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duminică, 5 august 2012

The Benefits Of Caffeine On Motor Impairment In Parkinson's Disease

Caffeine, which is widely consumed around the world in coffee, tea and soft drinks, may help control movement in people suffering from Parkinson's. This is the finding of a study conducted at the Research Institute of the McGill University Health Centre (RI MUHC) that was recently published in Neurology®, the official journal of the American Academy of Neurology. The study opens the door to new treatment options for Parkinson's disease that affects approximately 100 000 Canadians.

"This is one of the first studies to show the benefits of caffeine on motor impairment in people who have Parkinson's disease," stated Dr. Ronald Postuma, lead author of the study, a researcher in neurosciences at the RI MUHC, and Professor of Medicine in the Department of Neurology and Neurosurgery at McGill University. "Research has already shown that people who drink coffee have a lower risk of developing Parkinson's disease, but until now no study had looked at the immediate clinical implications of this finding."

Caffeine - one of the most widely used psychomotor stimulants in the world - it acts on the central nervous system and cardiovascular system by temporarily decreasing tiredness and increasing alertness. According to Dr. Postuma, sleepiness is commonly associated with Parkinson's disease. "We wanted to discover how caffeine could impact sleepiness as well as the motor symptoms of Parkinson's disease, such as slowness of movement, muscle stiffness, shaking and loss of balance."

The researchers followed a group of 61 people with Parkinson's. While the control group received a placebo pill, the other group received a 100 mg dose of caffeine twice a day for three weeks and then 200 mg twice a day for another three weeks.

"The people who received caffeine supplements experienced an improvement in their motor symptoms (a five-point improvement on the Unified Parkinson's Disease Rating Scale, a rating scale used to measure the severity of the disease) over those who received the placebo," said Dr. Postuma. "This was due to improvement in speed of movement and a reduction in stiffness." Caffeine had only borderline effects on sleepiness, and did not affect depression or nighttime sleep quality in the study participants.

Larger-scale studies need to be carried out over a longer period to clarify these caffeine-related improvements. "Caffeine should be explored as a treatment option for Parkinson's disease. It may be useful as a supplement to medication and could therefore help reduce patient dosages," concluded Dr. Postuma.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our parkinson's disease section for the latest news on this subject. Funding
This research was funded by the Canadian Institutes of Health Research (CIHR) and the Webster Foundation.
Research partners
The study was co-authored by Ronald B. Postuma, Silvia Rios Romenets and Robert Altman (Department of Neurology, McGill/MUHC); Amélie Pelletier (Department of Neurology, McGill/MUHC, RI MUHC); Kathia Charland (Department of Epidemiology, Biostatistics and Occupational Health, McGill); Anthony E. Lang, Rosa Chuang and Binit Shah from the Morton and Gloria Shulman Movement Disorders Centre and the Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, University of Toronto; Renato P. Munhoz, Mariana Moscovich, Luciane Filla and Debora Zanatta of the Pontifical Catholic University of Paraná, Brazil.
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joi, 15 decembrie 2011

Biochemical Signature Predicts Progression To Alzheimer's Disease

Main Category: Alzheimer's / Dementia
Also Included In: Biology / Biochemistry
Article Date: 15 Dec 2011 - 1:00 PST

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A study led by Research Professor Matej Oresic from VTT Technical Research Centre of Finland suggests that Alzheimer's disease is preceded by a molecular signature indicative of hypoxia and up-regulated pentose phosphate pathway. This indicator can be analysed as a simple biochemical assay from a serum sample months or even years before the first symptoms of the disease occur. In a healthcare setting, the application of such an assay could therefore complement the neurocognitive assessment by the medical doctor and could be applied to identify the at-risk patients in need of further comprehensive follow-up.

Alzheimer's disease (AD) is a growing challenge to the health care systems and economies of developed countries with millions of patients suffering from this disease and increasing numbers of new cases diagnosed annually with the increasing ageing of populations.

