BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Brain (Page 1 of 4)

Potential New Treatment Strategy for Brain Cancer!

Cancer is a disease characterized by the up-regulation of cell growth and it usually develops when normal cells are not able to repair damaged genetic material. New studies are revealing insights into the function of genetic mutations commonly found in a form of brain cancer, specifically the IDH mutation. Isocitrate Dehydrogenase(IDH) is a metabolic enzyme found in more than 70% of low grade gliomas and secondary glioblastomas, types of malignant brain tumors. In a normal cell, IDH enzymes help to break down nutrients and generate energy cells. When mutated, IDH creates a molecule that alters cells genetic programming and instead of maturing, the cell remain primitive. Studies have shown that cells holding this mutation also have an impaired ability to repair DNA. Strangely enough, low grade gliomas that have the IDH mutation are typically more sensitive to chemotherapy than those that lack the mutation. Why does this occur? We still don’t really know the answer.  Yet, researchers have discovered a potential new treatment option for the glial cells harvesting the IDH mutation– PARP Inhibitors.   A super cool future is waiting ahead.

When treating the IDH mutated cells with PARP Inhibitors, a substance in the form of a drug that blocks an enzyme called PARP, the cells were effectively killed. When the drug blocks PARP, it keeps the cancer cells from repairing their damaged DNA, and eventually they die off. The cells are extremely sensitive after the effects of the inhibitors, especially after taking the most common PARP drug called oliparib. PARP inhibitors are a form of targeted therapy–meaning the inhibitors work within a similar approach as radiation and chemotherapy– they simply damage or prevent the repair the DNA. Researchers have also found the up regulation of the unusual molecule called  2-HG(2-Hydroxyl-glutarate) within the IDH mutated enzymes. In a study with Dr. Brinda’s team at Yale, they found that 2-HG may be responsible for the defect, DNA repair inabilities, in these cells. When the production of 2-HG was blocked in these cells, the DNA repair defect was reversed and cells became unresponsive to the PARP inhibitor treatment. This finding further solidifies that PARP inhibitors may be the best new effective brain cancer treatment method. What do you think? I think this is pretty cool news!

Jto410 is the username of the radiologistwho took the picture

Low grade glioma MRI scan. Creative Commons Attribution-Share Alike 3.0 Unported license.

There are also many clinical trials occurring currently to observe 2-HG as a definite IDH biomarker for cells that are sensitive to treatment with PARP inhibitors. In addition, labs are also designing a clinical trial of olaparib and temozolomide, two PARB inhibitor drugs, in patients with low-grade gliomas. The results of these trials, are for sure going to make headlines within the Biology and Medical field! Even though, there are still many questions to answers and studies to conduct regarding brain cancer and the IDH mutation, we are definitely on the right track to cure the monster a.k.a “cancer.”

New Research Shows Possible Early Diagnosis of Autism

Normally autism in children is diagnosed at around ages two or three but studies have been done to try to predict autism before behavioral symptoms occur.  University of North Carolina partnered with other universities to experiment with MRI machines to see if they could diagnose autism earlier than 24 months (2 years)

Autism is a big problem in our country and the rest of the world.  About 3 million people have autism in the United States and millions more throughout the world.  The study focused on hyper-expansion of brain surface area in children of 6-12 months of age. According to this article “Brain overgrowth was tied to the emergence of autistic social deficits in the second year.” They found that 8 out of 10 kids with a hyper-expanded brain as well as an autistic sibling would be diagnosed with autism in the future.

The fact that MRI’s can show enlarged surface area of the brain at such a young age is important in predicting whether or not a child will be later diagnosed with autism.  This is an important experiment because if doctors can predict autism before symptoms occur there may be ways for them to intervene with brain growth before a child’s brain permanently has autism and behavioral changes occur at 24 months.

 

 

8 Genes That May Be Affecting Your Sleep Patterns

Have you ever wondered why you struggle to fall asleep at night, while your sibling has no issues sleeping soundly for eight hours? What causes your sleep patterns? While your sleep may occasionally be affected by a particularly stressful event, leading to irregular sleep patterns, for

While your sleep may occasionally be affected by a particularly stressful event, leading to irregular sleep patterns, for many, it is simply caused by the way their brains and bodies work. New research has identified for the first time eight specific genes that are linked to insomnia or excessive daytime sleepiness. The data also revealed that some of the genes associated with disturbed sleep identified in this study seemed to be linked to certain metabolic and neuropsychiatric diseases too, like restless leg syndrome, schizophrenia, and obesity.

Richa Saxena, one of the co-authors and assistant professor of  anaesthesia at the Massachusetts General Hospital and Harvard medical school, explained why this research was so important: while “it was previously known that sleep disturbances may co-occur with many diseases in humans, but it was not known that there are shared genetic components that contribute both to sleep problems and these conditions.” Furthermore, while studies have previously identified genes linked to some sleep disorders, this is the first study that has specifically linked genes to insomnia.

