Understanding smell loss, we think, will hold some clues about how to slow down this disease," Wesson said.

There is currently no effective treatment or cure for the disease, marked by eroding senses, cognition and coordination, leading to death.

Currently 5.3 million Americans suffer from Alzheimer's and the number is expected to triple to 16 million by 2050, according to the Alzheimer's Association.

Wesson worked with Anne H. Borkowski, a researcher at the Nathan S. Kline Institute in Orangeburg, N.Y., Gary E. Landreth, professor of neuroscience at Case Western Reserve School of Medicine, and Ralph A. Nixon, Efrat Levy and Donald A. Wilson, of the New York University School of Medicine.

They found that just a tiny amount of amyloid beta - too little to be seen on today's brain scans - causes smell loss in mouse models.

Amyloid beta plaque accumulated first in parts of the brain associated with smell, well before accumulating in areas associated with cognition and coordination.

Early on, the olfactory bulb, where odor information from the nose is processed, became hyperactive.

Over time, however, the level of amyloid beta increased in the olfactory bulb and the bulb became hypoactive. Despite spending more time sniffing, the mice failed to remember smells and became incapable of telling the difference between odors.

The same pattern is seen in people with the disease. They become unresponsive to smells as they age.

While losses in the olfactory system occurred, the rest of the mouse model brain, including the hippocampus, which is a center for memory, continued to act normally early in the disease stage.

"This shows the unique vulnerability of the olfactory system to the pathogenesis of Alzheimer's disease," Wesson said.

The team then sought to reverse the effects. Mice were given a synthetic liver x-receptor agonist, a drug that clears amyloid beta from the brain. After two weeks on the drug, the mice could process smells normally.

After withdrawal of the drug for one week, impairments returned.

Wesson and his team are now following-up on these discoveries to determine how amyloid spreads throughout the brain, to learn methods to slow disease progression.

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MRI Scans Show Structural Brain Changes in People at Risk for Alzheimer's Disease

Erica Teichert — Wed, 01 Dec 2010 11:34:57 -0500

ScienceDaily (Nov. 17, 2010) - New results from a study by neuroscientists at Rush University Medical Center suggest that people at risk of developing Alzheimer's disease exhibit a specific structural change in the brain that can be visualized by brain imaging. The findings may help identify those who would most benefit from early intervention.

The study will be presented at Neuroscience 2010, the annual meeting for the Society of Neuroscience in San Diego, Calif., on November 17.

"One of the main challenges in the field of Alzheimer's disease is identifying individuals at risk of developing Alzheimer's disease so that therapeutic interventions developed in the future can be given at the earliest stage before symptoms begin to appear," said Sarah George, a graduate student who co-authored the study with Leyla deToledo-Morrell, PhD, director of the graduate program in neuroscience at Rush University Medical Center and professor of neurological sciences at the Graduate College of Rush University.

"Our study has found that structural imaging techniques can be used to identify those at risk for developing Alzheimer's disease," said deToledo-Morrell.

For the study, experts from Rush followed individuals with mild cognitive impairment, which is thought to be a precursor of Alzheimer's disease and other forms of dementia. Those with mild cognitive impairment can exhibit memory decline known as amnestic mild cognitive impairment.

Researchers followed 52 individuals with amnestic mild cognitive impairment over a period of six years. Twenty-three participants progressed to Alzheimer's disease.

Study participants underwent magnetic resonance imaging (MRI) screenings. The researchers used MRI to look for structural changes in the substantia innominata (SI), a region deep within the brain that sends chemical signals to the cerebral cortex, the brain's outer layer that is largely responsible for reasoning, memory and other higher functions. Although no structural changes were found in the SI between the two groups, the MRI showed a thinning of the cortical areas that receive strong input from the SI in those who went on to develop Alzheimer's disease.

"Since we were able to distinguish those who progressed to Alzheimer's disease compared to those who remained stable, we believe that MRI techniques that examine patterns of structural alterations provide a sensitive biomarker for detecting risk of Alzheimer's disease," said George.