The progression of Alzheimer's disease (AD) is gradual, with the subclinical stage of illness believed to span several decades. The pre-dementia stage, also termed mild cognitive impairment (MCI), is characterised by subtle symptoms that may affect complex daily activities. MCI is considered as a transition phase between normal aging and AD. MCI confers an increased risk of developing AD, although the state is heterogeneous with several possible outcomes, including even improvement back to normal cognition.

What are the molecular changes and processes which define those MCI patients who are at high risk of developing AD? The teams led by Matej Orešic from VTT and Hilkka Soininen from the University of Eastern Finland set out to address this question, and the results were published on 13th Dec. 2011 in Translational Psychiatry.

The team used metabolomics, a high-throughput method for detecting small metabolites, to produce profiles of the serum metabolites associated with progression to AD. Serum samples were collected at baseline when the patients were diagnosed with AD, MCI, or identified as healthy controls. 52 out of 143 MCI patients progressed to AD during the follow-up period of 27 months on average. A molecular signature comprising three metabolites measured at baseline was derived which was predictive of progression to AD. Furthermore, analysis of data in the context of metabolic pathways revealed that pentose phosphate pathway was associated with progression to AD, also implicating the role of hypoxia and oxidative stress as early disease processes.

The unique study setting allowed the researchers to identify the patients diagnosed with MCI at baseline who later progressed to AD and to derive the molecular signature which can identify such patients at baseline.

Though there is no current therapy to prevent AD, early disease detection is vital both for delaying the onset of the disease through pharmacological treatment and/or lifestyle changes and for assessing the efficacy of potential AD therapeutic agents. The elucidation of early metabolic pathways associated with progression to Alzheimer's disease may also help in identifying new therapeutic avenues.

Article adapted by Medical News Today from original press release. Source: Technical Research Centre of Finland
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New Drug That Improves Memory And Prevents Brain Damage In Mice May Prevent Alzheimer's Disease Progression

Main Category: Alzheimer's / Dementia
Also Included In: Parkinson's Disease; Huntingtons Disease; Stroke
Article Date: 15 Dec 2011 - 7:00 PST

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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 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.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our alzheimer's / dementia section for the latest news on this subject. The research was funded by the Fritz B. Burns Foundation, the National Institutes of Health, the Bundy Foundation and the Alzheimer's Association.
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Study To See If Walking And/Or Memory Training May Prevent Memory Problems In People With Parkinson's Disease

Main Category: Parkinson's Disease
Also Included In: Stroke; Rehabilitation / Physical Therapy; Clinical Trials / Drug Trials
Article Date: 15 Dec 2011 - 0:00 PST

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Researchers from the University of Maryland School of Medicine and the Baltimore VA Medical Center have launched a study of exercise and computerized memory training to see if those activities may help people with Parkinson's disease prevent memory changes. The type of memory that will be examined is known as "executive function;" it allows people to take in information and use it in a new way. Many Parkinson's patients develop problems with executive function, which can prevent them from working and may eventually require a caregiver to take over more of the complex cognitive tasks of daily living.

"Studies of normal aging show that memory and executive function can be improved with exercise, such as walking several days a week," explains Karen Anderson, M.D., principal investigator and an assistant professor of neurology and psychiatry at the University of Maryland School of Medicine. Dr. Anderson is also a neuro-psychiatrist at the Maryland Parkinson's Disease and Movement Disorders Center at the University of Maryland Medical Center and a clinician in mental health at the Baltimore VA Medical Center.

She adds, "We want to see if exercise can slow or reverse some of these memory changes in Parkinson's patients. We will also investigate whether a computer game designed to improve executive function may make a difference as well. The other question is, what happens when you put the two interventions together - if there is memory improvement, will it be even better than with one of the interventions? Or is it more efficient to do just one or the other? We really do not know."

The researchers, who received funding through a VA Merit Award, plan to enroll about 90 patients who will be divided randomly into three groups: exercisers walking on a treadmill, memory game players and those doing both exercise and memory games. Participants in each group will receive a memory assessment at the beginning of the study. They will come in three times a week for their training for three months and will be then be tested again. Three months after that, the researchers will test the participants again to see if there may be longer term benefits to the training.