Link to Original Image

The study looked at the prevalence of insomnia, sleep problems and excessive daytime sleepiness in 112,586 European adults who had participated in a UK Biobank study. All participants had their genes mapped, as well as additional information like weight and diseases/chronic conditions. The results revealed fascinating linkages between certain genes. For example, the genes linked to insomnia were most strongly related to those associated with restless legs syndrome, insulin resistance, and depression, while the genes associated with excessive daytime sleepiness were also linked to obesity. Saxena remarked again that “it was not known until this study that there are shared genetic components- shared underlying biological pathways- that contribute to both sleep problems and these shared conditions.”

Of course, this study is not 100% conclusive- people who have trouble sleeping are not necessarily at higher risk for restless legs syndrome, schizophrenia, and obesity. In reality, it is likely that many different genes contribute to both sleep problems and these medical problems, Saxena said. But this new study does suggest that these problems share genes and underlying pathways.

So what does this research do for the average person? Well, not much. Right now, it’s just fascinating news that there may be a genetic reason people with these disorders are more likely to have troubled sleep. However, there is hope that in the future researchers will be able to design and test various drugs to target these genes. This would bring immense benefits to people who struggle to keep normal sleep patterns, as well as helping individuals proactively avoid diseases they may be more at risk for (for example, obesity).

 

Thylacine Brain Structure Reveals Predatory Lifestyle

The thylacine, also known as the Tasmanian Tiger, was the largest carnivorous marsupial of modern times. Native to Australia, Tasmania, and New Guinea, the thylacine quickly went extinct at the start of the twentieth century, following an increase of demand for its pelts. The last known thylacine died in 1936, in Beaumaris Zoo in Hobart, Tasmania, and little is known about the species’ natural behavior. New research however, gives humans a better glimpse into brains and programming behind one of Australia’s most fascinating predators.

Dr. Gregory Berns of Emory University and Dr. Ken Ashwell of the University of New South Wales scanned thylacine brains and reconstructed neural connections in an effort to better understand the specific functions of the thylacine brain and behavior. Only four surviving specimens of the brain exist, and their study gained access to two of them.

“One was provided by the Smithsonian Institution, taken from a male Tasmanian tiger after it died at the National Zoological Park in 1905. The other specimen, loaned to the researchers by the Australian Museum in Sydney, came from an animal that died during the 1930s.”, claimed researchers.

They compared the structure of Thylacine brains to those of Tasmanian devils. The researchers found that the thylacine brains had larger caudate zones than the Tasmanian devil brains. This suggests that thylacines devoted more of their brains to complex thinking, particularly action planning and decision making.

These findings match with what we know of the two animals. Tasmanian devils are known to be scavengers while thylacines were hunters. The neural rewiring done by the researchers provides anecdotal evidence that thylacines occupied a more complex predatory brain than their scavenger cousin, the Tasmanian devil.

These findings are fascinating because they give us new information regarding an animal less than 100 years extinct. It’s seems strange that we had never gathered much information about the thylacine prior to its extinction. However, the resurgence in fascination and curiosity about the animal is exciting to see. Hopefully new research and discoveries will be made in the near future, shedding more light on the thylacines life.

 

 

Image result for thylacine

Source Article: http://www.sci-news.com/biology/thylacine-brain-structure-04549.html

 

MRIs Catch Autism Prior to Symptoms

Mark Lythgoe & Chloe Hutton / Wellcome Images Image Link

Research

By using magnetic resonance imaging (MRI), researchers are now able to accurately study and predict which infants, among those with older autistic siblings, will be diagnosed by the age of 2. According to an article on Science daily, in the past couple of years, researchers have correctly predicted 80 percent of these infants who would later meet criteria for autism at 24 months of age.

A study published in Nature, shows how early brain biomarkers can be very beneficial in identifying infants at the highest risk for autism prior to any symptoms. Joseph Piven, professor of Psychiatry at the University of North Carolina-Chapel Hill, explains how typically autism cannot be detected in infants until they ages 2-4, but for infants with autistic siblings, it can be determined at an earlier age.

People diagnosed with Autism Spectrum Disorder (ASD), experience social deficits and  demonstrate very specific stereotypical behaviors. According to this study, it is estimated that one out of 68 children develop autism in the United States and that  for infants with older siblings with autism, the risk may be as high as 20 out of every 100 births. Despite these high numbers, it remains a difficult task to detect behavioral symptoms prior to 24 months of age.

Piven, along with a couple of other researchers, conducted MRI scans of infants at six, 12, and 24 months of age. They discovered that increased growth rate of surface area in the first year of life was linked to increased growth rate of overall brain volume in the second year of life. This meant that brain overgrowth was tied to the emergence of autistic social deficits in the second year. The researchers then took the information they had and used a computer program that classified babies most likely to meet criteria for autism at 24 months of age, and developed an algorithm that they applied to a separate set of study participants.

The researchers found that there were brain differences at 6 and 12 months of age in infants with older siblings with autism and infants with older ASD siblings who did not meet criteria for autism at 24 months.

Plans for the Future

This research and test would be very beneficial to a family who already has a child with autism and has a second child who may or may not be affected. The ideal goal would be to intervene and provide as much assistance to the infant and family prior to the emergence of symptoms. By intervening at early stages and when the brain is most susceptible, researchers hope to improve the outcomes of treatment.

