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September 23, 2009, 7:18 AM CT

Rethinking Alzheimer's disease and its treatment targets

Rethinking Alzheimer's disease and its treatment targets
The standard explanation for what causes Alzheimer's is known as the amyloid hypothesis, which posits that the disease results from of an accumulation of the peptide amyloid beta, the toxic protein fragments that deposit in the brain and become the sticky plaques that have defined Alzheimer's for more than 100 years.

Billions of dollars are spent yearly targeting this toxic peptide but what if this is the wrong target? What if the disease begins much earlier, fueled by a natural process? Reporting in the current edition of the journal Neurobiology of Aging, UCLA professor of psychiatry George Bartzokis argues just that and says that a better working hypothesis is the "myelin model." .

"The greatest promise of the myelin model of the human brain is its application to the development of new therapeutic approaches," Bartzokis said.

Like insulation around wires, myelin is a fatty sheath that coats our nerve axons, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functions and encoding of memories.

But the lifelong, extensive myelination of the human brain also makes it uniquely vulnerable to damage. The myelin model's central premise is that it is the normal, routine maintenance and repair of myelin throughout life that ultimately initiates the mechanisms that produce degenerative diseases like Alzheimer's. That is, the amyloid-beta peptide and the tau peptide, which is also implicated in Alzheimer's, as well as the signature clinical signs of the disease, such as memory loss and, ultimately, dementia, are all byproducts of the myelin breakdown and repair processes.........

Posted by: Daniel      Read more         Source


September 23, 2009, 7:04 AM CT

Trial of new treatment for advanced melanoma

Trial of new treatment for advanced melanoma
Berlin, Gera number of: Scientists have made significant advances in the therapy of metastatic cancerous melanoma one of the most difficult cancers to treat successfully once it has started to spread as per a research studyto be presented at Europe's largest cancer congress, ECCO 15 ESMO 34 [1], in Berlin on Thursday.

In the phase I extension study, scientists have seen rapid and dramatic shrinking of metastatic tumours in patients treated with a new compound that blocks the activity of the cancer-causing mutation of the BRAF gene, which is implicated in about 50% melanomas and 5% of colorectal cancers. In new results from 31 melanoma patients with the BRAF mutation who were treated with 960mg of PLX4032 twice a day, 64% (14) of the 22 patients who could be reviewed so far met the official criteria for partial response (this involves the diameter of tumours shrinking by at least 30% for at least a month). A further six of the 22 patients also showed a response, but, at the time of the congress presentation, it was too early to say whether the tumours would shrink far enough to meet these criteria.

Dr Paul Chapman, an attending doctor on the Melanoma/Sarcoma service at Memorial Sloan-Kettering Cancer Center (New York, USA) and who was one of the leaders of the trial, told a news briefing: "We are very excited about these results. Of the 22 patients we have been able to evaluate so far, 20 have had some objective tumour shrinkage. This is impressive as they all had metastatic disease and most of them had failed several previous therapies. A lot of these patients were pretty sick but a number of of them had a significant and rapid improvement in the way they function. We've had patients come off oxygen and we've got several patients who have been able to come off narcotic pain medicine soon after starting therapy".........

Posted by: Janet      Read more         Source


September 15, 2009, 7:38 AM CT

Neurons found to be similar to Electoral College

Neurons found to be similar to Electoral College
A tiny neuron is a very complicated structure. Its complex network of dendrites, axons and synapses is constantly dealing with information, deciding whether or not to send a nerve impulse, to drive a certain action.

It turns out that neurons, at one level, operate like another complicated structure -- the United States, especially its system of electing a president, through the Electoral College.

A new Northwestern University study provides evidence that supports the "two-layer integration model," one of several competing models attempting to explain how neurons integrate synaptic inputs. The findings appear in the journal Neuron

In this model, each dendritic branch of a neuron receives and integrates thousands of electrical inputs, deciding on just one signal to send to the axon. The axon then receives signals from all the dendrites, much like electoral votes coming in from state elections, and a final decision is made. The result could be an output in the form of an impulse, or action potential, or no action at all.

"There are more than 100 billion neurons in the human brain, so detailed knowledge of individual neurons will lead to a better understanding of how the brain works, including the processes of learning and memory," said Nelson Spruston, who led the research team. He is professor of neurobiology and physiology in the Weinberg College of Arts and Sciences at Northwestern.........

Posted by: Daniel      Read more         Source


September 14, 2009, 11:56 PM CT

New 'adjuvant' could hold future of vaccine

New 'adjuvant' could hold future of vaccine
Researchers at Oregon State University have developed a new "adjuvant" that could allow the creation of important new vaccines, possibly become a universal vaccine carrier and help medical experts tackle a number of diseases more effectively.

Adjuvants are substances that are not immunogenic themselves, but increase the immune response when used in combination with a vaccine.

However, due to concerns about safety and toxicity, there's only a single vaccine adjuvant aluminum hydroxide, or alum that has been approved for human use in the United States. It's found in such common vaccines as hepatitis B and tetanus. But even though widely used, alum is comparatively weak and will only work with certain diseases.