Additional co-authors on the study include Elliott J. Mufson, PhD., professor of neurological sciences at Rush University Medical Center, and Dr. Raj C. Shah, director of the memory clinic at the Rush Alzheimer's Disease Center at Rush University Medical Center.

Alzheimer's Fights Brain Cancer

Erica Teichert — Tue, 28 Sep 2010 09:12:26 -0400

SARASOTA, Fla., Sept. 27 /PRNewswire-USNewswire/ -- Scientists at the Roskamp Institute in Sarasota, Florida, have shown that mice that naturally develop Alzheimer's are able to ward off the growth of brain cancer. In a series of experiments published in the Journal of Neuroscience, they showed that mice that spontaneously develop Alzheimer's Disease are able to dramatically reduce the growth of a human brain cancer. Brain cancers affect 612,000 people in the United States and are particularly common in children and older adults. 10,000 Americans are diagnosed each year with one of the most deadly brain tumors called malignant gliomas, the type of brain tumor tested in the study. Only about 50% of patients are alive 1 year after diagnosis, and 25% after two years despite surgical and medical treatment. Scientists believe that the cancers in the brains of the Alzheimer mice don't grow as they normally would because their blood supply is choked. It has long been known that in order to grow cancers need large blood supplies which they hijack from existing normal blood supplies. This is true of the brain cancers tested in the mice. In the normal mice without Alzheimer's Disease the cancers grew rapidly and aggressively in the brain as they do in humans. But in the mice with Alzheimer's Disease the brain cancers grew much more slowly and their blood supplies were greatly reduced.

Dr Daniel Paris, lead author on the study paper: "We believe that the small protein that causes Alzheimer's Disease, called amyloid, stops cancer blood vessels growing and thus the supply of nutrients and oxygen to the cancer is stifled."

Studies of Alzheimer's Disease patients suggest that cancer rates may be lower than the general population which would be expected if amyloid can stop new blood vessel growth in cancers.

Dr Michael Mullan, Director of the Roskamp Institute: "We believe that small parts of the amyloid protein may be harnessed to bring about these beneficial effects against cancer while the negative effects (causing Alzheimer's Disease) are avoided."

The work was conducted in collaboration with a team led by Dr Steven Brem, neurosurgeon at the Moffitt Cancer center, Tampa

Alzheimer's Association Launches TrialMatch(TM) - First-of-its-Kind Clinical Trial Matching Service in Alzheimer's

Erica Teichert — Mon, 19 Jul 2010 07:30:16 -0400

Alzheimer's Association TrialMatch Connects People with Potentially Life-Altering Studies

HONOLULU, July 12 /PRNewswire-USNewswire/ -- The Alzheimer's Association announced today the launch of Alzheimer's Association TrialMatch(TM), a confidential and free interactive tool that provides comprehensive clinical trial information and an individualized trial matching service for people with Alzheimer's disease and related dementias. The Internet (www.alz.org/trialmatch) and phone-based (800-272-3900) service debuted during the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, HI.

There are as many as 5.3 million Americans living with the Alzheimer's and every 70 seconds someone in America develops the disease, according to the Association's 2010 Alzheimer's Disease Facts and Figures. This year, there will be one half million new cases of Alzheimer's; in 2050, there will be nearly a million new cases annually.

"Alzheimer's disease is clearly the #1 public health challenge of the 21st century and research is the only way to solve this problem," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association.

Recruiting and retaining trial participants is one of the greatest obstacles to developing the next generation of Alzheimer's treatments, perhaps second only to lack of funding.

"If patients are not enrolling in trials, there can be no advances in diagnosis, treatment and prevention, making the lack of study participants a significant public health issue," Thies said. "Alzheimer's Association TrialMatch provides a first-of-its-kind service in Alzheimer's by delivering a user-friendly and individualized guide to clinical trials for people with Alzheimer's, their healthcare professionals, caregivers and healthy volunteers."