In the nature study, Piven describes how Parkinson’s and Autism are similar in that when the person is diagnosed, they’ve already lost a substantial portion of the dopamine receptors in their brain, making treatment less effective.

One mother who has benefitted from this discovery and is extremely grateful is Rachel O’Connor. When interviewed by News12, she shared how early intervention “has brought out some language in [her] daughter,” and how her daughter “can now say what she wants and she desires. She makes better eye contact.”

 

Mouse Gut Research Could Save Your Brain

A new study in mice published by Nature Magazine suggests that a specific microbial balance results in a reduction of brain damage after a stroke. The severity of a stroke is determined by two types of intestinal cells: Regulatory T Cells and Gamma Delta T Cells. Regulatory T cells have a helpful inflammatory effect. However, Gamma Delta T Cells make a cytokine which results in harmful post-stroke inflammation.

Researchers at Weill Cornell Medical College and Memorial Sloan Kettering Cancer Center studied two different groups of mice in order to learn if gut cells could be altered in order to reduce stroke severity. One group of mice had gut bacteria that was unaffected by antibiotics, while the other group of mice’s gut bacteria was extremely vulnerable to antibiotics. The group of mice that was vulnerable to antibiotics had a higher ratio of good Regulatory T Cells to harmful Delta T Cells.

House mouse.jpg

https://en.wikipedia.org/wiki/Murinae#/media/File:House_mouse.jpg

The researchers then induced strokes in all of the mice, and the brain damage was 60% less devastating in the mice vulnerable to antibiotics than the other group. In order to ensure that the difference in stroke severity was solely as a result of the gut bacteria, the researchers took the feces of the mice with reduced stroke severity, and transplanted it into new mice. Those new mice also exhibited a resistance to brain damage, confirming the belief that the gut bacteria was responsible for the change.

These new findings in the research of mice may be able to benefit humans in the future. Antibiotics or a specific diet may be able to reduce the effect of stroke on the brain. However, the gut microbiome of a mouse is vastly different than the gut microbiome of a human, so it may be a while before new treatments are discovered.

When in doubt go with your gut!

The human gut has trillions of bacteria that help to regulate digestion and break down food.  An extremely important function they have is to keep out bad bacteria and potential harmful microbes.  The gut is a very important part of the body, because it affects not only your digestion and metabolism, but your brain too!

Often called your “second brain,” the human gut plays a big role in a human’s life.  The gut produces about 95% of serotonin, which is the drug that affects emotion.  An experiment with mice was done to see the effect that their gut had on their brain activity.

Each mouse received antibiotics, consisting of neurochemicals that enhanced mood, and were observed after this change occurred in their gut.  The mice became more energetic.  The article mentioned that even changing an animal’s gut by one bacteria can change their mood.  In this case altering one bacteria was tested which caused the mice to be more cautious than normal.

This article went in depth on how the bacteria in your gut can cause anxiety. “Bacteria communicate with the brain via the vagus nerve: When the vagus nerve is severed, effects of gut bacteria on brain biochemistry, stress response and behavior evaporate.”  They then went on to discuss how someone’s brain can affect the human gut, which was extremely fascinating.

Golden Snub-nosed Monkeys, Qinling Mountains - China

They first did tests with monkey’s and found that mothers who were exposed to loud noises during pregnancy caused their offspring to have less beneficial bacteria.  Another experiment was done with students in which they gave stool samples during exam week.  The results showed that their was less good bacteria in their gut, called lactobacilli.

In general the human gut plays a huge role on the brain and vice versa.  Stay healthy, don’t stress too much over school because you never know what anxiety could be doing to the good bacteria in your gut!

I chose this article because I have stomach issues and had to go gluten free.  I didn’t realize what goes into your gut had such a large effect on the brain!

 

Gut Microbes and the Brain

Neuroscientists are studying the idea that intestinal microbiota might influence brain development and behavior.

Neuroscientist Knickmeyer is looking to study 30 newborns and how they have grown into inquisitive, curious one-year olds through a series of behavioral and temperament tests. She is eager to see their faecal microbiota, bacteria, viruses and other microbes that live in their guts.

Studies of animals raised in sterile, germ-free conditions showed that these microbes in the gut influence behavior and can alter brain neurochemistry and physiology. Some research has drawn links with gut bacteria and their interactions with the brain.

Escherichia coli, a species of bacteria present in the human gut https://en.wikipedia.org/wiki/Gut_flora#/media/File:EscherichiaColi_NIAID.jpg

Gut Reactions

Prior to recent research, microbes and the brain have rarely been known to interact, with the exception of when pathogens penetrate the blood brain barrier. When they do, there can be intense effects. For example, the virus causing rabies elicits aggression, agitation and a fear of water. The idea that gut microbes could influence neurobiology was not ever thought of, but this is changing.

One research study showed that IBS lead to issues such as depression and anxiety. This lead scientists to wonder if psychiatric symptoms are driven by inflammation or a whacky microbiome caused by infection.

