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March 13, 2011, 11:26 AM CT

Potential way to protect neurons

Potential way to protect neurons
This is an illustration of a healthy neuron. A UT Health Science Center San Antonio study found a protective mechanism for neurons placed under mitochondrial stress.

Credit: Image courtesy of the NIH/National Institute on Aging.

Cell biologists pondering the death of neurons � brain cells � said today that by eliminating one ingredient from the cellular machinery, they prolonged the life of neurons stressed by a pesticide chemical. The finding identifies a potential therapeutic target to slow changes that lead to neurodegenerative disorders such as Parkinson's and Alzheimer's diseases.

The researchers, from The University of Texas Health Science Center San Antonio, observed that neurons lacking a substance called caspase-2 were better able to withstand pesticide-induced damage to energy centers known as mitochondria.

Master switch

Caspase-2 may be a master switch that can trigger either cell death or survival depending on the amount of cellular damage, the team found. Neurons that lacked caspase-2 showed an increase in protective activities, including the efficient breakdown of obsolete or used proteins. This process, called autophagy, delays cell death.

"This research shows, for the first time, that in the absence of caspase-2 neurons increase autophagy to survive," said co-author of study Marisa Lopez-Cruzan, Ph.D., investigator in the cellular and structural biology department at the Health Science Center.

Role of energy centers

Evidence suggests that mitochondrial dysfunction plays an important role in neuronal death in conditions such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease) and Huntington's disease.........

Posted by: Daniel      Read more         Source


March 13, 2011, 11:12 AM CT

Genius quality might be the result of hormonal influences

Genius quality might be the result of hormonal influences
A longstanding debate as to whether genius is a byproduct of good genes or good environment has an upstart challenger that may take the discussion in an entirely new direction. University of Alberta researcher Marty Mrazik says being bright appears to be due to an excess level of a natural hormone.

Mrazik, a professor in the Faculty of Education's educational psychology department, and a colleague from Rider University in the U.S., have published a paper in Roeper Review linking giftedness (having an IQ score of 130 or higher) to prenatal exposure of higher levels of testosterone. Mrazik hypothesizes that, in the same way that physical and cognitive deficiencies can be developed in utero, so, too, could similar exposure to this naturally occurring chemical result in giftedness.

"There seems to be some evidence that excessive prenatal exposure to testosterone facilitates increased connections in the brain, particularly in the right prefrontal cortex," said Mrazik. "That's why we see some intellectually gifted people with distinct personality characteristics that you don't see in the normal population".

Mrazik's notion came from observations made during clinical evaluations of gifted individuals. He and his fellow researcher observed some specific traits among the subjects. This finding stimulated a conversation on the role of early development in setting the foundation for giftedness.........

Posted by: Daniel      Read more         Source


March 10, 2011, 7:58 AM CT

Brain has 3 layers of working memory

Brain has 3 layers of working memory
Scientists from Rice University and Georgia Institute of Technology have found support for the theory that the brain has three concentric layers of working memory where it stores readily available items. Memory scientists have long debated whether there are two or three layers and what the capacity and function of each layer is.

In a paper in the recent issue of the Journal of Cognitive Psychology, scientists observed that short-term memory is made up of three areas: a core focusing on one active item, a surrounding area holding at least three more active items, and a wider region containing passive items that have been tagged for later retrieval or "put on the back burner." But more importantly, they observed that the core region, called the focus of attention, has three roles -- not two as proposed by prior researchers. First, this core focus directs attention to the correct item, which is affected by predictability of input pattern. Then it retrieves the item and subsequently, when needed, updates it.

The researchers, Chandramallika Basak of Rice University and Paul Verhaeghen of Georgia Tech, used simple memory tasks involving colors and shapes on a computer screen to determine the three distinct layers of memory. They also determined the roles of attention focus by exploring the process of switching items in and out of the focus of attention.........

Posted by: Daniel      Read more         Source


March 10, 2011, 7:34 AM CT

Selectively Controlling Anxiety Pathways in the Brain

Selectively Controlling Anxiety Pathways in the Brain
A new study supports the role of a brain region called the amygdala in processing anxiety. In this 3-D magnetic resonance imaging (MRI) rendering of a human brain, functional MRI (fMRI) activation of the amygdala is highlighted in red.

Credit: NIMH Clinical Brain Disorders Branch

A newly released study sheds light--both literally and figuratively--on the intricate brain cell connections responsible for anxiety.

Researchers at Stanford University recently used light to activate mouse neurons and precisely identify neural circuits that increase or decrease anxiety-related behaviors. Pinpointing the origin of anxiety brings psychiatric professionals closer to understanding anxiety disorders, the most common class of psychiatric disease.

A research team led by Karl Deisseroth, associate professor of psychiatry and behavioral sciences and bioengineering, identified two key pathways in the brain: one which promotes anxiety, and one which alleviates anxiety.

