Interestingly enough, in today’s society, it seems like depriving oneself of sleep is almost like a trophy to jokingly brag as people attempt to see who slept the least number of hours yesterday or who pulled the most number of all-nighters last week. In addition, with finals season approaching, it becomes tempting for most students to sacrifice their sleep to score a few more points on the exam, although one can’t help but to ask if it was really worth it. Sleep deprivation seems like a necessary part of life that many college students must go through to succeed academically. There is even a joke that college students can only choose two of the following: good grades, social life and enough sleep. However, one of the choices, social life, seems unlikely as a sustained pattern of sleep deprivation can have an impact on the social aspect of our lives.
A study conducted in UC Berkley showed that people who suffer from sleep deprivation tend to become recluse; instead of seeking protection from society, sleep deprived individuals withdraw from social situation in the hopes of obtaining rest. In this experiment, they showed participants a stranger with a neutral facial expression walking towards them, and they asked them to hit the panic button when they felt that the stranger was getting too close. They found that sleep deprived participants hit the button significantly earlier than those who did get sleep. Through fMRI scans, they tried to see what regions of the brain were responsible for this behavior. One region, called the near space network, was very active compared to the control group. This region allows one to orient oneself in space and get out of threatening situations that involve spatial elements. In addition, the theory of mind network, which allows people to interpret others’ intention, was less active in sleep deprived participants than the control group. Thus, sleep deprivation may lead to a more antisocial attitude and an inability to fully detect social cues.
Yet another study also shows increased anxiety and fear levels in people who suffer from sleep deprivation. Sleep deprivation can increase sensitivity in the amygdala, leading to stronger fear responses to a stimulus. As a result of the activation of the amygdala, the ventromedial prefrontal cortex (vmPFC) begins to regulate emotion and inhibit activity in the amygdala. Another area of the brain, the insula, does the opposite of vmPFC and increases the activity in amygdala which then leads to fear acquisition. In a study by Feng et al. (2017), participants’ brains were tracked with an fMRI while they were shown series of different shapes in which a certain consecutive pattern of shapes would indicate an electric shock. In sleep deprived participants, higher activity was seen in the connections between the amygdala and the insula, while for the control group a higher activity was seen between amygdala and vmPFC.
When comparing the results of the two studies, both makes sense; sleep deprived individuals have increased levels of anxiety and fear which could have led to earlier responses in pushing the panic button. Both studies also demonstrate that the lack of sleep can affect one’s mood and thus their ability to socially interact with others. Although it is difficult for college students to find time to get quality sleep, getting sleep can possibly improve the social aspects of one’s life.
Writer: Audrey Kim
Editor: Lauren Renehan
Over the past two decades, a neurosurgical technique known as Deep Brain Stimulation (DBS) has revolutionized the fields of both medicine and neuroscience. DBS has been able to accomplish incredible feats once deemed impossible, one of these being the extremely effective treatment of Parkinson’s Disease symptoms. DBS has also opened many doors to a bright future where debilitating neurological disorders and diseases may be eradicated.
So what exactly is Deep Brain Stimulation? Deep Brain Stimulation essentially consists of sending electrical impulses to certain brain areas via surgically implanted electrodes, resulting in the removal of adverse neurological symptoms. The exact mechanism by which DBS exerts its effect on neurons is still not fully understood, although many theories have been presented. One popular explanation for the mechanism behind DBS is that electrode stimulation of certain brain areas induces changes in neuronal activity in the respective neural circuits that would ultimately change physiological and cognitive behavior.