More than 100 clinical studies in Alzheimer's and dementia are currently taking place and dozens more experimental compounds are moving from the laboratory to clinical testing. For people with Alzheimer's and their caregivers, clinical trials present an opportunity to play a more active role in their own treatment - ultimately contributing to scientific discovery and benefiting future generations.

About Alzheimer's Association TrialMatch

Alzheimer's Association TrialMatch is designed to be easy to use for people with Alzheimer's, with web and phone support, specially trained staff, and tools developed with input from people with Alzheimer's.

The strength of this Web- and national 800 line-based service is that Alzheimer's Association TrialMatch contains a comprehensive, constantly updated database of institutional review board-approved Alzheimer's, mild cognitive impairment and other dementia trials taking place across the U.S. Specialists at the Alzheimer's Association's national Helpline - available 24-hours a day - assist in the process of matching individuals to clinical trials for which they are eligible based on study inclusion/exclusion criteria, diagnosis, treatment history and location.

By Association policy, telephone specialists will not recommend any particular clinical trial, but will describe all studies for which the person is eligible. They will answer questions about the trial process and connect individuals with trial sites based on their unique profile. Patients and caregivers will be encouraged to share their trial matches with their healthcare professionals to help decide whether a clinical trial is appropriate.

"We're looking to physicians to play a leadership role in referring their patients to Alzheimer's clinical trials and to Alzheimer's Association TrialMatch," said Marilyn Albert, PhD, Professor of Neurology at Johns Hopkins and Director of their Division of Cognitive Neuroscience. "As healthcare professionals, there is more we can do to help our Alzheimer's patients post-diagnosis by offering access to potential cutting-edge research and treatments being tested."

Alzheimer's Association TrialMatch can be accessed at www.alz.org/trialmatch or by calling toll-free, (800) 272-3900.

The technology and platform for Alzheimer's Association TrialMatch is provided by EmergingMed.

About the Alzheimer's Association

The Alzheimer's Association is the 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. www.alz.org/icad/

Researcher developing novel therapy for Alzheimer's disease

Erica Teichert — Tue, 13 Jul 2010 09:56:18 -0400

Researcher developing novel therapy for Alzheimer's disease

July 8, 2010 A University of Oklahoma researcher is developing a novel therapy for Alzheimer's disease using "biopharmaceutical proteases" to attack the toxic plaque that builds up in the brain of an Alzheimer's patient -- an approach that he predicts will be lower in cost and higher in effectiveness than current therapies.

Peter J. Heinzelman, an associate professor in the Department of Chemical, Biological and Mechanical Engineering, recently received a $75,000 grant from the Oklahoma Center for the Advancement of Science and Technology to pursue this research, which includes the development of a library of biopharmaceutical proteases for public use.

Heinzelman's previous research led to the idea that proteases, or proteins that degrade other proteins, would be more effective as a therapy for Alzheimer's disease than existing approaches. The brain is surrounded by a barrier of cells that allows glucose to pass through but is resistant to drug molecules and therapeutic proteins.

By virtue of a single protease molecule able to degrade thousands of the plaque molecules, these proteases should be capable of delivering a catalytic benefit even if only small amounts pass through the cell barrier surrounding the brain.

"Digestive enzymes are promiscuous," says Heinzelman. "We can create catalytic proteases that attack the beta-amyloid plaque that cause neurons in the brain to die. Current therapies use amyloid-binding antibodies that are created by the body or injected to get rid of the plaque, but these antibodies used to attack the problematic Abeta molecules can only bind one time and clear one Abeta molecule, then they are done."

The delivery system is problematic, too. Heinzelman suggests an approach that addresses both therapeutic efficacy and delivery. He wants to re-engineer an existing technology to link proteases with "ferrying" antibodies that can encourage passage of the proteases from the circulation side across the brain cell barrier and into the brain tissue. This approach has been demonstrated in the laboratory.

Another aspect of the OCAST grant is the development of a library of proteases that will be made freely available and could become a powerful tool for the scientific community. Heinzelman is working with researchers from the University of Wisconsin-Madison and the Oklahoma Medical Research Foundation on this grant.

Provided by University of Oklahoma