The pathways are in a brain region called the amygdala. Previous research suggests the amygdala plays a role in anxiety, but earlier studies used widespread modifications of the amygdala, through drugs or physical disruption of the brain region, to study the way in which it affects anxiety. This new work, published in this week's Nature, uses a tool called optogenetics--developed by Deisseroth and recently named Method of the Year by Nature Methods--to specifically tease out which pathways contribute to anxiety.

Optogenetics combines genetics and optical science to selectively manipulate the way a neuron fires in the brain. Neurons are electrically excitable cells that convey information through electrical and chemical signaling.........

Posted by: Daniel      Read more         Source


March 7, 2011, 7:22 AM CT

Stroke patients benefit from family involvement

Stroke patients benefit from family involvement
Your family's involvement in your exercise treatment could significantly improve your function and recovery after stroke, as per a research studyin the March print issue of Stroke: Journal of the American Heart Association.

Scientists observed that adding family-assisted exercise treatment to routine physical treatment after stroke improved motor function, balance, distance walked and ability to perform daily living activities. It also lowered the strain on the family member, who said participation lowered stress and was empowering.

"It's a win-win situation for everyone," said Emma Stokes, Ph.D., the study's principal investigator and Senior Lecturer in Physiotherapy at Trinity College Dublin in Ireland. "People with stroke, their families and healthcare providers share in the benefit".

The study involved 40 male and female stroke survivors, all Caucasian. Half received routine exercise treatment, while the others received the FAmily Mediated Exercise intervention (FAME) in addition to routine treatment.

The routine exercise treatment group included seven men and 13 women, average age 70. The FAME group had 13 men and seven women, average age 63. Family members helped the stroke patient do exercises in 35-minute increments seven days per week for eight weeks to improve leg function. The exercises were simple enough to be done at the bedside, either at the hospital or at home. Exercise was tailored to each individual and modified weekly to reflect improvement. Scientists assessed the outcome of the two groups after the therapy period and at three-month follow-up.........

Posted by: Daniel      Read more         Source


March 7, 2011, 7:14 AM CT

Protecting the brain from epileptic seizures

Protecting the brain from epileptic seizures
For years brain researchers have puzzled over the shadowy role played by the molecule putrescine, which always seems to be present in the brain following an epileptic seizure, but without a clear indication whether it was there to exacerbate brain damage that follows a seizure or protect the brain from it. A new Brown University study unmasks the molecule as squarely on the side of good: It seems to protect against seizures hours later.

Putrescine is one in a family of molecules called "polyamines" that are present throughout the body to mediate crucial functions such as cell division. Why they surge in the brain after seizures isn't understood. In a lengthy set of experiments, Brown neuroresearchers meticulously traced their activity in the brains of seizure-laden tadpoles. What they found is that putrescine ultimately converts into the neurotransmitter GABA, which is known to calm brain activity. When they caused a seizure in the tadpoles, they observed that the putrescine produced in a first wave of seizures helped tadpoles hold out longer against a second wave of induced seizures.

Carlos Aizenman, assistant professor of neuroscience and senior author of a study reported in the journal Nature Neuroscience, said further research could ultimately produce a drug that targets the process, potentially helping young children with epilepsy. Tadpoles and toddlers aren't much alike, but this basic aspect of their brain chemistry is.........

Posted by: Daniel      Read more         Source


February 21, 2011, 7:45 AM CT

Take care of your brain

Take care of your brain
As the average life span becomes longer, dementia becomes more common. Swedish scientist Laura Fratiglioni has shown that everyone can minimize his or her risk of being affected. Factors from blood pressure and weight to the degree of physical and mental activity can influence cognitive functioning as one gets older.

The lengthening of the average life span in the population has caused an increase in the prevalence of aging related disorders, one of which is cognitive impairment and dementia. An expert panel estimates that worldwide more than 24 million people are affected by dementia, most suffering from Alzheimer's disease. In the more developed countries, 70 percent of the persons with dementia are 75 years or older.

Age is the greatest risk factor for developing dementia. But there is growing evidence that the strong association with increasing age can be, at least partially, explained by a life course cumulative exposure to different risk factors.

Laura Fratiglioni's research group at Karolinska Institutet is a leader in identifying the risk factors that lie behind developing dementia and using this knowledge to develop possible preventative strategies. The group's research has shown that the risk is partly determined by an individual genetic susceptibility, and that active involvement in mental, physical and social activities can delay the onset of dementia by preserving cognitive functions. Further education early in life has a protective effect, and the group's research has shown that it is never too late to get started.........

Posted by: Daniel      Read more         Source


February 21, 2011, 7:29 AM CT

Higher triglyceride level increases stroke risk

Higher triglyceride level increases stroke risk
A study by scientists in Denmark revealed that increasing levels of non-fasting triglycerides are linked to an increased risk of ischemic stroke in men and women. Higher cholesterol levels were linked to greater stroke risk in men only. Details of this novel, 33-year study are now available online in Annals of Neurology, a journal published by Wiley-Blackwell on behalf of the American Neurological Association.