An example of DBS in action can be seen through one of its most common applications, Parkinson’s Disease treatment. Parkinson’s Disease is characterized by voluntary motor deficits and symptoms including resting tremor, bradykinesia, postural instability, extreme difficulty initiating voluntary movement, and more. These symptoms are caused by the loss of dopamine producing neurons in an area called the substantia nigra, which is a constituent of a much more complex brain circuit within the basal ganglia that controls the initiation of voluntary movement. Needless to say, this neurodegenerative disease is very debilitating for the patient. When medications such as L-DOPA fail to alleviate Parkinson’s Disease symptoms, DBS steps in to save the day. Electrodes are surgically inserted into brain areas such as the internal Globus Pallidus or the Subthalamic Nucleus and are connected to an internal pulse generator (IPG) located in the patient’s chest or abdominal cavity. Upon the initiation of electrical impulses to those certain brain areas via the implanted electrodes, the patient’s symptoms disappear immediately and the patient is able to execute normal voluntary motor function without difficulty.
DBS holds vast potential and unending applications in the fields of medicine and neuroscience. DBS research is currently being done to investigate its effect in treating a plethora of neurological disorders including major depressive disorder, OCD, PTSD, addictions, Alzheimer’s Disease dementia, chronic pain, schizophrenia, eating disorders, and more. As mentioned, DBS has opened the doors to a new and hopeful future in which neuroscience research and medicine can eradicate the most debilitating of neurological disorders. Ironically, although DBS was created to provide an answer to the many questions plaguing neuroscientists and doctors today, it has instead prompted us to ask infinitely more questions and has further shown how little we know about our own brains. I will end our short discussion of Deep Brain Stimulation with a quote by Santiago Ramon y Cajal, the father of modern neuroscience himself, which sums up what DBS, and neuroscience itself, is all about: “To know the brain…is equivalent to ascertaining the material course of thought and will, to discovering the intimate history of life in its perpetual duel with external forces.”
Writer: Richard Kuang
Editor: Audrey Kim
Why does the brain deteriorate with age? Researchers might finally have found a potential cause. The klotho protein has been found to be associated with the aging brain. Specifically, higher levels of klotho have been associated with longevity of the brain. As you grow older, however, your brain’s klotho levels decrease, and researchers believe that this decrease may be related to age-related impairments.
Experiments conducted at the Gladstone Institute of Neurological Disease measuring klotho levels in mice show decreasing levels of klotho with age in the choroid plexus, a brain structure whose cells are responsible for producing cerebrospinal fluid and forming a barrier between the central nervous system and the bloodstream. In addition, experimentally reduced klotho levels in mice resulted in increased inflammation in the brain. The researchers thus found that klotho plays a role in maintaining the integrity of the blood brain barrier – a gatekeeper for protecting the brain from the peripheral immune system. This observation is particularly important because brain inflammation is a prominent feature of neurodegenerative diseases such as Alzheimer’s disease and multiple sclerosis.
Klotho has also been shown to be therapeutic and saves cognitive functions such as spatial learning and memory that were impaired as a result of aging or dementias. Researchers at UCSF injected a small fragment of the klotho protein into 18-month-old mice (about the same stage in the mouse lifespan as a 65-year-old human). What they observed was that a single injection of klotho significantly improved the ability of the mice to navigate and learn new tasks. The researchers then injected the protein into mice that were engineered to produce abundant levels of alpha-synuclein in order to induce Parkinson’s disease-like symptoms, namely movement disturbances. As a result of klotho administration, these mice displayed improvement in motor function as well as improvement in learning to navigate and explore new territories. All of these improvements were shown in spite of the mice brains still containing the toxic alpha-synuclein, indicating that the klotho protein appears to play a protective role against toxicity in the brain.
So, given this potential protective role for klotho, a next step for researchers could possibly be to develop a potential klotho-related treatment for individuals suffering from neurodegenerative diseases.
Writer: Nathaniel Meshberg
Editor: Audrey Kim
A new study out of the Boston University School of Medicine shows the first evidence of a genetic link to developing chronic traumatic encephalopathy (CTE). CTE is a neurodegenerative disease that may be diagnosed in patients with repeated head trauma. These patients typically exhibit cognitive and emotional issues including difficulty planning, emotional instability, substance abuse, impulsivity, and short-term memory loss. However, CTE can only be diagnosed postmortem, and there is currently no reliable way to predict who will develop this disorder.