With both the treadmill walking and the memory game, the exercise or video game will become more challenging as the participant improves. The memory training works like a video game with players advancing to a higher level of difficulty. For the exercisers, trainers may increase the speed or slope of the treadmill to make it more aerobically challenging.

"This new study builds on our experience from a previous study of exercise for gait and mobility in Parkinson's disease. Since both motor function and cognitive function are important for mobility and performance of daily activities, this new study will investigate the individual and combined effects of treadmill training and cognitive training," explains Lisa Shulman, M.D., co-investigator and professor of neurology at the University of Maryland School of Medicine.

"Parkinson's patients are eager to know if there is anything they can do to give them greater control over their condition. Mobility and memory are the two key components to preserve independence. If these treatment strategies are found to be effective, we will learn important new approaches to delaying disability," says Dr. Shulman who is co-director of the Maryland Parkinson's Disease and Movement Disorders Center.

The treadmill training will take place at the Baltimore VA Medical Center in the Maryland Exercise and Robotics Center of Excellence, a gym facility with specialized equipment for people with physical limitations or balance issues. For safety, participants will wear a safety harness while walking on the treadmill. Experienced exercise physiologists will supervise each training session.

The computerized memory training game will take place both at the VA and University of Maryland School of Medicine.

"This study shows the commitment of our University of Maryland faculty to exploring new approaches, such as exercise and memory training, to help patients with illnesses such as Parkinson's disease around the world," says E. Albert Reece, M.D., Ph.D., M.B.A, vice president for medical affairs, University of Maryland, and dean, University of Maryland School of Medicine.

The Maryland researchers expanded the exercise studies to Parkinson's patients after first finding success with treadmill training for stroke patients. This research, also conducted at the University of Maryland School of Medicine and the VA Maryland Health Care System, found that regular exercise on a treadmill can improve stroke patients' walking ability even years after they've had a stroke.

Co-investigator Richard Macko, M.D., says, "With stroke patients, we have seen that the consistent, repetitive motion of walking may help the brain to develop new connections to compensate for the damaged ones. This new Parkinson's study takes the concept of exercise training for neurology patients in a new direction. We will be interested to see if this consistent training will produce benefits to memory." Dr. Macko is director of the Maryland Exercise and Robotics Center of Excellence at the VA Maryland Health Care System and professor of neurology at the University of Maryland School of Medicine.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our parkinson's disease section for the latest news on this subject. Parkinson's disease affects about one million people in the United States and Canada. Most people begin to develop symptoms in their late 50s or early 60s, although it can occur in younger people.
Parkinson's disease affects the brain's ability to produce dopamine, the neurotransmitter involved in the communication between the brain cells for motor control. Physical symptoms include tremor, muscle rigidity and slowness of movement. There are also non-motor symptoms such as changes in memory ability, sleep disturbances and depressed mood.
Parkinson's patients interested in enrolling in the exercise and memory study should call 443-827-0677.
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University of Maryland Medical Center. (2011, December 15). "Study To See If Walking And/Or Memory Training May Prevent Memory Problems In People With Parkinson's Disease." Medical News Today. Retrieved from
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marți, 13 decembrie 2011

Risk Of Death And Stroke In Those With Heart Disease Increased By Herbal Amphetamine

Main Category: Alcohol / Addiction / Illegal Drugs
Also Included In: Stroke; Heart Disease
Article Date: 13 Dec 2011 - 2:00 PST

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Chewing the natural stimulant khat increases the risk of death and stroke in patients with heart disease compared to those who are not users, according to new research in Circulation: Journal of the American Heart Association.

Since ancient times, people in the Arabian Peninsula and East Africa have chewed the fresh leaves of the Catha edulis plant which has effects similar to amphetamines and cocaine. It causes euphoria, hyperactivity, restlessness, loss of appetite and weight loss.

