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June 10, 2007, 7:26 PM CT

Drug may halt Parkinson's disease

Drug may halt Parkinson's disease
Northwestern University scientists have discovered a drug that slows and may even halt the progression of Parkinsons disease. The drug rejuvenates aging dopamine cells, whose death in the brain causes the symptoms of this devastating and widespread disease.

D. James Surmeier, the Nathan Smith Davis Professor and chair of physiology at Northwestern Universitys Feinberg School of Medicine, and his team of scientists have observed that isradipine, a drug widely used for high blood pressure and stroke, restores stressed-out dopamine neurons to their vigorous younger selves. The study is described in a feature article in the international journal Nature, which will be published on-line June 10.

Dopamine is a critical chemical messenger in the brain that affects a persons ability to direct his movements. In Parkinsons disease, the neurons that release dopamine die, causing movement to become more and more difficult.

Ultimately, a person loses the ability to walk, talk or pick up a glass of water. The illness is the second most common neurodegenenerative disease in the country, affecting about 1 million people. The occurence rate of Parkinsons disease increases with age, soaring after age 60.

Our hope is that this drug will protect dopamine neurons, so that if you began taking it early enough, you wont get Parkinsons disease, even if you were at risk. said Surmeier, who heads the Morris K. Udall Center of Excellence for Parkinsons Disease Research at Northwestern. It would be like taking a baby aspirin everyday to protect your heart.........

Posted by: Daniel      Read more         Source


June 10, 2007, 7:23 PM CT

Stroke study sheds light on left-right brain divide

Stroke study sheds light on left-right brain divide
Research into the effects of strokes has furthered our understanding of the different roles of the left and right sides of our brains. A study led by the University of Exeter has highlighted differences in the ability of people to perform basic tasks, depending on whether the left or right sides of their brains have been damaged by a stroke. The research identified the role of the right side of the brain in noticing and correcting errors.

The research focused on damage to the frontal lobes, the front part of the brain which is known to be responsible for aspects of language, decision making and learning. The team observed that people who had damage to their left side were more likely to realise they had made a mistake, and then correct it, in comparison to those who had damage to their right frontal lobes. Funded by the Wellcome Trust, the research is now reported in the journal Brain.

Dr Tim Hodgson, neuro-psychology expert at the University of Exeter and lead researcher on this study, said: We know that suffering a stroke in the left frontal region can affect aspects of speech and language, but this research highlights, for the first time, the additional challenges that people with right frontal-lobe damage might face in everyday life.

23 people, each with frontal lobe damage, performed a rule-switching task which involved learning rules linking the colour of a symbol on a computer screen with a movement to the left or right. All the participants made mistakes during the task, but it was those with right-brain damage who most frequently failed to spot their errors and had difficulty keep track of the changing task rules. The group with damage to the left frontal lobes corrected 68% of mistakes in the test, whereas people with right-brain damage only made corrections to 30% of their errors. This suggests that people who suffer damage to their right frontal lobe following a stroke may struggle in everyday situations which require attention to be switched flexibly from one thing to another.........

Posted by: Daniel      Read more         Source


June 6, 2007, 9:13 PM CT

Clues to Working Memory

Clues to Working Memory
A newly discovered interplay of cells in one of the brain's memory centers sheds light on how you recall your grocery list, where you laid your keys, and a host of important but fleeting daily tasks.

Researchers at Weill Cornell Medical College say their experiments with common goldfish are uncovering the secrets of a form of short-term recall known as "working memory".

"We've now identified a mechanism that can organize the activity of groups of cells involved in this important form of recall," says lead researcher Dr. Emre Aksay, assistant professor of computational neuroscience in the HRH Prince Alwaleed Bin Talal Bin Abdulaziz Al-Saud Institute for Computational Biomedicine at Weill Cornell Medical College in New York City.

"Furthermore, because deficits in working memory are often a precursor of schizophrenia, drugs that target this mechanism might someday help fight that debilitating disease," he says.

The findings have been published in Nature Neuroscience.

Humans rely on their working memory every day to keep track of faces and names, tasks at school or in the workplace, and other important bits of information. "This process is distinct, neurologically speaking, from the storage and retrieval of longer-term memories," explains Dr. Aksay, who is also assistant professor of physiology and biophysics at Weill Cornell.........

Posted by: Daniel      Read more         Source


June 5, 2007, 0:31 AM CT

Old memory traces in brain may trigger chronic pain

Old memory traces in brain may trigger chronic pain
Why do so a number of people continue to suffer from life-altering, chronic pain long after their injuries have actually healed".