This study, published in Acta Neuropathologica, is the first to show that there may be a genetic predisposition to developing CTE. Eighty-six brain samples from deceased American football players were examined for the presence of a missense mutation (rs3173615) in the TMEM106B gene. These players had all been diagnosed with CTE after their deaths. The mutation has been identified as playing a role in neuroinflammation and TDP-43 neurodegenerative diseases (such as ALS and Alzheimer’s). Thus, this specific mutation was of interest to researchers, who have been trying to find a possible genetic basis for the development of CTE.
Researchers identified that those diagnosed with CTE were more likely to have the missense mutation (rs3173615) on the TMEM106B gene than those without the disease. They also found that those with this gene variant were 2.5 more likely to have developed dementia. Researchers found that the presence of rs3173615 was associated with synaptic loss, dementia, and density of abnormal tau protein. However, these results were only seen when analyzing the brains of those diagnosed with CTE.
When compared to case-controls, the same associations were not observed. This study is the first to identify a possible genetic link to the development of CTE. The actual applicability of this study is limited, but it does provide possible paths for future research into the causes of CTE. There are likely to be many genes that contribute to the development of CTE, and as such, further research is needed. It is possible that this research could lead to preventative measures, diagnostic methods, and treatment of CTE; all of which are extremely limited as of now. CTE has been a popular topic in the news recently, with evidence accumulating that links head trauma from contact sports to CTE-like symptoms. A Boston University study in 2017 found that 99% of former NFL players’ brains that were studied showed signs of CTE. Evidence has also been produced to show that playing contact sports as a minor may contribute to cognitive deficits later in life. Studies like these have led to some arguing that contact sports (especially football) need to be altered to mitigate the risk of head trauma. Such alterations may include better helmets or rule changes. Some have even argued that children should not play football because of the risk of future brain trauma may be too great. More studies like this one are needed to assess the validity of these arguments, but in the meantime, these studies have ignited the debate around contact sports.
Writer: Jayden Font
Editor: Lauren Renehan
https://www.bostonglobe.com/metro/2018/11/03/study-hints-that-certain-gene-may-worsen-cte/ QORz6GjMsKCjqGvAOBblxN/story.html https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-018-0619-9 https://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/symptoms-ca uses/syc-20370921 https://www.cell.com/trends/molecular-medicine/pdf/S1471-4914(08)00186-X.pdf http://www.bu.edu/cte/2017/07/25/bu-researchers-find-cte-in-99-of-former-nfl-players-studied/ http://www.bu.edu/cte/2017/09/19/study-suggests-link-between-youth-football-and-later-life-emo tional-behavioral-and-cognitive-impairments/
With a computer or telephone in hand, it seems pointless to memorize simple facts, lists of things, poems, directions, dates or formulas. From an evolutionary standpoint before modern day technology, people would constantly have to exercise their mind and memorize what we currently leave the task for our computer or telephone in hand to remember. But schools are now switching their structures to provide students the skills to apply knowledge instead of reciting information, which seems logical. Except there may be a huge positive to memorizing what seems to be pointless information.
Memorizing information is the equivalent to lifting weights in the gym, but instead of building more muscle, the levels of acetylcholine increase in the brain. Acetylcholine is a neurotransmitter has been identified by scientists to keep the mind sharp; it is critical in creating and strengthening connections between neurons. People blame the lack in memory as a consequence of aging, but scientists are finding out it has more to do with how much the person is exercising the mind. More specifically, the brain produces acetylcholine when the person is exercising the mind, such as when a person is trying to pay attention1. Although many people’s memories increasingly start to fail after their mid-40’s, elderly people who constantly exercise their minds show high levels of acetylcholine, and their memory, as a result, does not deteriorate as rapidly. High levels of acetylcholine also reduce the risk of dementia; for example, cholinesterase inhibitors, which inhibit proteins that degrade acetylcholine and consequently lead to higher acetylcholine levels, have been used to slow down the effects of Alzheimer’s1.
