Some Jokes Activate Brain’s Reward Centers More Than Others

Posted on August 27, 2011 by admin

A funny thing happens to your brain when you hear a joke…. Specific neurons “light up” as you begin to laugh!

According to research published in the Journal of Neuroscience, the funnier the joke is, the more activity there is in the listener’s brain pleasure centers. A team of scientists using functional magnetic resonance imaging (fMRI), scanned the brains of 12 healthy people who volunteered for the study, to compare what goes on in their brains when they hear ordinary sentences and funny jokes, including puns.

Scans clearly demonstrated that the brain’s reward centers were activated much more when responding to jokes and puns than to everyday language. As if to  reinforce the phenomenon, the funnier each subject found an individual joke, the greater was their MRI response.

The researchers found a characteristic pattern of brain activity when the jokes used were puns. For example, jokes like ‘Why don’t cannibals eat clowns? Because they taste funny!’ involved language processing areas in the brain more than jokes that didn’t use wordplay.  Double entendres (i.e., words with more than one meaning) also exhibited their own characteristic fMRI pattern. Such studies help scientists gain further insight into how the brain works.

A more humane implication of this study involves patients in a vegetative state from severe acquired brain injury.  Scientists previously used fMRI to detect language comprehension in vegetative state patients who can’t communicate in any other way. This study shows that similar methods can be used to look for positive emotions in such patients which could be important for their families and friends wanting to find out whether someone in a vegetative state can experience positive emotions – a step that could help relatives understand their state of mind.

 

Posted in Assessment, Brain Injury, How the Brain Works, How the Memory Works, neuroscience, Stroke, Uncategorized | View Comments

Brain Stem Cells Restore Memory & Cognition After Brain Cancer Radiation Therapy

Posted on August 26, 2011 by admin

Radiation therapy utilizes high-energy radiation to shrink and kill cancer cells, but it may be doing much damage to the brain. Although radiation therapy has been the standard of care for patients with brain cancer, it can have severe and devastating side effects such functional learning and memory loss that is progressive, debilitating, and adversely impacts quality of life.

A new development in regaining cognition is the use of stem cells. Studies show that stem cell therapy may be the diagnosis in restoring cognition for patients with brain cancer.

Immature stem cells found in bone marrow, blood stream, and in umbilical cords will later develop into blood cells. Because stem cells can be damaged in certain cancer treatments, hospitals are developing techniques to add healthy stem cells back into your body post treatment. Under proper conditions, appropriate stem cells can develop into tissues and organs in virtually any part of the body.

A recent study published in Cancer Research, reported results of researchers who studied rats exposed to cranial radiation. They followed up their research with human neural stem cell transplants. Significant levels of these stem cells survived and converted into brain cells or neurons. Cognitive function also greatly improved compared with the control rats who did not receive stem cell transplantation. Their findings pave the way for human safety trials to be conducted within a few years.

This is one more example of how stem cells can provide innovative treatments for central nervous system diseases, especially repairing of damaged neurons from acquired brain injury such as stroke, as well as from neurodegenerative diseases such as dementias including Alzheimer’s disease.

 

Posted in Alzheimer's Disease, Brain Injury, How the Brain Works, How the Memory Works, Memory Health, Neuroplasticity, Stroke, Uncategorized | View Comments

Dopamine Involved In Neuroplasticity Through New Neuron Formation

Posted on August 20, 2011 by admin

Researchers at Karolinska Institute studying the brains of salamanders discover an unknown neuroplasticity capability of the brain neurotransmitter dopamine.

As published in Cell Stem Cell, researchers demonstrate how dopamine controls the formation of new neurons in the adult brain by switching on genes for new stem cells.

By studying the salamander, a tailed member of the frog family known for its ability to regenerate lost body parts including entire limbs, researchers where taking advantage of the ability of these non-mammals to be able to fully recover from a condition similar to Parkenson’s in only about one month. Parkinson’s is a neurodegenerative disease involving the death of dopamine-producing cells in the mid-brain.

When Salamanders lose their dopamine producing cells, the brain detects that these vital cells are missing and triggers the rebuilding of lost dopamine-producing neurons until the correct number are replaced.

Researchers found that when dopamine levels drop due to the death of dopamine-producing neurons, the salamander stem cells are automatically activated. The neurotransmitter effectively acts as a continual regulator of stem cell activity.

Such neuroplasticity studies shed light on how new nerve cell production can be resumed and how it can be stopped when no additional neurons are needed. It is precisely in this regulation that dopamine seems to play a vital part.

Further comparative studies may shed additional light on how neurotransmitters control stem cells in the brain— findings that may some day contribute to new treatments for neurodegenerative conditions such as Parkinson’s and Alzheimer’s disease.