In Yemen, some people have khat picnics, chewing the leaves for as much as three hours, like tobacco chewing. Its use has spread globally throughout Western Europe and into the United States. Seven metric tons of khat travel through Heathrow Airport in England each week, and fresh and dried khat has been seized and confiscated in the United States where it is illegal, researchers said.

In the 2nd Gulf Registry of Acute Coronary Events (Gulf RACE-2) Study, researchers - comparing 1,408 khat chewers to 5,991 people who didn't use khat - found: In the hospital, khat users had a 7.5 percent death rate from heart disease compared to 3.8 percent in those who were not khat users. At one month, the death rate was 15.5 percent among khat users and 6.4 percent for non-khat users. At one year, the death rate was 18.8 percent among khat users compared to 10.8 percent among non-users. For the study, researchers enrolled men and women from 65 hospitals in Saudi Arabia, Bahrain, Yemen, Qatar, United Arab Emirates and Oman.

About 96 percent of the khat users were from Yemen, where khat is legal and socially acceptable, unlike the other countries in the study.

"Global awareness of the negative impact of khat chewing on health and social life is warranted before it becomes endemic," said Jassim Al Suwaidi, M.B., Ch.B., study co-author and Consultant Cardiologist and Director of Cardiovascular Research in the Department of Cardiology and Cardiovascular Surgery at Hamad General Hospital in Doha, Qatar. "This report underscores the importance of improving education about the cardiovascular risks of khat chewing as well as the need for further studies in the field."

Furthermore, researchers found: Khat chewers were more likely to be men (only 14 percent were women) and had lower cardiovascular risk factors such as diabetes mellitus, hypertension and dyslipidemia. Death rates were consistently higher among khat users up to age 80, but khat chewing occurs across the spectrum of young and old, male and female. Users were more likely to experience adverse health effects, including heart failure, recurrent ischemia, a second heart attack, cardiogenic shock and stroke compared to non-users. Women were as likely as men to experience adverse heart effects. Male khat chewers were more likely to develop stroke, particularly hemorrhagic (bleeding) stroke, compared to non-users. The increased risk of stroke wasn't significant among women using khat. The worse in-hospital outcomes may be related to delays in people getting to the hospital after the onset of symptoms and failing to receive thrombolytic (clot-busting) therapy or treatment with beta blockers, researchers said. Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our alcohol / addiction / illegal drugs section for the latest news on this subject. Co-authors are: Waleed M. Ali, M.D.; Al Habib KF, M.D.; Ahmed Al Motarreb, M.D.; Rajvir Singh, Ph.D.; Ahmad Hersi, M.D.; Hassam Al Faleh, M.D.; Nidal Asaad, M.M.B.S.; Shukri Al SaiF, M.D.; Wael Almameed, M.D.; Kadhim Sulaiman, M.D.; Haitham Amin, M.D.; Jawad Al-Lawati, M.D.; Nizar Al Bustani, M.D.; Norah Q. Al-Sagheer, M.D.; and Awad Al-Qahtani, M.B.Ch.B.
Author disclosures and sources of funding are on the manuscript.
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In Rat Model Of Lou Gehrig's, Disease Progression Halted

Main Category: Neurology / Neuroscience
Also Included In: Genetics
Article Date: 13 Dec 2011 - 1:00 PST

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Amyotrophic lateral sclerosis (ALS; also known as Lou Gehrig's disease) is an incurable adult neurodegenerative disorder that progresses to paralysis and death. Genetic mutations are the cause of disease in 5% of patients with ALS.

Of immense interest, Hongxia Zhou, Xu-Gang Xia, and colleagues, at Thomas Jefferson University, Philadelphia, now show that progressive neuron degeneration can be halted in a rat model of familial ALS linked to mutations in the gene that carries the instructions for making the protein TDP-43.