The definitive answer -- and an effective therapy -- has long eluded scientists. Traditional analgesic drugs, such as aspirin and morphine derivatives, havent worked very well.

A Northwestern University researcher has found a key source of chronic pain appears to be an old memory trace that essentially gets stuck in the prefrontal cortex, the site of emotion and learning. The brain seems to remember the injury as if it were fresh and cant forget it.

With new understanding of the pain source, Vania Apkarian, professor of physiology, and of anesthesiology, at Northwesterns Feinberg School of Medicine, has identified a drug that controls persistent nerve pain by targeting the part of the brain that experiences the emotional suffering of pain. The drug is D-Cycloserine, which has been used to treat phobic behavior over the past decade.

In animal studies, D-Cycloserine appeared to significantly diminish the emotional suffering from pain as well as reduce the sensitivity of the formerly injured site. It also controlled nerve pain resulting from chemotherapy, noted Apkarian, who is a member of the Robert H. Lurie Comprehensive Cancer Center at Northwestern University.........

Posted by: JoAnn      Read more         Source


May 30, 2007, 0:12 AM CT

Yin, Yang And Alzheimer's disease

Yin, Yang And Alzheimer's disease
Scientists at Rensselaer Polytechnic Institute are challenging current thinking on the causes and prevention of Alzheimers disease, offering a new hypothesis that could be the key to preventing this form of dementia. The scientists have observed that a specific imbalance between two peptides may be the cause of the fatal neurological disease that affects more than five million people in the United States.

"We have observed that two peptides, AB42 and AB40, must be in balance for normal function," said Chunyu Wang, lead researcher and assistant professor of biology at Rensselaer. "They are like the Yin and Yang in Taiji, an ancient Chinese philosophy. When the peptides are produced in the correct proportions, the brain is healthy; but when that delicate balance is changed, pathological changes will occur in the brain and the persons memories become hazy, leading to eventual dementia."

Wang expects that this imbalance could be the main factor in the progression of Alzheimers disease. If correct, the addition of AB40 may stop the diseases development. Wang notes that further research is needed, but his preliminary results challenge the current mode of thinking about how these peptides contribute to the progression of the disease.

The research would be reported in the June edition of the Journal of Molecular Biology.........

Posted by: Daniel      Read more         Source


May 29, 2007, 11:56 PM CT

A living memory chip

A living memory chip
A new experiment has shown that it's possible to store multiple rudimentary memories in an artificial culture of live neurons. The ability to record information in a manmade network of neurons is a step toward a cyborg-like integration of living material into memory chips. The advance also may help neurologists to understand how our brains learn and store information.

Itay Baruchi and Eshel Ben-Jacob of Tel-Aviv University used an array of electrodes to monitor the firing patterns in a network of linked neurons. As prior studies have shown, simply linking the neurons together leads them to spontaneously fire in coordinated patterns. In the study published this month in the journal Physical Review E the scientists observed that they could deliberately create additional firing patterns that coexist with the spontaneous patterns. They claim that these new firing patterns essentially represent simple memories stored in the neuron network.

To create a new memory in the neurons, the scientists introduced minute amounts of a chemical stimulant into the culture at a selected location. The stimulant induced a second firing pattern, starting at that location. The new firing pattern in the culture along coexisted with the original pattern. Twenty-four hours later, they injected another round of stimulants at a new location, and a third firing pattern emerged. The three memory patterns persisted, without interfering with each other, for over forty hours.........

Posted by: Daniel      Read more         Source


May 21, 2007, 10:34 AM CT

Protein Protects Neurons from Stress Induced Cell Death

Protein Protects Neurons from Stress Induced Cell Death
Photo: ABDA
The researchers could show that Parkin prevents the induction of neuronal cell death. As published in the "Journal of Neuroscience", the protein activates a survival mechanism which had been known for its prominent role in immune response.

Usually, Parkinson's disease occurs after the age of 50 and in Gera number of about 400,000 people are affected. Typically it is characterized by a decline of neurons in the so-called Substantia Nigra, a structure in the midbrain that produces dopamine. The resulting deprivation of this messenger substance causes symptoms like muscular tremor at rest and restricted mobility and even complete immobility. Characteristic deposits are found in the brain, the Lewy corpuscles.

Little is known about the causes of Parkinson's disease. It has only been known for a few years that ten to fifteen per cent of all cases are linked to mutations in certain genes.