 

Posted in Alzheimer's Disease, How the Brain Works, How the Memory Works, Memory Health, Neuroplasticity, neuroscience, Uncategorized | View Comments

Statins May Even Reduce Risk of Stroke In Younger Adults

Posted on August 2, 2011 by admin

By far the most important risk factor for stroke is high blood pressure. Blood pressure medication substantially reduces your stroke risk. So does cessation of smoking. Now a study published in the journal Neurology indicates that a class of drugs known as statins – typically prescribed for high levels of low density cholesterol – can reduce the risk of a second stroke in younger stroke victims.

A stroke – an interruption of the blood supply to any part of the brain – is caused by one of two main types: Ischemic strokes— caused by the blockage of an artery supplying the brain and make up 85 percent of the total. The brain tissue beyond the blockage dies from the lack of supply of nutrients, oxygen and glucose. The other 15 percent of strokes are the result of ruptured blood vessels that bleed into the brain and are called hemorrhagic strokes.

Advisory Statements From the Stroke Council, American Heart Association and American Stroke Association all suggest that benefits from statins are considerable. Based on numerous large-scale randomized trials, the vast majority of patients with a history of ischemic stroke or transient ischemic attack could benefit from statin use. Multiple studies have shown that statins reduce risk of stroke in those with coronary artery disease and elevated total or low-density lipoprotein (LDL) cholesterol.

The average age for stroke is around 70. Younger people can suffer from stroke, but the causes are a little bit different than the average stroke caused by blood clots to the brain. In young people, one common cause is accidental tearing of an artery— it’s usually something that’s pretty hard to prevent. What’s unfortunate about strokes is that they often don’t offer many warning signs when they’re happening. Due to sudden onset of this type of stroke, it tends to be much more of a surprise than stroke caused by clots. The most important warning signs to recognize are weakness or numbness, loss of feeling on one side of the body, loss of balance, inability to walk, slurred speech, headache, and loss of vision, which might be in one eye or off to one side of your visual field.

Results of this study indicate younger adults who have a stroke could dramatically reduce their chances of another one by taking statins.  The study included 215 people. Those who had their first stroke between the age of 15 and 49, found that those who took statins at some point afterwards were 77 % less likely to suffer another, over a nine year period. Of the 36 people who took statins continuously after their first stroke, none had a second cardiovascular event of any kind during that time.

The principal investigator suggests that even though the number of subjects is low, young adults who have experienced a stroke for unknown reasons should consider treatment with cholesterol-lowering statin drugs.

 

Posted in Brain Injury, Memory Fitness, neuroscience, Stroke, Uncategorized | View Comments

Paying Attention To The Pleasures Of ADHD

Posted on July 30, 2011 by admin

Researchers at the Universitat Autònoma de Barcelona studying brain circuits involved in the development of ADHD found anomalies in aspects of attention related to the brain’s pleasure centers…. the brain’s dopamine-mediated reward system related to motivation and gratification.

In children with ADHD, the degree of motivation in carrying out an activity is related to the immediacy with which activity objectives are met. This would explain why attention level differs depending on the tasks—such as fast paced computer games or interesting videos that are more instantly gratifying and therefore provide greater incentive to pay attention.

However, recent research focused on neuronal gratification/pleasure circuits located within part of the brain’s reward system – the nucleus accumbens in an area of the brain known as the ventral striatum – which are in charge of maintaining levels of motivation from the task’s start until reaching the objective or “reinforcement”. In children with ADHD, unless great incentives are immediately present, motivational levels drop rapidly and immediate reinforcements are needed to continue in their task.

Researchers studied 84 participants aged 6 to 18 years, divided according to presence of ADHD symptoms (42 with ADHD in one group and a control group with no signs of mental or behavioral anomalies) paired by sex and age. Magnetic resonance images (MRIs) displayed brain structures of all participants. Differences in the structure of the ventral striatum – particularly on the right-hand side – could be seen between those with ADHD and those without the disorder. Children with ADHD exhibited reduced volumes in this region. These differences were associated with symptoms of hyperactivity and impulsiveness.

The study data backs up previous animal study regarding the importance of the reward system, the relation between nucleus accumbens, impulsive behavior and the development of motor hyperactivity.

Consequently, study authors believe ADHD is not only caused by brain alterations affecting cognitive processes, but also by anomalies which cause motivational deficiencies.

Overcoming lack of motivation is important because memory and learning must be preceded by paying adequate attention to the material if it is to be encoded into short term working memory. While medications are available to manage dopamine levels more evenly— to help increase natural pleasure incentives, it can be seen that managing the type of activity, for example using ‘attention grabbing’ videos versus printed text to teach a new subject might be more effective for people with ADD/ADHD.