Progressive motor neuron degeneration was stopped when expression of the ALS-associated mutant human TDP-43 was switched off. If expression of the mutant protein was switched off before many motor neurons had degenerated, the rats recovered function. Conversely, if expression was switched off after most motor neurons had degenerated, functional recovery was minimal. These data indicate that mutant TDP-43 in motor neurons is sufficient to promote the onset and progression of ALS and that progression of motor neuron degeneration (and thereby progression of disease) is partially reversible in the rat model.

TITLE: Mutant TDP-43 in motor neurons promotes the onset and progression of ALS in rats

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Significant Findings In Foot-And-Mouth Disease

Main Category: Veterinary
Also Included In: Infectious Diseases / Bacteria / Viruses
Article Date: 13 Dec 2011 - 0:00 PST

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Researchers at the University of Leeds have been studying an enzyme - called 3D - which plays a vital role in the replication of the virus behind the disease. They have found that this enzyme forms fibrous structures (or fibrils) during the replication process. What's more, they have found a molecule which can prevent these fibrils forming.

The project was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and its findings have been published by the Journal of Virology.

"It's too much of a jump to say that we've found a potential drug target for treatment of foot-and-mouth disease because there's still such a lot we don't know," says Dr Nicola Stonehouse of the University of Leeds' Faculty of Biological Sciences. "However, we do think these findings are significant and provide us with a new avenue for exploration."

Foot-and-mouth is a one of the most readily transmissible diseases known to man, but the mechanisms by which it infects animals are not well understood. The virus responsible for the disease is able to reproduce very quickly, enabling it to cause widespread devastation in a short space of time. The 2001 outbreak in the UK resulted in the deaths of around seven million sheep and cattle at an extremely high cost to the British agricultural sector. Another, more contained outbreak, occurred in 2007.

In laboratory experiments, the research team were able to see that the 3D enzyme forms fibrils when it is copying genetic information it requires to replicate. The implications of these fibrils are not yet fully understood, but it is thought they may play an important role in the reproduction process. If this is the case, having already found a molecule to block the fibril formation could be significant.

"The next stage of our research will be to investigate these fibrils further, to look at their structure and purpose," says PhD student Kris Holmes, who has been working on the project.

Because FMD is classed as a dangerous pathogen, only one laboratory in the UK - the Institute for Animal Health at Pirbright, in Surrey - is licensed to work with the actual virus. In this research, the Leeds team used a simple, non-harmful model of the virus.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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luni, 12 decembrie 2011

Missed Opportunity To Transform Global HIV/AIDS Fight Reported By Tropical Disease Experts

Main Category: Tropical Diseases
Also Included In: HIV / AIDS; Infectious Diseases / Bacteria / Viruses; Sexual Health / STDs
Article Date: 12 Dec 2011 - 1:00 PST

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Global HIV/AIDS prevention and treatment efforts are missing a major opportunity to significantly improve health conditions in poor countries by simply adding low-cost care for the many other chronic and disabling diseases routinely afflicting and often killing these same patients, according to a panel of disease experts who spoke at the annual meeting of the American Society of Tropical Medicine and Hygiene (ASTMH).

"People want better health; they do not understand why we silo diseases," said Judd Walson, a global health and infectious disease expert at the University of Washington. "If you die from malaria, you don't care that your HIV was treated. Communities want us to leverage the resources we have to treat and prevent disease as effectively as possible."

Walson and his colleagues on the panel noted that many victims of HIV/AIDS also typically suffer from one or more of about 17 neglected, but burdensome, tropical diseases often called "diseases of poverty" because they prey on the "bottom billion" - the world's poorest people. They include ailments such as trachoma, schistosomiasis, lymphatic filariasis, leishmaniasis, Chagas disease and onchocerciasis, all of which are either insect-borne disease, bacterial infections, or caused by parasitic worms.

Despite the illness and deaths attributable to these diseases, proposed US funding for fighting them was only about $155 million in 2011, or about 3 percent of the $5.6 billion invested in HIV/AIDS efforts. Moreover, the programs often exist in isolation from one another with, for example, many programs restricting support only to antiretroviral drugs to treat AIDS.