The new adjuvant is based on nanoparticles prepared with lecithin, a common food product. In animal models, it helped protein antigens to induce an immune response more than six times stronger than when alum was used. Scientists also showed that the lecithin nanoparticles were able to help induce a reasonable antibody response after only one shot, whereas it took at least two shots for the alum adjuvant to work.

Based on their studies, scientists believe the lecithin nanoparticles have wide potential applications and possibly a good safety profile. Their findings were just reported in the Journal of Controlled Release, a professional journal in the field of pharmaceutics, in work supported by the National Institute of Allergy and Infectious Diseases.........

Posted by: Scott      Read more         Source


September 9, 2009, 7:42 AM CT

Gene variant heightens risk of severe liver disease

Gene variant heightens risk of severe liver disease
Scientists at the University of North Carolina at Chapel Hill have discovered a genetic risk factor for severe liver disease in people with cystic fibrosis. Those who carry a particular variant of the SERPINA1 gene (also known as alpha-1-antitrypsin or alpha-1-antiprotease) are five times more likely to develop cirrhosis and other liver complications than patients who carry the normal version of the gene.

The study, which appears in the Sept. 9 issue of the Journal of the American Medical Association (JAMA), could lead to earlier detection and diagnosis of cystic fibrosis liver disease and better therapy options for the patients affected by the disease. In addition, it could pave the way for similar studies in more common forms of liver disease.

"I predict that as we uncover more risk factors of liver disease in cystic fibrosis we may also find that they play a role in how rapidly people with a more common malady, such as viral hepatitis, develop liver complications (or "fibrosis")," said senior study author Michael R. Knowles, M.D., professor of pulmonary and critical care medicine at UNC.

Cystic fibrosis is the most common fatal genetic illness among Caucasians. In the disease, defects in the CFTR gene cause the lungs, intestines and pancreas to become clogged with mucus, resulting in breathing problems and other difficulties. Though every patient with cystic fibrosis carries mutations in both copies of their CFTR gene (one inherited from the mother and one from the father), symptoms can vary widely from patient to patient. For instance, about five percent of cystic fibrosis patients develop liver disease so severe it requires a liver transplant.........

Posted by: Scott      Read more         Source


September 3, 2009, 7:27 AM CT

Canadian research breakthrough for cancer therapies

Canadian research breakthrough for cancer therapies
Scientists Dr. Marc Therrien at the Institute for Research in Immunology and Cancer (IRIC) of the Universit de Montral, and Dr. Frank Sicheri, at the Samuel Lunenfeld Research Institute of Mount Sinai Hospital in Toronto, have discovered a new target that appears to be instrumental in the development of new, more effective cancer therapies.

A recent article co-authored by Drs. Therrien and Sicheri and reported in the leading scientific journal Nature sheds new light on the activation mechanism of the RAF protein kinase which, when mutated, is responsible for more than 25 per cent of cancers. Understanding this mechanism may lead to novel anti-cancer agents designed to minimize the toxic side effects caused by chemotherapy.

The RAF family of kinases regulates various cellular processes including cell growth, differentiation and survival. The Therrien-Sicheri team is the first to show that the dimerization, or combination, of two RAF proteins is essential to its activation. Inhibiting the dimerization of RAF may therefore block its activation, thus stopping cancer cells from growing. The study exposes not only the activation mechanism of RAF, but potentially the mechanisms that control other protein kinases, a large number of which are associated with cancer and other diseases such as diabetes, high blood pressure and neurodegeneration.........

Posted by: Janet      Read more         Source


September 1, 2009, 11:18 PM CT

Computational Process Zeroes in

Computational Process Zeroes in
Rachel Karchin, right, an assistant professor of biomedical engineering, and doctoral student Hannah Carter led a Johns Hopkins team that developed software to narrow the search for mutations linked to cancer. Photo by Will Kirk.
Johns Hopkins engineers have devised innovative computer software that can sift through hundreds of genetic mutations and highlight the DNA changes that are most likely to promote cancer. The goal is to provide critical help to scientists who are poring over numerous newly discovered gene mutations, a number of of which are harmless or have no connection to cancer. As per its inventors, the new software will enable these researchers to focus more of their attention on the mutations most likely to trigger tumors.

A description of the method and details of a test using it on brain cancer DNA were reported in the August 15 issue of the journal Cancer Research.

The new process focuses on missense mutations, meaning protein sequences that each possess a single tiny variation from the normal pattern. A small percentage of these genetic errors can reduce the activity of proteins that commonly suppress tumors or hyperactivate proteins that make it easier for tumors to grow, thereby allowing cancer to develop and spread. But finding these genetic offenders can be difficult.

"It's very expensive and time-consuming to test a huge number of gene mutations, trying to find the few that have a solid link to cancer," said Rachel Karchin, an assistant professor of biomedical engineering who supervised the development of the computational sorting approach. "Our new screening system should dramatically speed up efforts to identify genetic cancer risk factors and help find new targets for cancer-fighting medications".........

