This disorder was thought to be an isolated condition, but doctors conducting follow-up studies on diagnosed patients are starting to rethink that. Anywhere from 80 to 100 percent of these RBD patients later develop neurodegenerative diseases such as Parkinson’s disease.

Doctors studying their patients conclude that there is a minimum of a 15 year difference between the onset of RBD and the onset of a neurological disorder. In some patients, the time between onsets was as much as 50 years. However long it is, this sleep disorder seems to prelude the disease by a significant amount of time. Doctors are hoping that this will allow the patient to be treated for a disease before the disease actually manifests. Perhaps one day if there is a neuroprotective treatment available, it can be used to treat these patients before the severe deterioration of their brain.

Well, it could be your family and it could be your environment. Studies have shown that addictions run in families. In fact, if a parent has an addiction, the child is 4 to 8 times more likely to have an addiction as well. It doesn’t necessarily have to be the same addiction, but an addiction nonetheless. Those with other family members with an addiction are more susceptible to the disease, but that also doesn’t mean that the disease is inevitable.

Saying that addiction runs in the family would speculate a possible genetic component. In fact, researchers are currently trying to link addiction to a cluster of genes in the human genome. Scientists are looking for “addiction genes” that are biologically different from others that might make someone prone to addiction. It also might affect the severity of withdrawals.

For example, in humans, a candidate gene for addiction includes the A1 allele of dopamine receptor gene DRD2 which is common in those with alcohol and cocaine addictions. Also, non-smokers are more likely to carry a protective gene, CYP2A6, which causes them to feel more nausea and dizziness from smoking.

Mice have been a model for studies on human addiction because the reward pathway functions in mice are very similar to those in the human brain.

Mice bred to lack serotonin receptor gene Htr1b are more attracted to cocaine and alcohol. Those with low levels of neuropeptide Y drink more alcohol while those with higher levels tend to abstain from alcohol.

It mainly all comes down to the reward pathway in our brains. The reward pathway is in the center of our brain and connects to other areas such as those controlling memory and behavior. It’s responsible for driving our feelings of motivation, rewards and behavior. The main job of the pathway is to make us feel good when we engage in behaviors essential to survival such as eating and drinking. Places in the brain gather information about what’s happening outside of our body and then strengthen circuits within the brain that control desirable behavior.

For instance, say you’re thirsty and someone hands you a cold water bottle. The brain will tell you that there’s cold water in front of you. Stored in your brain is a memory that says “if you drink that water, you won’t be thirsty anymore and you’ll feel good!” So you’ll drink the water. While drinking, you’re 5 senses will send a single to your brain about drinking the water. The brain, in response will release dopamine, giving you a jolt of pleasure which is your instant reward. The reward pathway will make you repeat the behavior for the same dopamine reward, like a dog doing a trick for a dog biscuit. The wiring in your brain for that particular activity has been strengthened.

Despite the genetic link, it’s not all due to our DNA makeup. Essentially, addiction is the combination of the interaction of several genes (not just a single gene) with social and environmental factors. Also, just because someone has all that’s necessary for an addiction doesn’t mean they’ll have an addiction problem. For example, I know I have an addictive personality but I look for other ways to expel or sedate the addiction and to put that addictive capability to better use.

Researchers have been searching for ways to treat and prevent addictions. One way is the identification of genes. The genes can become “drug targets,” in which researchers can work to modify the gene product’s activity resulting in stabilizing or reversing pathways to restore the brain to proper function.

Earlier this year, researchers at UT Southwestern Medical Center have a new hypothesis. They hope that by increasing a process known as neurogenesis it might prevent or treat addiction. Neurogenesis is a normally occurring process of making nerve cells in the brain. In previous studies, blocking neurogenesis had increased a rodent’s vulnerability for cocaine addiction and relapse. They hope that by stimulating the increase of neurogenesis, it might combat addiction. Another application is to use this increased neurogenesis in situations where a patient is required to use a potentially addicted medication such as Vicodin, a severe pain killer with a high addiction rate. Perhaps this treatment may be used in those who have quit their addiction in order to prevent a relapse.