In response to this trend of memory loss, researchers in New York discovered five compounds that naturally reinstate optimal levels of acetylcholine: Alpha GPC, Huperzine A, Bacopa Monnieri, Lion’s Mane Mushroom, and Ginkgo Biloba2. This formula was named RediMind. RediMind was created in order for people to use modern day technology without the consequence of drastically losing their memory through aging. After a placebo-controlled clinical trial by Princeton Consumer Reseach, the results showed that the group who took the RediMind drug had scored 45% better than the placebo group2. Another positive of RediMind is that it gives the brain a long-term boost for energy compared to short-term boosts of drugs like caffeine.
RediMind is now for sale but has not been reviewed by the FDA. This could one step closer to creating enhancers for superpower memorization, but this drug has not been tested enough to prove consistent improvement of memory and to be safe for the brain. So, for now, I would stick to memorizing directions, grocery lists, and more vocabulary words to work out my brain.
Writer: Lauren Renehan
Editor: Audrey Kim
- https://globenewswire.com/news-release/2018/07/24/1541146/0/en/Alzheimer-s-related-Study-B rain-Training-Upregulates-Acetylcholine.html
- https://www.nutreance.com/articles/redimind?utm_medium=google_display&utm_campaign=redimind_us_content&utm_source=neurosciencenews.com&utm_term=long%20term%20memory &gclid=EAIaIQobChMIg8z664a33gIVAhLTCh3CIg5VEAEYASAAEgJz_vD_BwE
Music is all around us. It’s in our ears as we walk to class with our earbuds in. It’s in the cars we drive and the ubers we take. It’s in malls and grocery stores. It’s even infiltrated the smallest of spaces, like elevators in hotel lobbies. This ubiquity of music may make it lose its significance in our eyes, however, this is not the case for people suffering from neurogenerative diseases such as Alzheimer’s and Parkinson’s. Music plays an important role in the lives of these people. While they may find themselves lost in their own minds, music can help guide them to lucidity, even for a little bit. Clinicians and researchers are utilizing music therapy as a supplemental treatment for people who suffer from neurodegenerative diseases. This approach has been found to be extraordinarily beneficial in such patients. In fact, in his book Musicophilia, Oliver Sacks writes: “ music therapy with such patients is possible because musical perception, musical sensibility, musical emotion, and musical memory can survive long after other forms of memory have disappeared. Music of the right kind can serve to orient and anchor a patient when almost nothing else can.”1
One of the most prevalent neurodegenerative diseases is Alzheimer’s disease with 5.7 million Americans suffering from it in 20182. So far there is no absolute ‘cure’ for AD. It is caused by an accumulation of p-tau and neurofilaments in the brain which cause cell death and neurodegeneration in the hippocampus. Music therapy has been found to be an effective non-pharmacological approach to manage AD. A study by Arroyo-Anlló EM et al was conducted on self-consciousness in people suffering from mild to moderate AD where they played familiar music for one group of people and unfamiliar music for another group. They found that familiar music intervention resulted in improvement in some aspects of self-consciousness such as personal identity, affective state, moral judgements and body representation. The researchers suggested that the improvement in self-consciousness may be due to the enhancement of general cognitive state by familiar music3.
Another study investigated the effects of background music on autobiographical memory of those with mild AD and also found encouraging results. The investigators conducted Autobiographical Memory Interviews (AMI) in which they asked questions related to major events in the individual’s lives that spanned over childhood, early adulthood and recent life. They found that subjects that had music ‘Spring’ movement from Vivaldi’s ‘Four Seasons’ in the background during the interview had higher AMI recall scores especially for recent personal semantic memories. Subjects in the music condition had reduced state anxiety levels and therefore the researchers attribute the enhanced autobiographical recall to an anxiety reduction mechanism brought on by music4.