One 2011 study showed that germ-free mice were less-anxious than mice with indigenous microbes. These studies also showed that many of these behaviors are formed during a critical period during which microbes have their strongest effects. Another problem is that “germ-free” is an unnatural situation. However, it allows for researchers to learn which microbial functions are important for development of organs or cell types.

Chemical Exploration

Recent studies have found that gut microbes directly alter neurotransmitter levels, enabling their communication with neurons.

Scientists are also studying whether or not altered serotonin levels in the gut trigger a cascade of molecular events, therefore affecting brain activity.

In 2015 research showed that myelination can also be influenced by gut microbes, at least in a specific part of the brain. Germ-free mice are protected from some conditions, for example multiple sclerosis, because it is characterized by demyelination of nerve fibers. These scientists wish to use these studies to help humans who suffer from MS.

A Move to Therapy

Tracy Bale, a neuroscientist, sought to study how microbes of pregnant mothers affect their offspring. Maria Dominguez-Bello, microbiologist, wants to see if babies born through Caesarean sections end up with microbiota similar to babies born vaginally if they are swabbed on the mouth and skin with gauze taken from their mothers’ vaginas.

For Knickmeyer, the amygdala and prefrontal cortex are the brain areas that interest her the most in her studies with the newborn infants. This is because both of these areas have been affected by microbiota manipulations in rodent models. Something she is worried might affect the study is the confounding factors such as diet, home lives and environmental exposure.

Source: http://www.nature.com/news/the-tantalizing-links-between-gut-microbes-and-the-brain-1.18557

For more information:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4228144/

https://www.sciencenews.org/article/microbes-can-play-games-mind

http://www.huffingtonpost.com/healthline-/gut-bacteria-and-the-brai_b_11898980.html

Tickle, Tickle!

You might be wondering, why am I ticklish? Or, why do I laugh if somebody else tickles me, but not when I try to tickle myself? The mystery of ticklishness has been sought after for decades, including by Darwin and Aristotle.

A recent study tested ticklishness on rats, and the results were astonishing! The rats reacted to human tickles with ultrasonic “laughter cells” and emitted various calls. While many humans are most ticklish on their armpits and stomachs, rats were found to be most ticklish on their bellies and underneath their feet. They performed “joy jumps” after being tickled, which is a behavior associated with joyful subjects in various mammals.

 

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Researchers continued searching for answers, and sought to discover how being ticklish relates to the brain and whether or not it is a trick of the brain that rewards interacting.

When researchers Shimpei Ishiyama and Michael Brecht investigated the response of the rat’s brain to tickling, they observed nerve cells that responded strongly to tickling and they found very similar responses during play behaviors as during tickling- even without the scientist touching the rat. These nerve cells also worked in reverse. For example, if the rats were made anxious, they were less ticklish and the activity in these cells were reduced. It was discovered that activity in the trunk somatosensory cortex is what led to ticklishness.

The discovery of the connection between brain responses to tickling and play was incredible.

 

Other Articles About This Topic:

http://www.npr.org/sections/health-shots/2016/11/10/501447965/brain-scientists-trace-rat-ticklishness-to-play-behavior

https://www.washingtonpost.com/news/speaking-of-science/wp/2016/11/11/watch-rats-giggle-and-jump-for-joy-at-being-tickled/

Number of strokes increased in children!

Sean Maloney stroke brainscan

Intel Free Press Image Link

Statistics 

According to new studies, strokes have been affecting younger generations more than ever. The average age for people having a first stroke has dropped from  71.1 in 2000 to 69.3 in 2012.What’s interesting is that in general, the number of strokes in the U.S. has actually gone down over the last few decades, according to Chengwei Li, an epidemiologist at the University of Michigan School of Public Health. However, Li’s study, shows that the rate of strokes in people under the age of 65 have not gone down, and that the rate of strokes in people under the age of 55 has actually increased.

Treatment

According to a study on WebMD, it is in some ways easier to treat the younger patients affected. People who get to the hospital within 4 and a half hours of their episode, or attack, can receive a drug that breaks up the clot in the brain and restores the blood flow. However, studies have shown that this treatment is more likely to benefit younger patients opposed to elder patients. Although this may be the case, young adults and females in particular, are often not eligible for the treatment because they ignore early symptoms or wait until the symptoms get severe, before they seek help.

As stated in an article from Live Science  and a journal from NCBI, the increase in stroke incidents at younger ages has great significance because strokes in younger patients carry out for a greater lifetime burden of disability.

While the total number of strokes in the U.S. has decreased, the number and severity of strokes in younger generations has increased. As a result, researchers, doctors, and medical staff continue to work together in order to seek ways to treat the newer generation of stroke patients.

Obesity Related to the Brain

Lauri Nummenmaa has done research the connects obesity to the brain.  This research shows that people struggling with obesity have a lower amount of μ-opioid receptors available for binding in the brain.  (To learn more about μ-opioid receptors click here.)  Due to evolution, our brains are still “wired” to search for food and nutrients.  Since eating gives off a sensation in the brain, related to the opioid receptors, people with fewer receptors that are able to bind will therefore eat more to make up for the loss in sensation.  This reaction is the same as a reaction to an addiction would be, causing more neurotransmitters to be secreted.  The next step that scientists are taking is to discover whether being obese causes a lack in opioid receptors, or if a lack in opioid receptors, caused by another source, is what causes obesity.  One test that scientists did was testing μ-opioid receptors in people that had bariatric surgery.  Bariatric surgery causes more receptors to work again, shown by the fact that scientists could not distinguish between the μ-opioid receptors or healthy people and the μ-opioid receptors of people who had the surgery.