As per the World Health Organization (WHO) cardiovascular diseases are the number one cause of death globally�responsible for an estimated 17.1 million deaths worldwide ( 2004), with 5.7 million due to stroke. The American Stroke Association states that stroke is the third leading cause of death in the U.S. and 87% of all cases are attributed to ischemic stroke, occurring when the supply of blood to the brain is obstructed. The obstruction or blockage is typically caused by the build-up of fatty deposits inside blood vessels (atherosclerosis).

Medical evidence suggests that elevated non-fasting triglycerides are markers of elevated levels of lipoprotein remnants, particles similar to low density lipoprotein (LDL), or bad cholesterol, both of which are thought to contribute to plaque build-up. "Interestingly, current guidelines on stroke prevention have recommendations on desirable cholesterol levels, but not on non-fasting triglycerides," said lead study author, Dr. Marianne Benn from Copenhagen University Hospital. "Our study was the first to examine how the risk of stroke for very high levels of non-fasting triglycerides compared with very high cholesterol levels in the general population."........

Posted by: Daniel      Read more         Source


February 17, 2011, 7:05 AM CT

Increasing brain enzyme may slow Alzheimer's disease

Increasing brain enzyme may slow  Alzheimer's disease
Stanislav Karsten, an LA BioMed principal researcher, is the lead author of a new study on Alzheimer's disease.

Credit: LA BioMed

Increasing puromycin-sensitive aminopeptidase, the most abundant brain peptidase in mammals, slowed the damaging accumulation of tau proteins that are toxic to nerve cells and eventually lead to the neurofibrillary tangles, a major pathological hallmark of Alzheimer's disease and other forms of dementia, as per a research studypublished online in the journal, Human Molecular Genetics

Scientists found they could safely increase the puromycin-sensitive aminopeptidase, PSA/NPEPPS, by two to three times the usual amount in animal models, and it removed the tau proteins in the neurons. Removing the tau proteins restored neuronal density and slowed down disease progression. Scientists detected no abnormalities caused by the increase in PSA/NPEPPS, suggesting that elevating PSA/NPEPPS activity appears to be a viable approach to treat Alzheimer's disease and other forms of dementia, known a tauopathies.

"Our research demonstrated that increasing the brain enzyme known as PSA/NPEPPS can effectively block the accumulation of tau protein that is toxic to nerve cells and slow down the progression of neural degeneration without unwanted side effects," said Stanislav L. Karsten, PhD, the corresponding author for the study and a principal investigator at Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed). "These findings suggest that increasing this naturally occurring brain peptidase, PSA/NPEPPS, appears to be a feasible therapeutic approach to eliminate the accumulation of unwanted toxic proteins, such as tau, that cause the neural degeneration linked to the devastating effects of Alzheimer's disease and other forms of dementia".........

Posted by: Daniel      Read more         Source


February 17, 2011, 7:00 AM CT

Tau-induced memory loss in Alzheimer's mice

Tau-induced memory loss in Alzheimer's mice
To test their capacity to learn, the mice are trained to find an underwater platform which is not visible to them from the edge of a water basin. The swimming path is marked in red. Normal mice learn to find the path after just a few training sessions; they remember it and swim straight to the platform (left) when tested. A mouse with too much aggregated tau protein in its neurons finds it difficult to learn and swims aimlessly around the basin (centre) for extended periods. If the gene for the toxic tau protein in this mouse is switched off for a few weeks using a genetic trick, the mouse is able to learn normally again and quickly finds its way to the platform (right). © Max-Planck-ASMB/Mandelkow
Amyloid-beta and tau protein deposits in the brain are characteristic features of Alzheimer disease. The effect on the hippocampus, the area of the brain that plays a central role in learning and memory, is especially severe. However, it appears that the toxic effect of tau protein is largely eliminated when the corresponding tau gene is switched off. Scientists from the Max Planck Research Unit for Structural Molecular Biology at DESY in Hamburg have succeeded in demonstrating that once the gene is deactivated, mice with a human tau gene, which previously presented symptoms of dementia, regain their ability to learn and remember, and that the synapses of the mice also reappear in part. The researchers are now testing active substances to prevent the formation of tau deposits in mice. This may help to reverse memory loss in the early stages of Alzheimer disease - in part, at least.

Whereas aggregated amyloid-beta protein forms insoluble clumps between the neurons, the tau protein accumulates inside them. Tau protein stabilises the tube-shaped fibers of the cytoskeleton, known as microtubules, which provide the "rails" for cellular transport. In Alzheimer disease, excess phosphate groups cause the tau protein to malfunction and form clumps (the 'neurofibrillary tangles'). As a result, nutrient transport breaks down and the neurons and their synapses die off. This process is accompanied by the initial stage of memory loss.........

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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