Recently, new research focusing on microRNA (miRNA) and gene expression might also have a potential effect on the fight with addiction. miRNAs are used in gene expression regulation and gene silencing. They bind to complementary mRNA strands and prevent translation to a protein. Raising the levels of miR-212, an miRNA, in the brains of cocaine-using rats have caused the rodents to take in less of the drug. Completely blocking the miRNA, and allowing full gene expression, increased the drug use. This would suggest a new drug target- a medication to raise miR-212 levels or at least creating something to mimic the miRNA’s function. Liked to miR-212 is an increase in the protein CREB. CREB holds promise in fighting drug addiction by decreasing the reward response, sometimes actually creating an aversion to it all together. The only obstacle with CREB drug targets is the regulation of it. The level cannot become too low (where the rewards are increased) because it can lead to addiction and anxiety, but it cannot become too high (where nothing is rewarding) which can lead to depression. This study has only been done with cocaine and is currently under investigation for the applications in nicotine and alcohol addictions.

Someday, possibly, there will be ways for those suffering from addictions, whether they be chemical addictions, which is heavily mentioned here, or an addiction to more physical things to overcome that addiction and lead healthier lives.

Typically, Alzheimer’s is diagnosed through cognitive testing.  Family members or health care professionals may realize that a person is experiencing forgetfulness, disorientation, or other symptoms. Unfortunately, by the time these symptoms are apparent and a diagnosis is made, the patient may have already experience a great deal of brain damage.

A new method to test for Alzheimer’s at a much earlier stage of the disease has been described in a paper in the journal Neurobiology of Aging, (10.1016/j.neurobiolaging.2010.04.025) where Laurel Beckett et.al. describe  a method of diagnosis based on a combination of imaging and sampling of cerebrospinal fluids to categorize individuals into at-risk groups before clinical signs of Alzheimer’s appear.

This important work could have a two-fold impact on the fight against Alzheimer’s. By identifying at-risk patients early, medical intervention may be able to at least delay the onset of the disease. The early identification of at-risk individual also would accelerate the development of clinical interventions because you have now isolated a population that can participate in clinical investigation and broaden the horizon of time investigators have to work with, increasing the rate at which further discovery can proceed.

E.coli gets a bad reputation and I understand that. My students immediately cringe and I know what goes through their minds. They think of the E.coli outbreaks we’ve had in our foods as of late such as the ones that are leading to cases of severe food poisoning and death. I can quickly reassure them that this bacteria does not have this capability. In fact, many are surprised to learn that not all bacteria can cause harm.  With the bad also comes the good and there are good bacteria as well. 

Bacteria have taken up residence everywhere on and in you. Hundreds of species of bacteria live on your skin, live in your mouth, and in your intestines. Everyone is born sterile (completely clear of bacteria), but soon after birth bacteria moves in and multiplies enough to include more bacteria cells than human cells in your body. 

Don’t get too grossed out! These bacteria strains are important. For example, Biologist Jeffrey Gordon of Washington University has a group of mice that are completely gut bacteria free. These mice are very different from their non-sterile cousins in the way that they are extremely skinny. Food passes right through their intestines, mainly undigested. Thus it is shown that the gut bacteria are more efficient at digesting our food than we are alone.

 Today, the bacteria in our guts seem to do more things than originally thought. They are currently under investigation in studies of Autism. There is a hypothesis that these gut bacteria might be releasing chemicals that are contributing to the onset of Autism. Autism has already been linked to gastrointestinal problems. These gastrointestinal problems also seem to appear around the same time as behavior symptoms, so perhaps these gastrointestinal microbes have something to do with it.

 Researchers in the UK are studying chemicals in the urine of people with Autism compared to those without the condition to detect any chemical differences. These metabolic changes might be detected in the urine. Using nuclear magnetic resonance (NMR) spectroscopy, the urine was analyzed. The results showed a clear difference between the two groups.

 There is a theory that these gut bacteria are producing a toxin that might interact and disrupt brain development. One compound that was identified using the NMR spectroscopy was N-methyl-nicotinamide (NMND) which has already been linked to Parkinson’s disease.