Music seems to have interesting effects on people who suffer from Parkinson’s disease as well. Parkinson’s is the second most common neurodegenerative disorder with approximately 60,000 Americans diagnosed with it every year5. It usually caused by cell death in the substantia nigra in the basal ganglia. This causes a depletion of dopamine in the brain which is responsible for the symptoms present in Parkinson’s such as gait abnormalities. Oliver Sacks makes another interesting observation in his book where he states, “The patient can regain a fluent flow with music, but once the music stops, so too does the flow. There can, however be longer-term effects of music for people with dementia – improvements of mood, behavior, even cognitive function – which can persist for hours or days after they have been set off by music.”6 Researchers have found some encouraging results in line with Sack’s conclusion. In a study conducted by Benoit et al, it was found that musically cued gait training showed improvement in gait, motor timing, and perceptual timing. They trained patients with Parkinson’s to walk to the beats of German folk music on their own but giving them exact instructions on how to do so. They found that not only did these patients show improvements in gait velocity and stride length, but this effect outlasted the duration of the training for up to one month7.
In the same study, they also found that music therapy has the ability to enhance perceptual timing. They assessed this using a tone duration detection task and found that the patients that had undergone musical intervention improved their performance in these tasks. The researchers state that both these effects may be attributed to a cerebello-thalamo-cortical tract which is activated by auditory cues and compensates for the dysfunction in the basal ganglia as the enhancement in perceptual timing is responsible for the improvements in the subjects’ gait 8.
While we may take music for granted, it can play a very important part in people’s lives – particularly those that have to live with neurodegenerative disorders like Alzheimer’s and Parkinson’s. Unfortunately, there’s no exact ‘cure’ for these diseases, but interventions such as music therapy can still help provide a unique approach to alleviate many of the debilitating symptoms presented by these disorders.
Writer: Farwa Faheem
Editor: Kawtar Bennani
- Musicophilia by Oliver Sacks
Recent studies have shown that the brains of children with Autism Spectrum Disorder (ASD) fold differently than a normal brain—either being unusually smoother or unusually convoluted depending on location and age. Researchers measure the development of neural tissue folds in the cortex as changes in the local gyrification index; a ratio which compares the area of the smooth outer surface with that of the inside the sulci. Using this information, researchers can understand the link between autism and the folds of a brain.
In a study at San Diego State University, it was found that school-age children and adolescents with autism had more intricately folded regions. The left temporal and parietal lobes, which are responsible for processing sound and spatial information, were shown to have these intricate folds in children with autism. Research also found increased gyrification in the right temporal and frontal lobes, which are responsible for decision making and motor skills. In contrast, a second study found that preschoolers with autism do not show this degree of intricate folding unless they had enlarged brains. Preschoolers with autism were also found to have an unusually smooth region in the occipital lobe (specifically in the region dedicated to recognizing faces). These studies, in juxtaposition, demonstrate that brain folding hints at the different developmental path that autism brains follow when compared to normal brains. According to Ruth Carper, a researcher at San Diego State, “many of the brain areas with exaggerated folding are among the earliest to develop folds during gestation.” Thus, the folding will increase in intricacy and convolution over time due to this developmental disruption. In another study at the University of California, Davis, researchers found that children with enlarged brains actually have a specific subtype of autism due to the fact that only children with enlarged brains exhibited this degree of increased and atypical folding. This study adds to the evidence that folding patterns depends on the development of the individual and where that individual lies within the autism spectrum.
It’s clear that ASD is a very complex subset of conditions and traits that are influenced by various genetic and environmental factors. A great deal of research is focused on identifying physical differences, such as brain folding patterns, which are present in the autistic brain. In doing so, resources may be found to aid and benefit a developing brain with ASD. Lastly, such research will only further our understanding of how all of our brains grow and evolve over time.
