Is it Alzheimer's disease or another dementia? Marker may give more accurate diagnosis

ScienceDaily (Nov. 30, 2011) — New research finds a marker used to detect plaque in the brain may help doctors make a more accurate diagnosis between two common types of dementia -- Alzheimer's disease and frontotemporal lobar degeneration (FTLD). The study is published in the November 30, 2011, online issue of Neurology®, the medical journal of the American Academy of Neurology.

"These two types of dementia share similar symptoms, so telling the two apart while a person is living is a real challenge, but important so doctors can determine the best form of treatment," said study author Gil D. Rabinovici, MD, of the University of California San Francisco Memory and Aging Center and a member of the American Academy of Neurology.

For the study, 107 people with early onset Alzheimer's disease or FTLD underwent a brain PET scan using a PIB marker, which detects amyloid or plaque in the brain that is the hallmark of Alzheimer's disease but not related to FTLD. The participants underwent another PET scan using a FDG marker, which detects changes in the brain's metabolism and is currently used to help differentiate between the two types of dementia.

The study found the PIB PET scan performed at least as well as the FDG PET scan in differentiating between Alzheimer's disease and FTLD, but had higher sensitivity and better accuracy and precision with its qualitative readings. The study found PIB had a sensitivity of 89.5 percent compared to 77.5 percent for FDG.

"While widespread use of PIB PET scans isn't available at this time, similar amyloid markers are being developed for clinical use, and these findings support a role for amyloid imaging in correctly diagnosing Alzheimer's disease versus FTLD," said Rabinovici.

The study was conducted at the University of California (UC) San Francisco, UC Berkeley and Lawrence Berkeley National Laboratory, and supported by the National Institute on Aging, the California Department of Health Services, the Alzheimer's Association, John Douglas French Alzheimer's Foundation and the Consortium for Frontotemporal Dementia Research.

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Yeast model connects Alzheimer's disease risk and amyloid beta toxicity

ScienceDaily (Oct. 27, 2011) — In a development that sheds new light on the pathology of Alzheimer's disease (AD), a team of Whitehead Institute scientists has identified connections between genetic risk factors for the disease and the effects of a peptide toxic to nerve cells in the brains of AD patients.

The scientists, working in and in collaboration with the lab of Whitehead Member Susan Lindquist, established these previously unknown links in an unexpected way. They used a very simple cell type -- yeast cells -- to investigate the harmful effects of amyloid beta (Aß), a peptide whose accumulation in amyloid plaques is a hallmark of AD. This new yeast model of Aß toxicity, which they further validated in the worm C. elegans and in rat neurons, enables researchers to identify and test potential genetic modifiers of this toxicity.

"As we tackle other diseases and extend our lifetimes, Alzheimer's and related diseases will be the most devastating personal challenge for our families and one the most crushing burdens on our economy," says Lindquist, who is also a professor of biology at Massachusetts Institute of Technology and an investigator of the Howard Hughes Medical Institute. "We have to try new approaches and find out-of the-box solutions."

In a multi-step process, reported in the journal Science, the researchers were able to introduce the form of Aß most closely associated with AD into yeast in a manner that mimics its presence in human cells. The resulting toxicity in yeast reflects aspects of the mechanism by which this protein damages neurons. This became clear when a screen of the yeast genome for genes that affect Aß toxicity identified a dozen genes that have clear human homologs, including several that have previously been linked to AD risk by genome-wide association studies (GWAS) but with no known mechanistic connection.

With these genetic candidates in hand, the team set out to answer two key questions: Would the genes identified in yeast actually affect Aß toxicity in neurons? And if so, how?

To address the first issue, in a collaboration with Guy Caldwell's lab at the University of Alabama, researchers created lines of C. elegans worms expressing the toxic form of Aß specifically in a subset of neurons particularly vulnerable in AD. This resulted in an age-dependent loss of these neurons. Introducing the genes identified in the yeast that suppressed Aß toxicity into the worms counteracted this toxicity. One of these modifiers is the homolog of PICALM, one of the most highly validated human AD risk factors. To address whether PICALM could also suppress Aß toxicity in mammalian neurons, the group exposed cultured rat neurons to toxic Aß species. Expressing PICALM in these neurons increased their survival.

The question of how these AD risk genes were actually impacting Aß toxicity in neurons remained. The researchers had noted that many of the genes were associated with a key cellular protein-trafficking process known as endocytosis. This is the pathway that nerve cells use to move around the vital signaling molecules with which they connect circuits in the brain. They theorized that perhaps Aß was doing its damage by disrupting this process. Returning to yeast, they discovered that, in fact, the trafficking of signaling molecules in yeast was adversely affected by Aß. Here again, introducing genes identified as suppressors of Aß toxicity helped restore proper functioning.