Yet tropical disease experts note that in places like sub-Saharan Africa, where neglected diseases affect 1.4 billion people, co-infections with HIV are common. And they see mounting evidence that dealing with multiple diseases at the same time and in the same place is more cost-effective and clinically beneficial.

Walson pointed to a program in Western Kenya that focused on a community suspected of having high levels of HIV but whose remote location made it hard to reach to conduct testing. The program promised access to free bed nets and water filters to those residents who came in for a test. In just six days, some 10,000 residents turned out for the free nets and filters. The result: 1181 people were found to be HIV positive and referred to care while thousands of people gained new tools for preventing malaria and water-borne diseases.

In another example of the potential benefits of targeting multiple problems in a single intervention, a study initially focusing on treatment for onchocerciasis, a parasitic disease also known as river blindness, was broadened to offer insecticide-treated bed nets (ITNs), malaria drugs and vitamin A. The study, which covered an area with 2.35 million people, increased bed net coverage by nine-fold.

Sten Vermund, Professor of Pediatrics and Director of the Vanderbilt Institute for Global Health, noted the need to address any co-infections that might increase HIV viral load. He pointed to studies linking higher viral load with a higher likelihood of transmitting HIV, and a low load with reduced disease progression and HIV transmission risk. He said a review of a wide number of studies revealed that treating a variety of co-infections, including TB, malaria, schistosomiasis, filariasis, herpes, gonorrhea and syphilis decreased viral load to varying degrees.

"If de-worming efforts for neglected diseases reduces the viral load even just a little, then you could expect some benefit for preventing or slowing HIV transmission," said Vermund. "But it's also helpful to keep in mind that a majority of people don't know they have HIV. An effective mass de-worming campaign could have huge effects without even knowing the community's HIV status."

Peter Hotez, ASTMH President and founding dean of the National School of Tropical Medicine at Baylor College of Medicine, and Alan Fenwick, Professor of Tropical Parasitology and Director of Schistosomiasis Control Initiative at the Department of Infectious Diseases Epidemiology at Imperial College of London, offered a presentation focused on improved treatment for schistosomiasis. Schistosomiasis is a preventable, chronic, inflammatory condition caused by a parasite infection that is found in approximately 220 million people, most of whom live in sub-Saharan Africa. The parasite swims in water and burrows into human skin on contact. It is linked to an estimated 280,000 deaths each year. In women, the disease often affects the cervix and vagina where it can cause infertility, painful intercourse, and post-coital bleeding. One type of schistosomiasis known as female urogenital schistosomiasis affects girls and young women and is associated with HIV infection.

"These women are at highest risk of HIV infection and should be the focus of public health interventions," said Fenwick.

The high prevalence of urogenital schistosomiasis appears to be associated with higher rates of HIV and the genital lesions seen with this type of schistosomiasis may contribute to the acquisition of HIV in women. The researchers believe schistosomiasis interventions can be seen as a type of HIV/AIDS control, with mass treatment in girls aimed at preventing the onset of genital lesions.

In his President's address to the ASTMH meeting, Hotez challenged his colleagues to move beyond a focus on individual conditions to embrace a concerted campaign against the totality of tropical diseases. Referencing Bill Gates' call for adopting an "audacious goal" of eradicating malaria, Hotez called for expanding the "audacious goal" to ridding the world of all its neglected tropical diseases.

He portrayed neglected diseases as everyday manifestations of the Four Horsemen of the Apocalypse in that they cause pestilence, death, underlie famine and worsen the conditions of war. Hotez noted the importance of fighting disease to the success of international anti-poverty initiatives. "These diseases don't just occur in a setting of poverty; these diseases are a stealth cause of poverty in low and middle income countries," he said.

He quoted John Gardner, the Secretary of Health under President Lyndon Johnson, who said: "There are no better grounds on which we can meet other nations and demonstrate our own concern for peace and the betterment of mankind than in a common battle against disease.