Some body fat, however, is helpful to the brain.  This article describes that “fat tissue in the bodies of mice releases an extracellular form of nicotinamide phosphoribosyltransferase (eNAMPT), an enzyme that travels to the hypothalamus, and gives animals energy during fasting.”  (To learn more about eNAMPT click here.)

This photo shows how a neurotransmitter is sent from neuron to neuron generally.

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(Link to Photo Page and Link to Licensing Page)

Yawning and Brain Size

macaca_fuscata_juvenile_yawning

Recently, scientists discovered a correlation between yawning and brains: the longer the average duration of a specie’s yawn, the bigger that specie’s brain size,  as measured by brain weight and total number of cortical neurons.

The study was conducted on 109 individuals from across 19 different species, including cats, humans, mice, camels, and more. The investigators found that the duration of yawns was shortest in mice, who averaged 0.8 seconds, and longest in humans, who averaged 6.5 seconds. The scientists plan on investigating whether this correlation holds true amongst individual members of a species.

The study was created in response to the ideas set forth in Gallup’s 2007 paper on the thermoregulatory theory of yawning, one of the strongest theories about why we yawn (we do not yet definitively know the biological purpose of yawning). The thermoregulatory theory indicates that yawning cools down the brain in homeotherms via three potential mechanisms. But whether or not this brain-cooling is simply a side effect or the primary function of yawning is up for debate.

Based on Gallup’s paper, the investigators of this study hypothesized that longer yawns would produce greater physiological responses, in terms of blood flow and circulation to the brain– which would be evolutionarily necessary for species with larger, more complex brains.

There are other theories about why we yawn, such as a 2014 paper stating that yawning stimulates cerebrospinal fluid circulation, which in turn increases species’ alertness. A common theory that yawning increases blood oxygen levels has largely been disproved. How would such alternate theories have different implications for the discovered correlation between yawning and brain size?

How Did Our Baby Learn That Word?!?!

Jason Sudeikis’ character is hosting a nice dinner party with his wife played by Jennifer Aniston, and all seems to be going great. Then, all of a sudden, their 12- month-old baby blurts out a curse word! “How could our baby learn such a thing?” In a flashback 8 months earlier, we see the less-experienced parenting pair blurt out some pretty R-rated things in a fit of frustration on the road with their baby in the backseat. And so the punch line sinks in.

In modern day parenting comedies, scenes like this fabricated one are a dime a dozen. But these humorous takes on life always get at least one thing right: babies are sponges. Let’s take a look at why on a cellular level.

image source: https://commons.wikimedia.org/wiki/File%3AComplete_neuron_cell_diagram_en.svg

Prior to birth, most neurons migrate to the frontal lobe of the brain where, during postnatal development, they link together and forge connections, allowing a baby to learn proper responses to stimuli. The “circuits” formed by the neural connections are incredibly flexible during the early months of development (roughly the first 6 months) and can quickly be formed or severed, resulting in a remarkable neonatal human ability to rapidly pick up new knowledge about our surroundings. But how are they so malleable?!

Researchers at the University of California, San Francisco may have the answer! In a study coauthored by neuropathologist Eric Huang, they found neurons forming a chain moving towards the frontal lobe from the sub ventricular zone, a layer inside the brain where nerve cells are formed, in infants up to 7 months old!

This research seems to point to the idea that these new brain cells form connections with the pre-existing neurons in the frontal lobe later in the infant’s development, resulting in more cognitive flexibility for a longer period of time.

To quote the original article by Laurel Hamers, what the new neurons are doing is analogous to “replenishing the frontal lobe’s supply of building blocks midway through construction”.

Huang’s team observed postmortem infant brain tissue under an electron microscope and discovered a group of neurons synthesizing migration proteins, but the real major discovery came with the observation of rare tissue acquired moments after death. The team injected viruses tagged with glowing proteins into the neurons (thus making the nerve cells glow) in the sample and tracked their movement. While infants up to 7 months old were observed with migrating neurons, the researchers recorded the number of migrating cells at its highest at 1.5 months old and saw it diminish thereafter. The migrating neurons usually become inhibitory interneurons which, to quote the original article, are “like stoplights for other neurons, keeping signaling in check”.

So there you have it! To make sure your baby doesn’t learn that bad word, just suck up all the migrating neurons from its brain!

All jokes aside, this research presents an amazing window into the brain development of the most intelligent species on earth! It’s fascinating how it breaks down psychological mysteries using cellular evidence. And it raises new questions about these mobile neurons: When are they created and how long does it take them to move to the frontal lobe?

How do you think this new research will influence our understanding of the creation of social biases? Do you think this will lead to breakthroughs in research on the foundation of Autism spectrum disorders?  Do you have any funny baby stories? Let me know in the comments.