Much remains to be learned, but the work provides a new and promising avenue to explore the mechanisms of genes identified in studies of disease susceptibility.

"We now have the sequencing power to detect all these important disease risk alleles, but that doesn't tell us what they're actually doing, how they lead to disease," says Sebastian Treusch, a former graduate student in the Lindquist lab and now a postdoctoral research associate at Princeton University.

Jessica Goodman, a postdoctoral fellow in the Lindquist lab, says the yeast model provides a link between genetic data and efforts to understand AD from the biochemical and neurological perspectives.

"Our yeast model bridges the gap between these two fields," Goodman adds. "It enables us to figure out the mechanisms of these risk factors which were previously unknown."

Members of the Lindquist lab intend to fully exploit the yeast model, using it to identify novel AD risk genes, perhaps in a first step to determining if identified genes have mutations in AD patient samples. The work will undoubtedly take the lab into uncharted territory.

Notes staff scientist Kent Matlack: "We know that Aß is toxic, and so far, the majority of efforts in the area of Aß have been focused on ways to prevent it from forming in the first place. But we need to look at everything, including ways to reduce or prevent its toxicity. That's the focus of the model. Any genes that we find that we can connect to humans will go into an area of research that has been less explored so far."

This work was supported by an HHMI Collaborative Innovation Award, an NRSA fellowship, the Cure Alzheimer's Fund, the National Institutes of Health, the Kempe foundation, and Alzheimerfonden.

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The above story is reprinted from materials provided by Whitehead Institute for Biomedical Research. The original article was written by Matt Fearer.

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Sebastian Treusch, Shusei Hamamichi, Jessica L. Goodman, Kent E. S. Matlack, Chee Yeun Chung, Valeriya Baru, Joshua M. Shulman, Antonio Parrado, Brooke J. Bevis, Julie S. Valastyan, Haesun Han, Malin Lindhagen-Persson, Eric M. Reiman, Denis A. Evans, David A. Bennett, Anders Olofsson, Philip L. Dejager, Rudolph E. Tanzi, Kim A. Caldwell, Guy A. Caldwell, Susan Lindquist. Functional Links Between Aß Toxicity, Endocytic Trafficking, and Alzheimer’s Disease Risk Factors in Yeast. Science, 2011; DOI: 10.1126/science.1213210

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Strides made toward drug therapy for inherited kidney disease

ScienceDaily (Oct. 27, 2011) — Scientists at UC Santa Barbara have discovered that patients with an inherited kidney disease may be helped by a drug that is currently available for other uses. The findings are published in this week's issue of the Proceedings of the National Academy of Sciences.

Over 600,000 people in the U.S., and 12 million worldwide, are affected by the inherited kidney disease known as autosomal-dominant polycystic kidney disease (ADPKD). The disease is characterized by the proliferation of thousands of cysts that eventually debilitate the kidneys, causing kidney failure in half of all patients by the time they reach age 50. ADPKD is one of the leading causes of renal failure in the U.S.

"Currently, no treatment exists to prevent or slow cyst formation, and most ADPKD patients require kidney transplants or lifelong dialysis for survival," said Thomas Weimbs, director of the laboratory at UCSB where the discovery was made. Weimbs is an associate professor in the Department of Molecular, Cellular and Developmental Biology, and in the Neuroscience Research Institute at UCSB.

Recent work in the Weimbs laboratory has revealed a key difference between kidney cysts and normal kidney tissue. They found that the STAT6 signaling pathway -- previously thought to be mainly important in immune cells -- is activated in kidney cysts, while it is dormant in normal kidneys. Cystic kidney cells are locked in a state of continuous activation of this pathway, which leads to the excessive proliferation and cyst growth in ADPKD.

The drug Leflunomide, which is clinically approved for use in rheumatoid arthritis, has previously been shown to inhibit the STAT6 pathway in cells. Weimbs and his team found that Leflunomide is also highly effective in reducing kidney cyst growth in a mouse model of ADPKD.

"These results suggest that the STAT6 pathway is a promising drug target for possible future therapy of ADPKD," said Weimbs. "This possibility is particularly exciting because drugs that inhibit the STAT6 pathway already exist, or are in active development."