Writer: Ava Genovese
Editor: Farwa Faheem
Everyday a person may be ignored by someone, not get a job or internship they wanted, not get invited somewhere, or not have their opinion factored into an important decision. The result of this is the person feeling unwanted or not valued. Multiple fMRI scans have shown that the brain processes rejection in similar parts of the brain that process physical pain. This feeling can escalate to depression, violence, suicide, or be covered up by the usage of drugs. So what’s the trick to overcome this feeling? Mindfulness.
Mindfulness is “maintaining a moment-by-moment awareness of our thoughts, feelings, bodily sensations, and surrounding environment, through a gentle, nurturing lens” (Kabat-Zinn). It is crucial to live in the present moment verses lingering on what could or could not have happened in the past or fearing what could happen in the future.
Dr. Chester and doctoral candidate Alexandra Martelli conducted a study looking at how specific brain circuits are able to help more mindful people cope with rejection, focusing on the connections between the ventrolateral prefrontal cortex (VLPFC), which inhibits negative emotions, with the amygdala and dorsal anterior cingulate cortex (DACC), which generates emotions, with the amygdala and dorsal anterior cingulate cortex (DACC), which generates questionnaire for the scientists to see how mindful they are. The participants returned two weeks later to play a ball-tossing game on a computer that was pre-programmed, but the participants were told that it was other students playing the game. The game started with an equal number of passes and ended by excluding the participant. During this, the participants were in an fMRI scanner, and after the game they were removed from the fMRI scanner and reflected on the experience with another questionnaire of agree and disagree statements.
The outcome of the study was that the people who were proven to be more mindful in the previous questionnaire showed less distress from being excluded during and after the game. The fMRI results showed that the more mindful people had less connections between the VLPFC with the amygdala and the DACC, and overall less activity in the VLPFC. This is due to their accepting the experience of rejection instead of suppressing it. When people overwork their VLPFC by trying to control their emotions or trying to change the way they think about the situations, distress and anger are able to build up, eventually being expressed in a negative way.
Researcher Gaelle Desbordes is currently taking fMRI scans of clinically depressed patients before and after an eight-week course in mindfulness-based cognitive therapy (MBCT) developed by Kabat-Zinn. This included focusing on their heart beats and then reflecting on their negative thoughts, while the control group completed muscle relaxation. Her goal is to better understand mindful meditation and what types of people it can benefit the most in order to provide an alternative way other than medication to treat depression and stress-related disorders. Since mindfulness is commonly associated with the ancient traditions of meditation, Desbordes hope to find out what types of meditation help and the mechanisms behind it.
Mindfulness has shown a lot of other benefits to the body, though it is unknown the exact reasoning on how it works and is challenging to design and execute a well-run study on. Seminal studies have shown that after eight weeks of MBCT, the immune system, blood pressure, sleep, memory, attention, and decision-making are improved. Studies have also shown it helps veterans with PTSD. Ways to incorporate mindfulness into your day are paying attention to your breathing and all the senses that surround you, especially the body’s physical sensations. This can include driving, eating, listening to music, and walking. Focus on your current thoughts and emotions, with the realization that any negative thought or feelings are not permanent. Focus on the moments of the day that provided a positive mindset and provided you a sense of purpose. Write down and observe your thoughts to clear your head if it is hard to understand and focus on the stream of thoughts. Most importantly remember not to reject the next time you get rejected.
Writer: Lauren Renehan
Editor: Samantha Stoker
A large amount of research has demonstrated the power of exercise to support cognitive function, the effects of which can last for considerable time. An emerging line of scientific evidence indicates that the effects of exercise are longer lasting than previously thought – to the extent in which future generations can inherit these effects. The action of exercise on epigenetic regulation of gene expression appears central to building an “epigenetic memory” to influence long-term brain function and behavior. There have been new developments in the epigenetic field connecting exercise with changes in cognitive function, including DNA methylation, histone modifications, and microRNAs (miRNAs). The understanding of how exercise promotes positive long-term cognitive effects is crucial for directing the power of exercise to combat the issue of neurological and psychiatric disorders.