 At the University of Western Ontario in Canada, Derrick MacFabe and his colleagues have discovered that clostridium bacteria produce a short-chain fatty acid that many cause autism-like behavioral and biochemical changes in rats that can be reversed.

 With this possible link, there might be a simple urine test for Autism. This test, done early enough, might then lead to earlier therapy and treatment options.

Physicians, Psychologists, and people in general have always held differences of opinion when it comes to how to think about mental conditions. Some people may think depression is simply a “bad mood” that should be “snapped out of” while medical evidence has shown that physiological components of  these diseases make them just as “real” as a broken bone.  The link between hypertension and bipolar disorder is just one of the latest correlations between mental disorders and other conditions such as diabetes and heart disease.

While in many cases it is not totally clear what causes what (i.e. does the stress of bipolar predispose the development of hypertension, or the other way round) the study by Dale D’Mello does suggest the need for doctors to consider the importance of tending to physical health as a complement to treating mental conditions. Without getting into the mind/brain/body debate, it only makes sense that any contribution to “physical” health will ultimately improve patient outcome, if even only indirectly.

When your body enters sleep, your brain undergoes several sleep cycles, four to fives times a night. Each cycle has its own purpose. The cycles range from drowsiness and light sleep to deep sleep. After deep sleep, the body (or more technically the brain) will enter a stage called Rapid Eye Movement, abbreviated REM sleep. It is during this REM stage where many of our dreams happen. 

Why do we dream? Many of them are strange, eerie, weird or impossible. They could be about being late to work because a big purple and blue spotted rhino decided to take up residence on the LIE (Long Island Expressway). Why do we have to watch or take part in these strange events while we sleep? Throughout history, people have sought meanings for their dreams. It’s been believed that these dreams can coincide with divination or contain messages from the Gods or the deceased. If you go to your local bookstore you could probably find what are called Dream Dictionaries- books that break down the meanings of dreams. Were you in front of the class naked? Well that might mean you’re unprepared for something. Did you dream of fire? Then it might be a warning of a dangerous or risky situation.  

Ever have a dream catcher? You’ve probably seen one before. I have a little one beside my bed. Dream catchers can be linked back to Native American traditions. Dream Catchers are made from earthy materials and objects from the person it’s for. They are used to keep any negative dreams away from the sleeping person. All positive dreams make their way through the hole in the center of the string web of the catcher and down the feathers to the person. Any negative dreams are stopped by the web and trapped. Those dreams then disappear at the first rays of the new morning sun. 

What’s interesting about dreams (other than the total bizarre-ness of them) is the physiological side of sleep. The body cycles into REM several times a night. REM occupies 20-25% of total sleep which equals about 90-120 minutes a night. During this stage, the brain is active. Brain scans of sleeping subjects show that around every 90 minutes, brain waves indicate that the person is “awake” yet clearly they are still asleep. In fact, when we enter REM sleep, the brain is very lively but our bodies undergo atonia, or paralysis of the muscles. The brain neurons become very active but neurotransmitters are completely shut down, preventing the stimulation of motor neurons and thus no movement can occur. The body literally paralyses you and makes you watch your dreams. 

There are some individuals that have what is referred to as REM Behavior Disorder. In these individuals, atonia is absent. Without the paralysis of the muscles, these people actually act out their dreams. 

So now why are we forced to have these dreams that can cause such strong reactions and emotions, yet are immobilized and unable to do anything about it? Why would our brains subject us to this? 

There have been some theories. Sigmund Freud believed that dreams are forbidden urges that we are trying to hide. He also suggested that dreams act as practice for our brain. He said that bad dreams let the brain learn how to handle specific situations and emotions resulting from distressing experiences. Negative emotions are more common in our dreams than positive ones, whether it is panic, fright, sorrow, or anger. 

Have you ever remembered a dream? Or remembered it once you woke up but forgot it a few hours later? At least 95% of dreams aren’t remembered. Chemicals in the brain that are required to turn short term memories into long term memories are also suppressed during REM. In order to remember a dream, it would have to be vivid enough to wake you during an REM stage or immediately after REM. Keeping a dream diary or journal often helps remember them as well. But without that, it’s often difficult. 