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E. E. Olsan, S. Mukherjee, B. Wulkersdorfer, J. M. Shillingford, A. J. Giovannone, G. Todorov, X. Song, Y. Pei, T. Weimbs. Signal transducer and activator of transcription-6 (STAT6) inhibition suppresses renal cyst growth in polycystic kidney disease. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1111966108

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Step toward unraveling Alzheimer's disease

ScienceDaily (Oct. 27, 2011) — Scientists outline new methods for better understanding links between specific proteins and the risks associated with Alzheimer's disease in an article co-authored by University of Alabama researchers and publishing in Science Express.

In experiments using a series of model organisms, including yeast, microscopic roundworms and rats, the researchers show how basic mechanisms inside cells are disrupted when a specific human protein, known as the amyloid beta peptide, fails to properly fold. This study also shows the role a second protein, referred to by the scientists as PICALM, can play in modifying the problem.

"By using these yeast models, in combination with worms, we really are hopeful of finding a way by which we can understand and maybe combat Alzheimer's disease more rapidly," said Dr. Guy Caldwell, professor of biological sciences at The University of Alabama and one of three UA-authors on the Science article.

The research involved scientists from several universities and research institutes, including the Whitehead Institute and Massachusetts Institute of Technology, where the lead author, Dr. Sebastian Treusch, is affiliated. Treusch works in the lab of Dr. Susan Lindquist, a renowned expert in cell biology and collaborator with Caldwell on a grant from the Howard Hughes Medical Institute that funded part of this research.

While the repeated misfoldings of amyloid beta peptides within the human brain were previously known to trigger the death of neurons, resulting in Alzheimer's, Caldwell says the underlying mechanisms of toxicity weren't as well understood.

Properly functioning cells must efficiently deliver proteins and chemicals to other parts of the cell, Caldwell said. This research shows how the amyloid beta peptide interrupts a specific cellular pathway called endocytosis, preventing the delivery of other needed proteins to other parts of the cell.

"Understanding what is going wrong inside a cell, or what pathways or proteins might be directly linked to the mechanisms that are involved in Alzheimer's, is really a much more fruitful strategy for drug development."

Information drawn from the brains of deceased Alzheimer's patients, who previously donated their bodies to science, was also significant in the effort, Caldwell said.

Rapid advances in DNA sequencing methods and human genetic population studies are generating an overwhelming number of leads for researchers; those genetic studies, taken in combination with advantageous attributes of simple organisms, can reveal basic functions of genes and proteins and can be an insightful combination, Caldwell says.

"What this paper shows is that simple systems, like yeast and worms, can be engineered to discern mechanisms that might be associated with complex human diseases, and, by that, we may accelerate the path of discovery for advancing therapeutics for those diseases."

UA's lead author is Dr. Shusei Hamamichi, a former post-doctoral researcher in the Caldwell lab who earned his doctorate at UA while working alongside Caldwell and Dr. Kim Caldwell, also a co-author of the paper and an associate professor of biological sciences at UA.

In the paper's conclusion, the researchers describe the potential significance of the development in light of the challenges faced in understanding and treating Alzheimer's disease.

"The treatments available for AD are few and their efficacy limited," the scientists wrote. "Determining how best to rescue neuronal function in the context of the whole brain is a problem of staggering proportions."

"On a personal level," Caldwell said, "so many of us have been affected by family or loved ones who have suffered from Alzheimer's. It's a great privilege for us to be able to contribute to the respective avenues of our understanding of the disease. It's a devastating disorder. The societal cost of Alzheimer's disease is tremendous."

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Sebastian Treusch, Shusei Hamamichi, Jessica L. Goodman, Kent E. S. Matlack, Chee Yeun Chung, Valeriya Baru, Joshua M. Shulman, Antonio Parrado, Brooke J. Bevis, Julie S. Valastyan, Haesun Han, Malin Lindhagen-Persson, Eric M. Reiman, Denis A. Evans, David A. Bennett, Anders Olofsson, Philip L. Dejager, Rudolph E. Tanzi, Kim A. Caldwell, Guy A. Caldwell, Susan Lindquist. Functional Links Between Aß Toxicity, Endocytic Trafficking, and Alzheimer’s Disease Risk Factors in Yeast. Science, 2011; DOI: 10.1126/science.1213210

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To diagnose heart disease, visualization experts recommend a simpler approach

ScienceDaily (Oct. 27, 2011) — A team of computer scientists, physicists, and physicians at Harvard has developed a simple yet powerful method of visualizing human arteries that may result in more accurate diagnoses of atherosclerosis and heart disease.

The prototype tool, called "HemoVis," creates a 2D diagram of arteries that performs better than the traditional 3D, rainbow-colored model. In a clinical setting, the tool has been shown to increase diagnostic accuracy from 39% to 91%.

