Drug 'may slow down Parkinson's'

Drug 'may slow down Parkinson's'
(NSI News Source Info) August 27, 2008: Early use of medication may be able to slow down progression of Parkinson's disease, preliminary research suggests.
Patients who took the drug rasagiline soon after diagnosis had a less aggressive form of Parkinson's than those who did not take it until later.
The international study involved more than 1,000 patients, but doctors stress it could be 10 to 15 years before the long-term benefits become clear.
Details were presented at a neurological conference in Madrid.
This work suggests that giving drugs at an early stage has an effect over and above what you would expect
Dr Kieran BreenParkinson's Disease Society
More than 120,000 people in the UK have Parkinson's and around 10,000 new cases are diagnosed each year.
Symptoms of the progressive neurological disorder include shakes, memory loss and stiffening of the muscles.
Rasagiline, also known as Azilect, is already approved for use by the NHS to ease symptoms of Parkinson's.
However, some doctors are reluctant to prescribe medication at an early stage, due to concern that the effect can wane with time.
The latest study, presented at the European Federation of Neurological Societies Congress, involved patients from the UK, US and Europe.
It found that patients who took rasagiline immediately after diagnosis were in better shape after 18 months than those whose treatment with the drug was delayed by nine months.
The researchers believe that the drug could work by creating a long lasting protection for brain cells.
However, they stressed that many patients had been taking part in the study for just 18 months, and much more work was required to pin down the long-term impact.
'Exciting' results
Professor David Burn, from the University of Newcastle, one of the researchers who took part in the study described the results as "exciting".
He said: "The data show that early treatment can result in a slowing of clinical progression. These data are also consistent with an earlier trial with rasagiline which showed a similar outcome.
"This may offer real benefit to patients who are treated promptly after diagnosis."
Dr Kieran Breen, director of research for the Parkinson's Disease Society, said: "There is a feeling among doctors that you should not put somebody on a drug until you really, really have to, but this work suggests that giving drugs at an early stage has an effect over and above what you would expect."
However, Dr Breen said it was unclear whether the effect of early medication was specific to rasagiline, or a general phenomenon also associated with other drugs for the condition.
He said the research showed that the effect of the drug was very subtle. Patients given a regular 1mg dose of rasagline showed benefit, but not those given a higher dose of the drug.

Frequently Asked Questions Relating To Parkinson's Disease

Frequently Asked Questions Relating To Parkinson's Disease
(NSI News Source Info) August 24, 2008

*Is there a cure for Parkinson’s disease?
*Can Parkinson’s be prevented?
*Is there a difference between Parkinson’s disease and essential tremor?
*If I undergo Deep Brain Stimulation surgery, how soon after will my symptoms improve?
*Does essential tremor increase the risk for Parkinson’s disease?
*When will my Huntington’s symptoms begin to show?
*If Huntington’s disease runs in the family, can I be tested?
*Are there warning signs for dystonia?
*Can you die from dystonia?

Is there a cure for Parkinson’s disease? Currently, there is no cure for Parkinson’s. Great discoveries are being made that will likely point researchers toward the underlying causes of the disease. As the environmental and genetic factors become more clear, we are hopeful that targeted medications and interventions will bring us closer to a cure in the years ahead.

Can Parkinson’s be prevented? Patient’s often want to know if something they did caused them to have Parkinson’s. We simply don’t yet know what causes the majority of cases of Parkinson’s disease. Perhaps it is an interaction of environmental factors and genetic predisposition. Until we have more clearly identified these “risk factors” we cannot prevent anyone from getting Parkinson’s.

Is there a difference between Parkinson’s disease and essential tremor? Parkinson’s and Essential Tremor are two different disorders that share tremor as a major feature. The exact nature of the tremor, however, is very different and can usually be distinguished by a movement disorder specialist. A small number of patients have both Essential Tremor and Parkinson’s but usually it is one or the other. Knowing which one a patient has is important because treatments are different.