Overall, it is known that dreaming (or at least REM sleep) is purely physiological. The brain stem signals REM sleep. Dreams are probably just responses to regular neural processes as we sleep and reflections in the subconscious. 

Well, whatever dreams are, and for whatever reason we have then, they can be very important. Dreams have led to 2 Nobel Prizes, and the creation of several drugs and medicines. Despite how strange they are, I can live with them. At least they give me something to talk about in the office the next day (that is if I remember them!).

Spring arrived on March 20^th and it was hard to ignore. It was a hot day in Central Park with fellow New Yorkers rushing out to sit in the sun, play ball, or ride their bikes. In my hometown people rushed to the Bluff just to sit in the sand and stare off into the water of Long Island Sound. There were some die hard jet skiers that took the opportunity to get their jet skies into the water (even though the water was an icy 40 degrees). People are craving to be outside; to shake off the feeling that winter has left behind.

 Here on Long Island we had a nasty winter. Every time it snowed it wasn’t  in inches, but in feet. We had record breaking amounts of  snow so when Spring came around the corner, we all rejoiced. For the last few weeks, the temperature has jumped into the 50s and 60s sometimes jumping into the high 80s.

A lot of changes happen once Spring arrives. Migrating birds return. The flowers bloom. The grass begins growing like a weed. But not all the changes are happening in nature. People are changing as well.

Have you ever heard of the winter blues? The winter blues is a set of symptoms closing resembling depression. These symptoms are present in the winter but commonly fade once warmer seasons arrive. Winter blues is another name for Seasonal Affective Disorder, or SAD. SAD is a mood disorder in which people who have normal mental health throughout most of the year experience depression symptoms in the winter months, repeatedly year after year. It has been estimated that 2-9% of adults suffer from SAD.

 Those who experience SAD can experience difficulty waking up in the morning, a craving for carbohydrates, a lack of energy, and difficulty concentrating among other symptoms. When the spring comes, it is essentially a role reversal. Those who have been diagnosed with a form of depression in their past have a greater chance of experiencing these winter changes.

There have been some theories on why people suffer from SAD. There is depression, a chronic disorder characterized by depression symptoms all year round. But why have depression only during the winter months and be fine in the spring and summer? The answer may lie in studying other species including our past ancestors.

 In many species, activity is diminished during the winter months due to less available food supplies and the difficulties involved in surviving during the cold weather. Several species like bears and box turtles, hibernate during the winter as an extreme way of surviving. A major clue resides in species that don’t hibernate, but still develop changes in their behavior during these less favorable times.

It can be argued that SAD is an evolved adaptation (like our fear of spiders and snakes). This adaptation in humans can be a variant of a hibernation response from an earlier ancestor. Since food was scarce during human prehistory, a low mood would reduce the need for the intake of calories, a good adaptation for the winter months.

 If these theories are correct, then Seasonal Affective Disorder would not be a disorder as once assumed. Instead, it would be considered a normal response to colder seasons.

Now, we are not talking Hypnotoad or Professor-X style mind control (not yet at least) but a simple experiment that demonstrates how mind and brain interact and can be manipulated.

In the study conducted by Rebecca Saxe of MIT (http://www.pnas.org/content/early/2010/03/11/0914826107.full.pdf+html)

used a technique call transcranial magnetic stimulation (TMS) to disrupt a region of the brain known as the right temporo-parietal junction (TPJ).  As every child knows, one of the best ways to figure out how something works is to take it apart and put it back together. Of course, this method does not exactly work when studying the brain, however, it is possible to disrupt certain brain regions without lasting harm, and this is how TMS works. Previous studies had indicated that when people are making moral judgments, the TPJ is one of the involved regions of the brain.
In order to learn more about how the TPJ impact moral judgments, the research team disrupted it using TMS while subjects were asked to moral judgment. The moral judgments evaluated by subjects during the experiments were simple stories where one could guess the intention of one of the characters of the story, as well as evaluate the outcome.
For example, you are touring a chemical factory and made a cup of coffee for your friend. Next to the coffee machine was a white powder marked toxic. You put this in your friend’s coffee, but it turns out that it was just sugar (you thought it was toxic) and your friend was fine when she drank it.