The positive effect of exercise on learning and memory in humans and animals has received abundant support. In older adults, exercise has been shown to improve cognitive performance and counteract the mental decline associated with aging, and these effects have been associated with modifications in hippocampal size. In one study, 21 women between the ages of 67 and 81 participated in exercise for 80 minutes per day. After 24 weeks, their hippocampal volume increased. In children, exercise has been found to be associated with cognitive performance: children who engaged in greater amounts of aerobic exercise generally performed better on verbal, perceptual, and mathematical tests. Recently, a meta-analysis study reported that a single bout of moderate aerobic exercise improves inhibitory control, cognitive flexibility, and working memory in preadolescent children and in older adults, indicating that beyond the well-known effects of long-term exercise on the brain, acute exercise also can be used as a tool for situations demanding high executive control. Interestingly, a single session of both aerobic and resistance exercise has been found to enhance memory consolidation in rats.
Epigenetic research has been centered on the analysis of changes on top of the genome that do not involve alterations in the nucleotide sequence. The two most studied epigenetic mechanisms are covalent modifications of DNA (methylation) or of histone proteins (i.e. acetylation and methylation), and their resulting effects on altering gene expression. The phosphorylation and methylation of histones are also tightly associated with regulation of learning and memory.
In agreement with its role in cognition, physical exercise can coordinate the action of genes involved in synaptic plasticity with resulting effects on memory preservation. For example, while exercise enhances the expression of genes (i.e. Bdnf, igf-1 and creb) that positively regulate memory consolidation, it downregulates genes (i.e. PP1and calcineurin) with a repressive role in these events. Evidence shows that DNA methylation is an important mechanism by which exercise affects gene expression. It is known that exercise differentially modulates the methylation pattern of specific CpG islands located at Bdnf gene, decreases hippocampal expression of DNMTs, attenuates the global methylation changes induced by stress, and increases Bdnf transcription through demethylation of its promoter IV.
It has been shown that the acetylation of histone proteins is a requisite for long term memory . For example, intrahippocampal injection of global HDAC inhibitors enhances long term potentiation. The pro-cognitive function of HDAC is partially attributed to their ability to increase histone acetylation. Interestingly, a previous study has shown that, like HDAC, physical exercise has the ability to transform a learning event that does not normally lead to a stable memory trace into a long-lasting form of memory (Intlekofer et al, 2013). Additionally, it was found that physical exercise increases histone acetylation and reduces HDAC expression and neural activity in the hippocampus.
In a recent study, Zhong et al. (2016) observed that exercise-induced memory improvements were associated with enhanced expression of cAMP response element-binding protein (CREB)-binding protein (CBP) in the hippocampus. Mechanistically, the recruitment of CBP triggers histone acetylation and the formation of a transcriptional complex at the promoters of many CREB-target genes to activate transcription. CBP mutant mice exhibit profound deficits in synaptic plasticity and LTM. Altogether, the aforementioned findings raise the idea that physical exercise promotes synaptic plasticity and memory improvements by altering the balance of HDAC enzymatic activity to favor a permissive state of chromatin, leading to the transcriptional activation of a myriad of genes with preponderant roles in cognition.
College students are known for being arguably the unhealthiest kind of humans. Between studying and managing social lives, exercise and self-care can be neglected despite their obvious importance. Sadly, this neglect might be prohibiting us from performing at our best as students. So, let me ask you this: how are you going to exercise today?