 

Posted in Attention, How the Brain Works, How the Memory Works, Memory Fitness, neuroscience, Uncategorized | View Comments

Age-Related Memory Loss Reversed in Animal Study

Posted on July 28, 2011 by admin

Age-related memory problems occur in virtually everyone. Some are due to declines in the neural networks of the prefrontal cortex— responsible for higher cognitive and executive functions, including working memory and the ability to multitask and inhibit distractions. Working memory facilitates abstract thought and reasoning, and enables recall of current information such as where you left your reading glasses.  The ability to inhibit distractions is, by the way, a hallmark of Attention Deficit Disorder (ADD).

Yale University researcher’s findings, reported in the journal Nature, uncovers the cellular defects that cause this type of working memory forgetfulness.  Results found that the older lab animals (monkeys) have weaker connections in the prefrontal cortex and that they fire less robustly than in younger animals, but that this problem may be reversible.

The study recorded prefrontal cortex neuronal electrical activity, a region especially vulnerable to aging in both humans and primates. Previous research demonstrated that these neural circuits are organized to create a sustained level of activity crucial for working memory. Analysis of activity recorded from young, middle-aged and old monkeys showed that the firing rate of neurons in this area slows with age even though other aging neurons, such as those that respond to cues in the environment, still fired normally.

The study also found that certain compounds — such as guanfacine used in a medication approved for treating high blood pressure in adults — helped improve prefrontal cortex neuronal firing rates in older monkeys.   Delivering guanfacine to the brain, researchers could make neurons in old monkeys behave like those in young monkeys. While studies involving animals often fail to produce similar results in humans, clinical trials of a promising generic compound are currently underway.

The need grows for maintaining memory fitness in order to live independently as we age. These findings support the possibility that some key brain changes occurring with age are very specific and may be preventable.

 

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Epigenetics And Neuroplasticity Control Brain Development Right From The Start

Posted on July 21, 2011 by admin

A study published in the journal Neuron, illustrates the effect of environmental inputs (epigenetics) on the developing brain’s neuroplasticity. Exposure to just 20 minutes of intensive visual stimulation during development led to enhanced visual acuity and higher sensitivity to finer and smaller visual targets than non-conditioned controls.

Employing time-lapse imaging to chart changes in brain circuitry during development, researchers studied developing brain neuronal circuitry, the network of connections between nerve cells (wiring), found the brain’s dynamic neuronal connections are plastic, changing and adapting to the demands of the environment (neuroplasticity). Many brain diseases are thought to result from errors in brain wiring due to a disruption of the complex interactions between genetic and epigenetic environmental influences during neuroplastic brain development.

In the developing brain from birth to about 3-5 years of age, there is an initial overproduction of imprecise connections between nerve cells. During development and learning, these connections are pruned, leaving only those that are appropriately strong and more specific.

For example, hearing spoken language from birth stimulates neuronal connections for correct pronunciation. Adult language learners speaking with an accent do so because their developing brains cannot hear and say ‘foreign’ sounds easily. That’s why teaching a languages before the age of 5 is so effective. This study focused on environmental stimulation from intense visual stimulation on refinement and enhancement of neuronal receptivity for visual acuity (clearness of vision due to sharpness of retinal focus).

Sensory experience during development leads to rapid production of key proteins (Brain Derived Neurotrophic Factor, or BDNF) which play a major role in the plasticity of neurons. BDNF has two forms: proBDNF (prunes poor connections) and mature BDNF (strengthens effective connections).

In the developing visual system, nerve cells from the retina at the back of the eye connect with very specific points within the visual part of the brain, the tectum, in order to ensure that the retina is properly represented in the brain and able to relay accurate visual signals using a highly sophisticated guidance cue system. This process was analyzed by the researchers in making their conclusions.

Research such as this is advancing knowledge about neuroplasticity (changes in networks) and epigenetics (effects of environmental factors) on how the brain develops and is vital to finding advanced therapies, treatments and even early intervention.

Additional research seeking advanced treatments for brain injuries from traumatic brain injury and stroke as well as therapies for developmental disorders such as autism and attention deficit disorder (ADD) is ongoing.

Posted in Brain Injury, epigenetics, How the Brain Works, How the Memory Works, Neuroplasticity, Stroke, Uncategorized | View Comments

Structures Required for Brain Neuroplasticity Identified

Posted on July 18, 2011 by admin

To store the new information gained during learning and memory formation, the brain builds or remodels its nerve cells, or neurons, using tiny structures on the surface of its nerve cells, known as dendritic spines. Small spines, extending like tree branches, receive chemical signals from other neuronal dendritic spines, each communicating with its counterpart on a nearby neuron. Together each pair of communicating structures form the “synapse” linking neurons.