"The parkin gene is of special interest here", says Winklhofer. "One effect of its inactivation is that the Parkin protein loses its physiological function. This genetic defect plays a role for hereditary Parkinson's disease, which may lead to an early onset of the disease".

However, inactivation of the Parkin protein could also contribute to sporadic forms of the disease. In these cases massive oxidative stress probably results in misfolding and aggregation of the protein. "Interestingly, misfolding of Parkin proteins has recently been observed in the brain of patients with sporadic Parkinson's disease", Winklhofer reports.........

Posted by: Daniel      Read more         Source


May 16, 2007, 10:30 PM CT

Violent sleep disorder linked to dementia

Violent sleep disorder linked to dementia
Mayo Clinic scientists and a group of international collaborators have discovered a connection between an extreme form of sleep disorder and eventual onset of parkinsonism or dementia. The findings appear in the current issue of the journal Brain

Clinical observations and pathology studies, as well as research in animal models, led to the findings that patients with the violent rapid eye movement sleep (REM) behavior disorder (RBD) have a high probability of later developing Lewy body dementia, Parkinsons disease or multiple system atrophy (a Parkinsons-like disorder), because all of these conditions appear to stem from a similar neurodegenerative origin.

"Our data suggest that a number of patients with idiopathic (not linked to any other neurologic symptoms) RBD may be exhibiting early signs of an evolving neurodegenerative disease, which in most cases appear to be caused by some mishap of the synuclein protein," says Bradley Boeve, M.D., Mayo Clinic neurologist and lead author of the study. Synuclein proteins are linked to synapses in the brain, and clumps of abnormal alpha-synuclein protein are present in some forms of dementia. "The problem does not seem to be present in the synuclein gene itself, but its something that happens to the protein following gene expression. Just what happens to it to cause the conditions isnt clear".........

Posted by: Daniel      Read more         Source


May 15, 2007, 11:22 PM CT

Alzheimer's weight gain initiative

Alzheimer's weight gain initiative
Swedish scientists have found a way to increase the weight of people with Alzheimer's, by improving communication and patient involvement, altering meal routines and providing a more homely eating environment.

During the three-month study, reported in the recent issue of Journal of Clinical Nursing, 13 of the 18 patients in the intervention group put on weight, compared with just two of the 15 patients in the control group.

Patients who gained weight also displayed improved intellectual abilities.

"Weight loss is a common issue among people with dementia and in particular Alzheimer's" explains lead researcher Anna-Greta Mamhidir from the Karolinska Institutet in Stockholm, Sweden.

"Meal environment, communication difficulties, loss of independence and confusion are just some of the factors that appear to contribute to this problem.

"Malnutrition can also lead to other serious issues, such as increased infection rates, delayed wound healing and increased risk of hip fractures".

The aim of the study was to measure weight changes in patients with moderate and severe dementia and analyse whether providing staff training and a more supportive environment could lead to weight gain.

Two nursing home wards with similar staffing profiles and numbers of patients were selected. Both received meals from the same central kitchen.........

Posted by: Daniel      Read more         Source


May 14, 2007, 9:06 PM CT

Migraines And Retinopathy

Migraines And Retinopathy
Middle-aged men and women with a history of migraine and other headaches are more likely to have retinopathy, damage to the retina of the eye which can lead to severe vision problems or blindness, than those without a history of headaches,.

as per a research studyfrom the University of North Carolina at Chapel Hill.

For the study, reported in the May 15, 2007, issue of Neurology, scientists evaluated the headache history and eye health of 10,902 men and women who participated in the Atherosclerosis Risk in Communities (ARIC) study. Participants, who were from communities in Maryland, Minnesota, Mississippi and North Carolina, were black and white and between the ages of 51 and 71 at the time of their examination.

Twenty-two percent of the participants had a history of migraine or other headaches. Those with a history of headaches were slightly younger, more likely to be female, and more likely to be white than those without a history of headaches.

The study found people with headaches were between 1.3 and 1.5 times more likely to have retinopathy than those without headaches. Among participants who did not have a history of diabetes or hypertension, the association was stronger and limited to those with migraine headaches and other headaches with aura (visual disturbances).........

Posted by: Daniel      Read more         Source



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Did you know?
The drug Ativan is better than Valium or Dilantin for controlling severe epileptic seizures, according to a new review of studies.Ativan, or lorazepam, and Valium, or diazepam, are both benzodiazepines, the currently preferred class of drugs for treating severe epileptic seizures. Dilantin, or phenytoin, is an anticonvulsant long used for the treatment of epileptic seizures.

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