Presented Oct. 27 at the IEEE Information Visualization Conference(InfoVis 2011), the new visualization methodoffers insight to clinicians, imaging specialists, engineers, and others in a wide range of fields who need to explore and evaluate complex, branching structures.

"Our goal was to design a visual representation of the data that was as accurate and efficient for patient diagnosis as possible," says lead author Michelle Borkin, a doctoral candidate at the Harvard School of Engineering and Applied Sciences (SEAS). "What we found is that the prettiest, most popular visualization is not always the most effective."

HemoVis takes data from patient-specific blood flow simulations, combined with traditional imaging data, and visually displays a tree diagram of the arteries with areas of disease highlighted to assist in diagnosis.

Tools for artery visualization in both clinical and research settings commonly use 3D models that portray the shape and spatial arrangement of vessels of interest. These complex tools require users to rotate the models to get a complete perspective of spatial orientation.

By contrast, the new visualization requires no such rotation or interaction. The tool utilizes 2D, circumference-adjusted cylindrical cross sections arranged in tree diagrams.

Though this visualization method may seem less high-tech, the team demonstrated through quantitative evaluation with medical experts that the 2D model is actually more accurate and efficient for patient diagnosis.

"In the 3D case, the more complex and branched the arteries were, the longer it took to complete the patient diagnosis, and the lower the accuracy was," Borkin reflects. "In the 2D representation, it didn't matter how many branches we had or how complex they were -- we got consistently fast, accurate results. We weren't expecting that."

Tree diagrams are hardly new, as evolutionary biologists will attest, but scientists in many fields are using them to solve a range of very modern and complex problems. In fact, Borkin applied her own experience in astronomy and physics to transform the concept of visualization for SEAS' Multiscale Hemodynamics research group. In prior work, she had used a very similar type of tree diagram to determine the structure of nebulae in outer space.

"With the consultation and cooperation of clinicians, we were able to draw on fairly well known visualization techniques and principles from computer science to solve a practical clinical problem," says Hanspeter Pfister, Gordon McKay Professor of the Practice of Computer Science at SEAS.

Borkin, Pfister, and their colleagues relied on the input of physicians and others with clinical or laboratory imaging experience throughout the process. Through extensive surveys and interviews, they identified the most popular options for display, accurate layout, and coloring of these arterial projections.

However, Borkin drew on well supported research that is less well known outside the visualization community:

"For years, visualization, computer science, and psychology researchers have identified that color is critical for conveying the value of data, but that the rainbow coloring is not well-attuned to the human visual system."

Accordingly, HemoVis departs from the traditional practice of rainbow color-coding in favor of a graded single-color scheme (red to black) that can represent placement along a continuum.

In tests, diagnostic accuracy, as measured by the proportion of diseased areas identified, increased dramatically with the new color scheme.

Widespread adoption of visual representations like those in HemoVis could have the effect of not only optimizing tasks that are critical for doctors, but also changing long-entrenched mindsets and making scientists "think twice" about their assumptions in data visualization, Borkin says.

"This approach to visualization design and validation is broadly applicable in medicine, engineering, and science," notes Pfister. "We hope that people will use this process as a template for transforming their own visualizations."

Borkin and Pfister acknowledged that while HemoVis represents an important step forward, traditional 3D artery models still play a role, particularly in providing a spatially intuitive tool for surgical planning.

With this in mind, the next steps for this research include further development and optimization of the 2D tool and investigation into how it might complement, rather than replace, its 3D counterpart.

A paper about this work will be published later this year in the journal IEEE Transactions on Visualization and Computer Graphics.

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The above story is reprinted from materials provided by Harvard University. The original article was written by Mureji Fatunde.

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Body’s molecular sensors may trigger autoimmune disease

ScienceDaily (Oct. 27, 2011) — Bruce Beutler, MD, a co-recipient of the 2011 Nobel Prize in Medicine, has coauthored an article describing a novel molecular mechanism that can cause the body to attack itself and trigger an autoimmune disease. The article is published online ahead of print in the Journal of Interferon & Cytokine Research, a peer-reviewed journal published by Mary Ann Liebert, Inc.

In the article, entitled "Intracellular Nucleic Acid Sensors and Autoimmunity," Argyrios Theofilopoulos, Dwight Kono, Bruce Beutler, and Roberto Baccala, The Scripps Research Institute (La Jolla, California), review the scientific evidence that supports the role of molecular sensors located inside cells in the initiation not only of protective and inflammatory immune responses, but also in an autoimmune response. These sensors recognize nucleic acid signatures that may be shared by foreign pathogens and the body's own DNA and RNA.