Lead Leads to Neurotoxitity

Have you ever heard of using bottled water to shower? Sounds ridiculous right, but the people of Flint, Michigan need to do this to save their lives. The city of Flint switched their water supply from Lake Huron to the Flint River in April 2014. The river was later discovered to be contaminated. Since the changeover, scientists have linked the high lead levels in children’s blood to the contaminated water. This is a serious problem.

Lead is a highly toxic substance that permanently affects humans’ brains by killing nerve cells. Not only does lead harm kids’ brain processes, it also may cause various future mental diseases, such as Alzheimer’s disease and Schizophrenia. Throughout U.S. history, people have been exposed to lead poisoning through basic everyday mediums, such as paint, water (from lead-contaminated water pipes), and dust. Children who eat paint chips or lick their fingers after coming in contact with products that have a lead component are poisoning themselves. The lead enters into the bloodstream and travels throughout the body, stealthily making itself at home, poisoning the body.

So how does lead poisoning work? Basically, lead disguises itself as zinc. Zinc is needed to anchor proteins that switch genes on and off. When zinc is replaced with lead, the switches cannot function properly, eventually leading to mental diseases.

Lead Poisoning

Scientists have been researching the possibility that lead is transferable in DNA to offspring. This could be devastating to a population of a town like Flint, Michigan, where the mothers who have lead poisoning could pass this on to their babies. The worst part is that there is no cure for lead poisoning.

Because of the devastating effects of lead in bloodstream, governments have debated the topic of legalizing contaminated water as a bioweapon, using lead as the contaminant. Governments in the past have used poisoned water as an assassination method, proving the effectiveness of this strategy.

Preventing lead exposure and poisoning is critical for children’s health and for future generations.

 

Source Article

For more info on the biowarfare, click here.

Possible Connections between the Gut Microbiome and the Brain

It is not a new concept that gut bacteria affects a person’s health. But this article published in The Atlantic explains how they may even affect the human brain. Some researchers believe that the microbiome may play a role in regulating how people think and feel. Scientists have found evidence that this community of bacteria (trillions of cells that together weigh between one and three pounds) could play a crucial role in autism, anxiety, depression, and other disorders.

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 https://en.wikipedia.org/wiki/Fecal_bacteriotherapy#/media/File:E_coli_at_10000x,_original.jpg

Much of the most intriguing work has been done on autism. For years, it has been noted that about 75 percent of people with autism also have some gastrointestinal abnormality, like digestive issues or food allergies. This has prompted scientists to search for potential connections between the gut microbiome and autism; recent studies find that autistic people’s microbiome differs significantly from those of control groups. Caltech microbiologist Sarkis Mazmanian specifically focuses on a species called Bacteroides fragilis, which is seen in smaller quantities in some children with autism.  Mazmanian and several colleagues fed B. fragilis from humans to mice with symptoms similar to autism. The treatment altered the makeup of the animals’ microbiome, and more importantly, improved their behavior: They became less anxious and communicated more with other mice.

Perhaps the most well-known human study was done by Emeran Mayer, a gastroenterologist at UCLA. He recruited 25 subjects (all healthy women) for four weeks. He had 12 of them eat a cup of commercially available yogurt twice a day, while the rest didn’t. Yogurt is a probiotic, meaning it contains live bacteria. In this case it contained four species: bifidobacterium, streptococcus, lactococcus, and lactobacillus. Before and after the study, subjects were given brain scans to gauge their response to a series of images of facial expressions—happiness, sadness, anger, and so on.

To Mayer’s surprise, the results showed significant differences between the two groups. The yogurt eaters reacted more calmly to the images than the control group. “The contrast was clear,” says Mayer. “This was not what we expected, that eating a yogurt twice a day for a few weeks would do something to your brain.” He thinks the bacteria in the yogurt changed the makeup of the subjects’ gut microbes, and that this led to the production of compounds that modified brain chemistry.

As scientists learn more about how the gut-brain microbial network operates, they think it could be manipulated to treat psychiatric disorders. And because these microbes have eons of experience modifying our brains, they are likely to be more precise and subtle than current pharmacological approaches, which could mean fewer side effects. “I think these microbes will have a real effect on how we treat these disorders,” neuroscientist John Cryan says. “This is a whole new way to modulate brain function.”

Just Because My D1 Neurons Are Excited, Doesn’t Mean My Risk of Alcoholism Increases…Does it?!

Alcoholism can now not only be studied and analyzed at the psychological level, but also at the molecular level, thanks to researchers at the Texas A&M Health Science Center College of Medicine. They recently conducted a study that found how alcohol influences the dorsomedial striatum, the part of the brain that participates in decision-making and goal-driven behaviors.

The dorsomedial striatum is composed of medium spiny neurons, neurons that have many branches, or spines, protruding off their dendrites.