If I undergo Deep Brain Stimulation surgery, how soon after will my symptoms improve? About two weeks after the brain surgery, the pacemakers will be turned on and programming will begin. Many patients experience very rapid improvement in many of their symptoms. Other symptoms can take a few months to improve. The programming of the pacemaker is a very individually tailored experience so predictions of improvement vary based on the type and severity of symptoms being treated. In general, however, most patients should certainly hope for significant improvement by 6 months from the date of the surgery.

Does essential tremor increase the risk for Parkinson’s disease? A small percentage of people with Essential Tremor do develop some symptoms of Parkinson’s disease after many years. Most patients with Essential Tremor, however, do not develop Parkinson’s.

When will my Huntington’s symptoms begin to show? It is impossible to predict when the symptoms of Huntington’s will develop. This can cause a great deal of anxiety for individuals who know the Huntington’s Disease gene status. For this reason, it is recommended that both symptomatic and non-symptomatic individuals with Huntington’s or at risk for Huntington’s consider routine visits to a movement disorder center. A specialist can review your condition and discuss any changes or potential treatments.

If Huntington’s disease runs in the family, can I be tested? Yes. Whether you want to be tested or not is a personal choice. You should discuss the possibility of being tested with a Huntington’s Center. An experienced counselor and geneticist can discuss the test options and help you make the best decision.

Are there warning signs for dystonia? Dystonia can begin very subtly. Early symptoms can be mild turning in of a hand or foot, sometimes at rest and sometimes during a specific task. Mild cramping doing tasks that didn’t previously cause cramping is another possible sign. If you are finding it much harder to do something specific (like playing an instrument or writing) you might want to have it evaluated instead of “toughing it out.”

Can you die from dystonia? It is very rare to die from dystonia. Untreated dystonia can lead to a variety of complications that can, themselves, be dangerous (like pneumonia or falls). With treatment, many dystonia patients lead active lives.

The Human Brain

New Map IDs The Core Of The Human Brain

(NSI News Source Info) August 22, 2008: An international team of researchers has created the first complete high-resolution map of how millions of neural fibers in the human cerebral cortex -- the outer layer of the brain responsible for higher level thinking -- connect and communicate. Their groundbreaking work identified a single network core, or hub, that may be key to the workings of both hemispheres of the brain.The work by the researchers from Indiana University, University of Lausanne, Switzerland, Ecole Polytechnique Federale de Lausanne, Switzerland, and Harvard Medical School marks a major step in understanding the most complicated and mysterious organ in the human body.

It not only provides a comprehensive map of brain connections (the brain "connectome"), but also describes a novel application of a non-invasive technique that can be used by other scientists to continue mapping the trillions of neural connections in the brain at even greater resolution, which is becoming a new field of science termed "connectomics."

"This is one of the first steps necessary for building large-scale computational models of the human brain to help us understand processes that are difficult to observe, such as disease states and recovery processes to injuries," said Olaf Sporns, co-author of the study and neuroscientist at Indiana University.

The findings appear in the journal PLoS Biology. Co-authors include Patric Hagmann and Reto Meuli, University Hospital Center and University of Lausanne; Leila Cammoun and Xavier Gigandet, Ecole Polytechnique Federale de Lausanne; Van J. Wedeen, Massachusetts General Hospital and Harvard Medical Center; and Christopher J. Honey, IU.Until now, scientists have mostly used functional magnetic resonance imaging (fMRI) technology to measure brain activity -- locating which parts of the brain become active during perception or cognition -- but there has been little understanding of the role of the underlying anatomy in generating this activity.

What is known of neural fiber connections and pathways has largely been learned from animal studies, and so far, no complete map of brain connections in the human brain exists.

In this new study, a team of neuroimaging researchers led by Hagmann used state-of-the-art diffusion MRI technology, which is a non-invasive scanning technique that estimates fiber connection trajectories based on gradient maps of the diffusion of water molecules through brain tissue.A highly sensitive variant of the method, called diffusion spectrum imaging (DSI), can depict the orientation of multiple fibers that cross a single location. The study applies this technique to the entire human cortex, resulting in maps of millions of neural fibers running throughout this highly furrowed part of the brain.