In a separate presentation at ASTMH, Paul Farmer, founder of Partners in Health, also underscored the importance of attaching the fight against neglected diseases to a broader agenda.

"We need to understand the impact we can have when we link our understanding of improvements in people's lives to policy endeavors that can changes the lives of millions," he said. "Often this does not happen. The question is how can we build consensus in the scientific community and among our allies; how can we build coalitions to pull those policy levers more effectively? All of the diseases that affect the poor are neglected."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Personalized Treatment For Crohn's Disease A Step Closer Following Gene Mapping

Main Category: Crohn's / IBD
Also Included In: Genetics
Article Date: 12 Dec 2011 - 0:00 PST

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Three new locations for Crohn's Disease genes have been uncovered by scientists at UCL using a novel gene mapping approach.

The complex genetic and environmental causes of Crohn's Disease (CD) have long been difficult to untangle. CD, a type of Inflammatory Bowel Disease that affects about 100 to 150 people per 100,000 in Europe, is characterised by inflammation in the gastrointestinal tract. Even though twin and family studies suggest a high heritability for CD of 50-60%, so far the locations of much of the genetic information implicated in this chronic disease have remained elusive.

Now, three newly identified gene regions on chromosome 16 have filled in some of the missing gaps, as well as showing that different patients carry different sets of faulty genes. Published today in the American Journal of Human Genetics, the findings could pave the way for personalised treatment and also lead to improved understanding of how complex diseases are inherited.

Dr Nikolas Maniatis, senior author from the UCL Research Department of Genetics, Evolution and Environment, said: "This paper shows how personalised medicine could work and also help to separate out patients. For example, just as there are many different types of cancer with different underlying genes, it seems that there are also mutations in different genes for different types of Crohn's Disease."

The research team used UK data provided by the Wellcome Trust Case Control Consortium (WTCCC), which includes genetic information of 1698 CD patients. The team's results were also replicated using independent US data provided by the American National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), which contains genetic information of 813 patients with CD.

Instead of comparing lots of genomic sites, one at a time, across the entire genome, the team instead looked at segments of DNA, each of which contains many variable sites. They used a mapping technique based on refined genetic maps that have the ability to show how stretches of DNA have been passed down together through the generations. By taking this into account when analysing genetic information from patients with CD the team were able to localise the faulty genes.

Dr Maniatis said: "This project essentially maps the most likely location of faulty sites for Crohn's Disease in the genome. By combining several pieces of information together, our technique lets us increase the power of our analysis."

Applying their technique on chromosome 16, which has long been known to harbour NOD2, an important gene for CD, the team indentified three novel genes, called CYLD, IRF8 and CDH1/CDH3, associated with CD and involved with inflammation and immune dysregulation in the body. Although these genes have different functions, all three are implicated in pathways involved in CD.

Dr Maniatis said: "These are very exciting times, as we can use these genetic maps to pinpoint where the causal sites of Crohn's Disease are located. Although it has been shown in the past that a proportion of patients suffering from Crohn's Disease do not carry the NOD2 mutations, up until now no other genes on chromosome 16 have been published in genome-wide analyses."

Professor Dallas Swallow, collaborator and co-author, also from the UCL Research Department of Genetics, Evolution & Environment, said: "This research will complement the work of those examining cellular and molecular changes, and ultimately lead to more personalised strategies for treatment. The next step is to search the rest of the genome.

"Importantly the work also shows that this method will allow more information to be derived from the valuable datasets collected by organisations such as the Wellcome Trust. This method can also be used to analyse other complex disorders, allowing us to make similar progress on other diseases, such as diabetes and Parkinson's disease."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our crohn's / ibd section for the latest news on this subject. 'Dissecting the Genetics of Complex Inheritance: Linkage Disequilibrium Mapping Provides Insight into Crohn's Disease' is published in the American Journal of Human Genetics.

University College London

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University College London. "Personalized Treatment For Crohn's Disease A Step Closer Following Gene Mapping." Medical News Today. MediLexicon, Intl., 12 Dec. 2011. Web.
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