Normally people would probably say that this was morally unacceptable, even if the outcome was ok. People who were subjected to TMS while making this judgment seemed to count the outcome of the situation as more important to their moral judgment, and did not characterize the above scenario as reprehensible as control subjects. In other words, all’s well that ends well.

Now people subject themselves to mind control all the time. People behave a certain way under the influence of alcohol as opposed to when they are sober. The same goes for television shows, and being in a group of friends. We can now add powerful magnetic stimulation to this list. While I won’t indulge in speculation on what future technologies this might be turned into by DARPA for example, I would be careful about anyone giving me a hat that requires batteries.

In the United States, an estimated 1.4 million people a year are victims to traumatic brain injuries obtained from motor vehicle accidents, falls, abuse, assault, and sporting accidents. Our brains are organs full of connections and to sever or damage a connection can lead to devastating consequences. Researchers have been trying to uncover why even a small injury has so much of an impact on the brain.

The answer lies in the condition of the brain after an injury. Many traumatic injuries result when the brain undergoes fast acceleration and deceleration. When the head is struck or shaken violently, this rapid acceleration and deceleration occur, causing injuries to the tissues on impact with the cranium.

Scientists at the University of Pennsylvania have been researching the brain and what happens to the brain upon impact. It has been known that blows to the brain can damage the very fragile fibers of our neurons, called axons, referred to as Diffuse Axonal Injury (DAI). DAI is one of the most common and devastating types of traumatic brain injury and is typically the underlying injury in shaken baby syndrome. An infant’s neck muscles aren’t developed enough to support the head and thus with shaking, there is very quick movement of the brain against the sides of the cranium causing damage.

Our neurons are cells made for connections. They consist of a central body (called a soma), dendrites, and an axon. The dendrites receive the message, which then pass down the long axon and over a synapse to the next neuron. Researchers at the University of Pennsylvania have been studying what inside the axon actually breaks. They have found that sudden blows to the brain damages microtubules that bring stability to the axon. These microtubules cannot withstand the quick stretching that results from the injury and then break in response.

In the lab, they are running experiments on these axons to see the effects of stretching and the possible use of medication to minimize axon stretching. The drug Taxol, used for cancer treatment seems to have some promise but it is too early to say if this drug will work on traumatic brain injuries.

For more information, please refer to www.sciencenews.org/view/generic/id/56455/title/Brain_at_the_breaking_point

While this is a very focused study, it is clear from a variety of scientific findings that music education is an essential and indispensible component of childhood education in general. Findings from Dr. Kraus’ lab have also indicated that the areas of the brain that are enhanced by musical training are the same areas found deficient in cases of dyslexia.

How many students with possible attention deficits, dyslexia, or other developmental difficulties could be helped by music education? Yet these programs are often the first to be cut when school budgets are tightened.

I’ve often wondered how professional musicians are so wonderfully educated, given the enormous amount of time they have to dedicate to their craft. But when you think about how music could help students better hear and comprehend sounds even in a complex aural environment (e.g. a classroom), it is not surprising given that in music, you are in a real sense listening to perhaps a half a dozen or more conversations or more. In an orchestra, you have to listen to yourself, your section, and all the other instruments in order to play correctly. As a skilled listener, every note is an important component of the piece, and you are easily disturbed (and perhaps later delighted) when you first listen to another recording of your favorite work to find some notes emphasized, diminished, or seemingly eliminated.

The Mozart effect (or at least the over-hyped media and commercialization of it) notwithstanding, music is more than entertaining, it can be educational.

Check out this youtube video (http://www.youtube.com/watch?v=PmWRttCo7lo ) of one of my favorite (educated) musicians, Mistko Uchida, as she explains the Schoenberg Piano Concerto (a personal favorite). I love her explanations of what you are hearing, especially at around 5:20 in this particular clip. To the uninitiated some “classical” music sounds like a jumble, but there is really so much beneath the surface. Look and listen to her play in this clip (http://www.youtube.com/watch?v=ct47T9_liOU) for a good brain workout.