Dr. Beutler is one of three recipients awarded the Nobel Prize in Physiology and Medicine. He shares half of the prize with Jules Hoffman, PhD for their discoveries related to how the body's immune system fights disease through the activation of an innate immune response. The third recipient, Ralph Steinman, MD, who died before the Nobel Prizes were announced, previously published an article in AIDS Research and Human Retroviruses. Mary Ann Liebert, Inc. congratulates the three winners for the work and contributions to medicine for which they are being recognized.

The Journal of Interferon & Cytokine Research, led by Co-Editors-in-Chief Ganes C. Sen, PhD, Chairman, Department of Molecular Genetics, Cleveland Clinic Foundation, and Thomas A. Hamilton, PhD, Chairman, Department of Immunology, Cleveland Clinic Foundation, is an authoritative peer-reviewed journal published monthly in print and online that covers all aspects of interferons and cytokines from basic science to clinical applications. Journal of Interferon & Cytokine Research is the Official Journal of the International Society for Interferon and Cytokine Research. Tables of content and a free sample issue may be viewed online at www.liebertpub.com/jir

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Argyrios N. Theofilopoulos, Dwight H. Kono, Bruce Beutler, Roberto Baccala. Intracellular Nucleic Acid Sensors and Autoimmunity. Journal of Interferon & Cytokine Research, 2011; 111027061355005 DOI: 10.1089/jir.2011.0092Ralf Ignatius, Yang Wei, Sylvie Beaulieu, Agegnehu Gettie, Ralph M. Steinman, Melissa Pope, Svetlana Mojsov. Short Communication: The Immunodeficiency Virus Coreceptor, Bonzo/STRL33/TYMSTR, Is Expressed by Macaque and Human Skin- and Blood-Derived Dendritic Cells. AIDS Research and Human Retroviruses, 2000; 16 (11): 1055 DOI: 10.1089/08892220050075318

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Healthy mouth bacteria provide ideal conditions for gum disease

ScienceDaily (Oct. 27, 2011) — Normal bacteria which live in our mouths provide the catalyst for the development of gum disease, a debilitating condition which leads to painful gums and the loosening of teeth, new research from Queen Mary, University of London has found.

The unexpected finding could pave the way for the development of preventative measures in tackling gum, or periodontal disease*, by manipulating the normal bacteria in the same way that probiotic yoghurt works to protect the intestine.

Researchers at Queen Mary's Blizard Institute, including Medical Research Council Clinical Research Training Fellow Mark Payne, worked with scientists in the US and published their findings in the journal Cell Host and Microbe.

The scientists introduced the oral bacterium Porphyromonas gingivalis to mice living in two different test conditions. The mice with normal bacteria in their mouths developed periodontal bone loss but the mice raised under germ-free conditions, in the absence of any normal bacteria, remained disease-free.

Professor Mike Curtis, Director of the Blizard Institute and co-author on the paper, said when the oral bacterium P. gingivalis was introduced under normal conditions "it stimulated the growth of normal bugs leading to a large increase in the number of those organisms already there."

"P. gingivalis was introduced at very low levels yet it had a major affect on both the immune system and the inflammatory system," he said.

"This oral bacterium only appears in small numbers but appears to have a major influence on the overall ecology. It has a keystone effect in a community -- working in the same way that starfish, which have relatively small numbers, control the shell fish communities in the sea.

Professor Curtis said although the findings were encouraging in terms of understanding the way gum disease develops, there was still "some way to go" before there was a similar product on the market for gum disease as a probiotic yoghurt is available for the intestine.

"Now we know that periodontal disease only develops through P. gingivalis interacting with the existing bacteria in our mouths, we need to understand the role played by our normal bacteria in both the development of disease and protection from it," he said.

"This may then provide the means to develop preventative measures for the disease."

Professor Farida Fortune, Dean for Dentistry at Queen Mary said the research was encouraging for people who suffer from gum disease which results in bleeding gums and ultimately loose teeth which cause difficulty in both speaking and eating.

"The public still need to be mindful of the way they look after their teeth and gums. People need to pay more attention to their oral hygiene. Their local hygienist, dental therapist and dentist can all assist in teaching them effective cleaning techniques."

"Just these simple preventative measures, as well as not smoking, will go some way to helping them avoid developing gum disease."

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Michael A. Curtis, Camille Zenobia, Richard P. Darveau. The Relationship of the Oral Microbiotia to Periodontal Health and Disease. Cell Host and Microbe, 2011; 10 (4): 302-306 DOI: 10.1016/j.chom.2011.09.008

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