(Source: https://commons.wikimedia.org/wiki/File:Confocal_image_of_spiny_neuron_-_1.jpg)

Spiny neurons have receptors for dopamine, which is further categorized into dopamine D1 and D2 neurotransmitters. D1 neurons have receptors for D1 neurotransmitters. They send excitatory postsynaptic potentials and encourage the action potential/signal to continue. D2 neurons counteract D1 neurons; they send inhibitory postsynaptic potentials and discourage further actions. In this study, D1 neurons prove to be a major part of alcoholism and addiction.

High consumption of alcohol, scientists learned, excites D1 neurons. The more excited they become, the more compelled one feels to perform an action…in this case, the action is drinking another alcoholic beverage.

More drinking induces more D1 neuron excitement, which leads to even more drinking.

Not only does it affect a D1 neuron’s excitability, alcohol also makes physical changes to the neuron itself at the molecular level, and consequently affects the neuron’s function.

In their study, researchers divided their test subjects into two groups: one that’s exposed to alcohol and one that’s not. Analyzing their spiny neurons, scientists saw that though the number of spines in the neurons of the individuals of each group didn’t change, the ratio of the difference between mature and immature spines was dramatic. The subjects that drank alcohol had notably longer branches and a high number of mature mushroom-shaped spines. The abstainers’ neurons had shorter branches and more immature mushroom-shaped spines. Mature, mushroom-shaped spines are involved in long-term memory; activation of long-term memory through alcohol underlies addiction.

However, there’s promising news! The study also showed results that blocking, or at least partially blocking, D1 receptors via a drug can inhibit and reduce the desire for consumption of another drink.

This is a huge step towards finding a cure for alcoholism. Alcoholism is a disease that affects not only the individual, but also his or her family, relatives, friends, etc…With this study, the scientific community has more of an understanding of how to go about creating new drugs and combating alcoholism.

If we suppress this activity, we’re able to suppress alcohol consumption. This is the major finding. Perhaps in the future, researchers can use these findings to develop a specific treatment targeting these neurons.

-Jun Wang, M.D., Ph.D., the lead author on the paper and an assistant professor in the Department of Neuroscience and Experimental Therapeutics at the Texas A&M College of Medicine.

What do you think? Do you think this study promotes a viable option towards curing alcoholism and addiction, or is there another method out there that we should be pursuing? Leave a comment below!

 

Original Article

The Not-So-Sweet Truth

Trick-or-treaters excitedly hoard candy every Halloween, aware of its dangers to the extent that sugar causes cavities. However, sugar’s stealth effects extend far beyond tooth decay. Research shows that consuming high-concentrations of sugar slows down brain function and is detrimental to both physical and mental health. Continuing overindulgences in sugar-laden products may even lead to Alzheimer’s disease. Children, teenagers, and adults need to understand the damages that a high-fructose diet could cause in order to avoid sugar.

For consumers, sugar is extremely difficult to avoid since it is found in most processed foods in the form of honey, sucrose, and high fructose corn syrup. As soon as sugar is consumed and absorbed into the body, it causes the brain to release hormones, such as dopamine, that generate good feelings. The good feelings from the release of dopamine are temporary. Once the high sugar level in the bloodstream drops, feelings of depression, irritability, or fatigue take over. Sugar thus stimulates the body to intensely crave for more sugar intake.

In addition to affecting the hormones, research shows that sugar-heavy diets causes changes in gut bacteria, which makes the brain’s ability to adapt and switch to new concepts more difficult to comprehend. The gut bacteria influences the way the brain functions, so any change in this type of bacteria is unhealthy for neurological health. The level of sugar intake and cognitive abilities are interconnected; therefore, restricting sugar from entering the bloodstream is an intelligent dietary choice.

The negative consequences of diets high in sugar have been studied and the conclusive evidence shows that sugar is toxic to good health. Scientists conducted experiments on a group of rats to prove that sugar consumption hinders the ability to effectively think. One group was given normal water to drink, while the other group was given a fructose-infused water to drink for six weeks. After the six weeks, the rats were timed to see how fast they could escape a maze. The group that drank the sugar water took thirty percent longer than the group that drank plain water. The researchers ultimately concluded that fructose disrupts plasticity: the brain’s ability to retain short-term and long-term memories and generate new ideas using new information.

It is important for everyone to be aware of the harmful effects that sugar has on the human body. Cavities should not be the thing people worry about when they eat candy, as they are petty compared to the dangers sugar has on the brain. Sugar weakens mental and physical health, and should be avoided like the death it could cause.

Original Article 

 

Epigenetics and Dopamine Activity

Researchers at the University of California in Irvine have correlated erratic dopamine activity as an underlying cause of complex neuropsychiatric disorders, specifically because of the epigenetic alterations caused by low levels of dopamine. This study, overseen by Emiliana Borelli, a UCI professor of microbiology & molecular genetics, provides clues to the possible causes of complicated disorders like schizophrenia.

Dopamine is a neurotransmitter (and hormone) that fuels our daily life, acting as our prime motivator and pleasure inducer, while also being linked to memory, and cognitive function. Many addictive drugs increase the amounts of dopamine released to exhausting levels, eventually wearing out the neurotransmitters notwithstanding the negative effects of the drugs themselves. High dopamine levels can also be achieved via everyday pleasures like exercise or sex, which can also spur addiction.