In anything involving learning or memory, the brain stores new information by changing the structure and properties of synapses in ways that make it easier for connected neurons to communicate with each other. This “plasticity” can occur in two ways. One way is structural, in which a synapse changes in size or shape; the other way is functional, in which connections between the synapses are strengthened by increasing the chemical signals sent or received by connected neurons.

In previous studies, researchers found that cellular structures called recycling endosomes – recycling used proteins within the cell – play a key role in the functional type of plasticity. In this study, Published in the journal Neuron, researchers found that recycling endosomes are also involved in the structural type of plasticity. Researchers were able to observe inside dendritic spines, that the recycling endosomes deposited pieces of recycled proteins that grew new spines or changed the shape and size of existing spines.

By providing a clearer understanding of neuroplasticity – how cells develop new synapses or strengthen existing synapses – researchers gain new ideas for developing drugs that target these critical cellular processes.

This discovery may lead to advances in understanding Alzheimer’s disease and age-related memory loss, and could point to potential treatments for these and other neurological conditions such as autism which are characterized by the loss of synapses or by the abnormal structural development of dendritic spines.

 

Posted in How the Brain Works, How the Memory Works, Memory Fitness, Neuroplasticity, Uncategorized | View Comments

Researchers Trace Alzheimer’s Process Seeking Breakthrough For Effective Treatment

Posted on July 12, 2011 by admin

Neurological researchers at Rush University Medical Center report a breakthrough in treatment that may lead to halting the progression of Alzheimer’s disease. The treatment focuses on a new therapeutic target neutral sphingomyelinase, a hydrolase enzyme involved in sphingolipid metabolism that can potentially lead to a new way to stop the progressive disease. Study results appear in the Journal of Neuroscience.

Researchers speculate that stopping the activation of the neutral sphingomylinase enzyme may stop Alzheimer’s disease (AD) progression and memory loss. Alzheimer’s, an irreversible, progressive disease, is the most common cause of dementia affecting as many as 5.3 million Americans over 60.

Multiple, neurotoxic, disease-causing pathways converge on the neutral sphingomyelinase that can cause neuronal loss in the brain of an AD patient.

Two abnormal structures – plaques and tangles – are prime suspects in damaging and killing brain nerve cells. While neurons (grey Matter) die, other glial (white matter) brain cells (e.g., astroglia and microglia) do not. Rather, these glial cells which form the first line of immune defense, become activated.  Glial cell activation plays a key role in the destruction of neurons. Until now, the molecular mechanisms by which activated glial cells can kill neurons have been poorly understood.

Development of a clinical medication that would target the neutral sphingomyelinase enzyme, might allow doctors to halt memory loss in Alzheimer’s patients. These results are promising, according to researchers, who will be turning their efforts to clinical interventions. A breakthrough in stopping AD could provide hope for an aging population in the US that could otherwise see 14 million cases of AD by 2050.

For more information about the latest in Alzheimer’s research select this link.

 

 

 

 

Posted in AD Drug Research, Alzheimer's Disease, neuroscience, Uncategorized | View Comments

Don’t Forget Your Vitamin D To Maintain Memory Fitness

Posted on July 10, 2011 by admin

Memory fitness, a measure of memory function and cognitive vitality, is related to how well the brain is able to manage and use available information for activities of daily life. At a time when baby boomers, ages 47 through 65, are now entering their Golden Years, interest in health-enhancing foods is high.

A study by Agricultural Research Service (ARS)-funded scientists adds to a growing body of evidence linking vitamin D and cognitive function. Published in Journals of Gerontology, a study involving more than 1,000 participants receiving home care, suggests aging boomers can slow cognitive decline by getting plenty of vitamin D.  But people tend to spend less time outdoors and get less Vitamin D as they grow older.

Metabolic pathways for vitamin D in the brain’s hippocampus and cerebellum involved in planning, processing, and forming new memories, suggest that vitamin D may be involved in a variety of cognitive processes.

The study participants underwent neuropsychological and blood testing: results were analyzed among the three categories of vitamin D blood concentrations: deficient, insufficient, or sufficient.

The 35 percent with sufficient vitamin D blood levels had better cognitive performance on the tests of “executive performance” – cognitive flexibility, perceptual complexity, and reasoning – than those in the deficient and insufficient categories. Researchers considered other variables that could also affect cognitive performance.

Alzheimer’s disease, the most common form of age-related dementia, affects about 47 percent of Americans 85 or older. Identifying nutritional factors that lower cognitive dysfunction and help preserve independent living provides economic and public health benefits.

This study suggests senior citizens and baby boomers entering their Golden Years can slow cognitive decline and maintain memory fitness by getting plenty of vitamin D.

Posted in Alzheimer's Disease, How the Brain Works, How the Memory Works, Memory Fitness, Uncategorized | View Comments