Writer: Kawtar Bennani
Editor: Nathaniel Meshberg
Vitamin B6 is a water-soluble molecule that is involved in many vital body functions such as metabolism of glucose, synthesis of neurotransmitters, immune function, and hemoglobin formation. Adults usually only need around 1.3 mg of vitamin B6 per day, but one study led by Pfeiffer found that taking 240 mg of vitamin B6 before sleep can improve dream recall. The study also concluded that inability to recall dreams can be due to a lack of vitamin B6 in the diet. Ebben et al. (2002) also found that ingesting high doses of vitamin B6 can intensify emotions, color, vividness, and bizarreness of dreams. In this study, 12 participants were asked to take placebo, 100 mg of vitamin B6, and 200 mg of vitamin B6 for five days each with two days washout period between each condition. They found that when people took 100 mg of vitamin B6, their dream salience score was 30% higher than the placebo, and when 200 mg of vitamin B6 was taken, dream salience score was 50% higher. Thus, there seems to be a dose-dependent relationship between vitamin B6 and dream salience. But why does vitamin B6 have this effect? Ebben theorized that vitamin B6 helps synthesize serotonin, which represses REM sleep in the first few hours of sleep, and REM sleep is responsible for dreams that people can remember. As a result, in the last few hours of sleep, there is a REM sleep rebound in which there is a more significant amount of REM sleep with intensified dreaming, leading to higher dream salience. Another theory proposed by Goodenough (1991) was that vitamin B6 also causes a lot of sleep disturbance, leading to frequent wake-ups during sleep. This gives the brain a chance to convert the short-term memory of the dream into long-term memory.
However, one study by Aspy et al. (2018) suggested that vitamin B6 does not increase dream saliency, but only increases the amount of dream content that is recalled. This study used a larger sample size of 100 participants with around 30 people in each group: placebo, vitamin B6, and B complex. Dream recall frequency and dream count were not statistically significant between placebo and vitamin B6 groups; dream recall frequency examines how many people in the sample recall any dreams and dream count tests how many dreams people remember. However, when using the Dream Quantity measure to test significant differences, the vitamin B6 group demonstrated a more significant dream content of 64.1% compared to the placebo group. They also found that vitamin B6 did not have any significant effects on sleep disturbance, sleep quality, or tiredness after waking, discounting Goodenough’s theory. On the other hand, the B complex group did show a significant decrease in sleep quality and increase in tiredness after waking, despite ingesting the same amount of vitamin B6. This indicates that one of the vitamin B counters the effects of vitamin B6; Aspy suggests that it is vitamin B1. This study seems to undermine the effects of vitamin B6 in dream salience and recall; however, there is a limitation to these findings due to the way the study was conducted. Aspy et al. (2018) used different participants in each conditional group, while Ebben et al. (2002) used the same participants in each conditional group. As a result, Ebben’s study can account for the subjective individual differences, and measure the differences more objectively. Nevertheless, Aspy did use a bigger sample size, which may make his data more reliable.
Although more future studies should be conducted to test the effects of vitamin B6 on sleep and dream saliency, there seems to be one strong indication from all these studies: vitamin B6 increases your ability to recall more dream content. The research also suggests that vitamin B6 aids in lucid dreaming, but again, further studies need to be conducted. If you cannot seem to remember any of your dreams after waking up, try increasing the intake of vitamin B6 in your diet with caution, and perhaps you will be able to recall more dreams.
Writer: Audrey Kim
Editor: Sophia Hon
Ebben, M., Lequerica, A., & Spielman, A. (2002). Effects of pyridoxine on dreaming: A preliminary study. Perceptual and Motor Skills, 94, 135–140.
Pfeiffer, C. (1975). The sleep vitamins: Vitamin C, inositol, and Vitamin B-6. In C. Pfeiffer (Ed.), Mental and elemental nutrients. New Canaan, CT: Keats.
Goodenough, D. R. (1991). Dream recall: History and current status in the field. In S. J. Ellman & J. S. Antrobus (Eds), The mind in sleep: Psychology and psychophysiology (2nd ed.). Oxford, England: John Wiley.
Aspy, D. J. (2018). Effects of Vitamin B6 (Pyridoxine) and a B complex preparation on Dreaming and Sleep. Perceptual and Motor Skills. 0(0), p 1-12