Dopamine_3D_ball

Dopamine, therefore, has an irrefutable role in our everyday lives, and according to Borelli, “Genes previously linked to schizophrenia seem to be dependent on the controlled release of dopamine at specific locations in the brain. Interestingly, this study shows that altered dopamine levels can modify gene activity through epigenetic mechanisms despite the absence of genetic mutations of the DNA.”

In short, it is quite likely that Dopamine is an epigenetic hub of sorts, that can cause powerful changes in gene regulation when functioning in a disrupted or excessive manner. Borelli, knowing the consequences of excess dopamine release, tested the opposite effect on mice, hindering dopamine release by turning off mid brain dopamine receptors in rats, leading to mild dopamine synthesis. The results were profound, as Borelli found there to be decreased expression in approximately 2,000 genes in the prefrontal cortex. This epigenetic surge of decrease in genetic expression was reinforced by the increase in change of DNA proteins called histones, which are associated with reduced gene activity. The now mutated mice suffered from ranging psychotic behavior and episodes, and were then treated with dopamine activators for a duration of time before seeing their behavior normalize.

Borelli’s and others’ work will provide useful clues for understanding these complex neurological disorders, while serving to reinforce the newfound importance of comprehending gene regulation and expression. These studies seem to point to a new era in which it is not just your genetic make up that determines your future, but also the regulation of your genes.

 

 

Editing the Brain Using Epigenetic Tools

Epigenetics is a huge part of our life and influences us in ways we may not be aware of. Did you know that it is impossible to create and save new memories without epigenetic tags? The brain is heavily reliant on Epigenetics to do its functions, and this makes it a huge topic of research to figure out the ways in which the epigenetics of the brain could affect certain diseases or memory. Recently special epigenetic molecular tools have been created that can erase specific epigenetic markers throughout the genome. The possible effects these tools could have on the curing of diseases of the brain or psychological ailments are tremendous.

These “epigenetic editing” procedure use either CRISPR (clustered, regularly interspaced, short, palindromic repeats) or TALE (Transcription activator-like effector) systems of modification. These systems can carry an Epigenome modifying enzyme and deliver it a specific site they are programmed to go to. This allows researchers to target very specific epigenetic changes and either shut them down or turn them on and possibly determine their correlation with certain ailments of the brain. “We’re going from simply being able to observe changes to being able to manipulate and recapitulate those changes in a controlled way,” Day said. This quote from Day, one of the researchers of this project, shows that we advance from only being able to observe epigenetic influences on the brain, to being able to manipulate and control them to potential aid us in combating diseases.

Researchers can catalog all of the epigenetic changes involved in forming and preserving a new memory. If we are able to track these epigenetic changes, then could we implant memories in to a person’s mind, by copying similar epigenetic changes? These researchers where also able to trigger not only the place where epigenetic change happens, but also the exact time using optogenetics. This form of using light to control neurons allows researchers to use the TALE system and a light switch apply epigenetic change to very specific brain regions or cell types.

One of the final goals of this research is to eventually be able to use epigenetic as a form of therapy to benefit PTSD, depression, schizophrenia, and cognitive function using the ability to alter epigenetic marks. This can also be used in a similar way to silence mutated genes that are damaging the cells or the body as whole. This form of using TALE and CRISPR to alter epigenetic tags creates a lot of hope for PTSD, depression, schizophrenia, Alzheimer’s, Parkinson’s, Huntington’s and other similar disease treatment options.

Epigenetics and Brain Development

Pre-natal human brain development helps determine many major qualities a person may have in life. Research at the University of Exeter found that a type of Epigenetics, DNA methylation, helps us understand the differences between male and female brains. They studied that this type of gene regulation in pre-natal brain development may help us grasp more information about “sex differences in behavior, brain function, and disease.”

In the womb, as organs are developing, the brain has extreme plasticity. Professor Jonathan Mill of the University of Exeter explains how it is extremely vulnerable to changes because the brain is creating the structures that “control neurobiological function across life.” The research consisted of measuring genomic patterns of DNA methylation in the womb between 23 and 184 days after conception. DNA methylation is a chemical modification to one of the 4 nitrogen bases that helps create one’s unique genetic code. By studying the DNA methylation, or turning on of selected genes, in the pre-natal period when the brain is being developed, it helps scientists understand the susceptibility of different neurological diseases based on one’s sex. Helen Spiers from King’s College London explains how male and females have unique differences with certain disorders, such as Autism. She says how “autism affects five males to every female.”

The molecular switches that regulate genes were found to be gender specific. They also help differentiate brain cells from other cells in the body. This research gained traction in understanding the unique qualities of the DNA “blueprint” of males and females in their developing stages. The genetic switches that are turned on in pre-natal development for each gender are unique, and a deep topic of study. By doing so, in the future, scientists can research deeper into neurological diseases that are unique to males or females, and how they may be created in the womb.

 

Original Article: http://www.sciencedaily.com/releases/2015/02/150203190223.htm

Link to picture:

http://commons.wikimedia.org/wiki/File:Brain_01.jpg#mediaviewer/File:Brain_01.jpgBrain_01

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