Posted by: Janet      Read more         Source


August 28, 2009, 6:56 AM CT

Genes and psoriasis

Genes and  psoriasis
A specific genetic region that has been increasingly identified as the strongest genetic link to psoriasis has an even more significant role in the chronic skin disease than has been suspected, University of Utah medical scientists show in a newly released study.

In the Aug. 13 issue of PLoS Genetics, scientists in the U School of Medicine's Department of Dermatology confirm that the presence of HLA-Cw*0602, a gene variation or allele on chromosome 6 found to be linked to psoriasis by numerous investigators, is the "major genetic determinant" of psoriasis, but that other nearby genetic variations also play an independent role in contributing to the disease.

"The HLA-Cw*0602 gene variation stands alone as a high risk for psoriasis," said Gerald G. Krueger, M.D., professor of dermatology, Benning Presidential Endowed Chair holder, and a co-author on the study. "A major question has been: are there other genetic variations in this region that associate with psoriasis?".

The study reported in PLoS Genetics identifies two other genetic variations on chromosome 6 that also have significant association with psoriasis. People who have all three genetic variations are nearly nine times more at risk for psoriasis.

Psoriasis is a chronic disease that causes red scaly patches on the skin and affects up to 7.5 million people in the United States. About 25 percent of subjects with the disease also develop a painful inflammation of the joints called psoriatic arthritis.........

Posted by: George      Read more         Source


August 26, 2009, 7:08 AM CT

Immune System's Role In Bone Loss

Immune System's Role In Bone Loss
Rita Effros, UCLA professor of pathology and laboratory medicine
Got high cholesterol? You might want to consider a bone density test.

A new UCLA study sheds light on the link between high cholesterol and osteoporosis and identifies a new way that the body's immune cells play a role in bone loss.

Published Aug. 20 in the journal Clinical Immunology, the research could lead to new immune-based approaches for treating osteoporosis. Affecting 10 million Americans, the disease causes fragile bones and increases the risk of fractures, resulting in lost independence and mobility.

Researchers have long recognized the relationship between high cholesterol and osteoporosis, but pinpointing the exact mechanism connecting the two has proved elusive.

"We've known that osteoporosis patients have higher cholesterol levels, more severe clogging of the heart arteries and increased risk of stroke. We also knew that drugs that lower cholesterol reduce bone fractures too," said Rita Effros, professor of pathology at the David Geffen School of Medicine at UCLA. "What we didn't understand was why".

Effros suspected a clue to the mystery involved oxidation - cell and tissue damage resulting from exposure of the fatty acids in cholesterol to molecules known as free radicals.

In the study, UCLA scientists focused on low-density lipoprotein (LDL), the so-called "bad" cholesterol. They examined how high levels of oxidized LDL affect bone and whether a type of immune cell called a T cell plays a role in the process.........

Posted by: Scott      Read more         Source


August 20, 2009, 7:04 AM CT

New targets for treatment of invasive breast cancer

New targets for treatment of invasive breast cancer
Research led by Suresh Alahari, PhD, Associate Professor of Biochemistry and Molecular Biology at LSU Health Sciences Center New Orleans, has demonstrated for the first time that a tiny piece of RNA appears to play a major role in the development of invasive breast cancer and identified a gene that appears to inhibit invasive breast cancer. The research is reported in the August 21, 2009 issue of the Journal of Biological Chemistry

The LSUHSC scientists are the first to demonstrate that miR-27b, a novel microRNA, not only inactivates the ST14 gene which they found suppresses the growth of breast tumor cells, but also that miR-27b stimulates the breast cancer to invade other cells.

MicroRNAs are a new class of small, single-stranded RNA molecules which play an important regulatory role in cell biology. They bind to target genes and decrease their function. MicroRNAs may act as oncogenes (a gene that contributes to cancer development) or tumor suppressors.

In this study working with a line of human breast cancer cells, Dr. Alahari's team observed that aggressively invasive breast tumor cells contain a large quantity f miR-27b molecules, while normal cells do not. Further analysis revealed that miR-27b increases during cancer progression, in direct proportion to the decrease in function of the ST14 gene. They observed that miR-27b promotes cell growth and cell invasion, suggesting that miR-27b acts as a breast cancer oncogene. They also observed that ST14 inhibits both cell growth and cell invasion, suggesting that ST14 is a breast cancer tumor suppressor gene and that it may also serve as a marker for the early detection of breast cancer.........

Posted by: Janet      Read more         Source



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Did you know?
Scientists at Yale have brought to light a mechanism that regulates the way an internal organelle, the Golgi apparatus, duplicates as cells prepare to divide, according to a report in Science Express.Graham Warren, professor of cell biology, and colleagues at Yale study Trypanosoma brucei, the parasite that causes Sleeping Sickness. Like a number of parasites, it is exceptionally streamlined and has only one of each internal organelle, making it ideal for studying processes of more complex organisms that have a number of copies in each cell.

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