Sporns then carried out a computational analysis trying to identify regions of the brain that played a more central role in the connectivity, serving as hubs in the cortical network. Surprisingly, these analyses revealed a single highly and densely connected structural core in the brain of all participants.

"We found that the core, the most central part of the brain, is in the medial posterior portion of the cortex, and it straddles both hemispheres," Sporns said.

"This wasn't known before. Researchers have been interested in this part of the brain for other reasons. For example, when you're at rest, this area uses up a lot of metabolic energy, but until now it hasn't been clear why."

The researchers then asked whether the structural connections of the brain in fact shape its dynamic activity, Sporns said. The study examined the brains of five human participants who were imaged using both fMRI and DSI techniques to compare how closely the brain activity observed in the fMRI mapped to the underlying fiber networks.

"It turns out they're quite closely related," Sporns said. "We can measure a significant correlation between brain anatomy and brain dynamics. This means that if we know how the brain is connected we can predict what the brain will do."

Sporns said he and Hagmann plan to look at more brains soon, to map brain connectivity as brains develop and age, and as they change in the course of disease and dysfunction.

Parkinson's Disease: What Causes It?

Parkinson's Disease: What Causes It?
Parkinson's disease is caused by the progressive impairment or deterioration of neurons (nerve cells) in an area of the brain known as the substantia nigra. When functioning normally, these neurons produce a vital brain chemical known as dopamine. Dopamine serves as a chemical messenger allowing communication between the substantia nigra and another area of the brain called the corpus striatum. This communication coordinates smooth and balanced muscle movement. A lack of dopamine results in abnormal nerve functioning, causing a loss in the ability to control body movements.
Why Does Parkinson's Occur?
Why Parkinson's disease occurs and how the neurons become impaired is not known. However, there is increasing evidence that Parkinson's disease may be inherited (passed on genetically from family members).
There is considerable controversy surrounding the possibility of a genetic cause of Parkinson's disease. In a small number of families, specific genetic abnormalities leading to the illness have been identified. However, the vast majority of people with Parkinson's disease do not have one of these identified genetic abnormalities. It is probable that in people who develop Parkinson's disease early in life (young-onset Parkinson's disease) there is a genetic component. Because we don't understand very much at this point about how Parkinson's disease is inherited, the implications for children of people with Parkinson's disease are unclear.
There is also some evidence that certain toxins in the environment may cause Parkinson's disease. Scientists have suggested that external or internal toxins may selectively destroy the dopaminergic neurons, causing Parkinson's disease. Toxins that may be linked to Parkinson's include manganese, carbon monoxide, carbon disulfide and some other pesticides.
Also, it is believed that oxidative stress can cause Parkinson's disease. Oxidation is a process in which free radicals (unstable molecules lacking one electron), in an attempt to replace the missing electron, react with other molecules (such as iron). Free radicals are normally formed in the brain and body, but usually the brain and body have mechanisms to get rid of free radicals. In people with Parkinson's disease, the mechanisms may not be effective or they may produce too many free radicals. It is also possible that environmental toxins may contribute to abnormal free radical formation and lead to Parkinson's disease. Oxidation is thought to cause damage to tissues, including neurons. In most cases, antioxidants protect cells from free radical damage.
While it is not clear what events cause the abnormal nerve function linked to Parkinson's disease, there are certain conditions and medications that can cause Parkinson's disease-like symptoms. These include:
Certain medications. Certain drugs such as antipsychotics used to treat severe paranoia and schizophrenia can cause a person to experience symptoms that resemble Parkinson's disease (Parkinsonism).
Shy-Drager syndrome. This is a rare degenerative condition that produces symptoms similar to Parkinson's disease.
Street drugs. MPTP, a synthetic heroin contaminant, can cause severe Parkinson's disease-like symptoms.
Blood vessel disorders. Although rare, stroke and atherosclerosis (hardening of the arteries) can cause symptoms similar to Parkinson's disease.
Most researchers suggest that a combination of these factors may cause the disease.
Can Parkinson's Be Prevented?
To date, there is no known prevention or cure for Parkinson's disease. But, there are several treatment options, including drug therapy and/or surgery that can reduce the symptoms, and make living with the disease easier.