For a Healthier 2018!

Dancing together is good for your health!


By Jesica Levingston Mac leod, PhD


Social dancers know the amazing feeling that a synchronized dance could bring. When your follower or leader is connected and it feels like you are one mind and body following the music, it is mystical and magical… Well, it turns out that synchronized dancing is also good for your health. I started dancing salsa because a good friend was going crazy about it and she recommended it, this inspired me to join a class. At this point I was a solitary belly dancer only following in team dances where you have choreography and if you are coordinated enough you feel this celestial connection with the other dancers…but without any physical contact.

On the other hand, in social dances like salsa, bachata, tango, zouk or swing, the connection is the base of a good dance. Nobody wants to be the person stepping to the left when 5 other dancers moved to the right while performing in a stage in front of hundreds of people, as well as nobody enjoys turning to the wrong side for misreading your dance partner lead, or watching how a follower does a completely different step that the one the leader indicated. Furthermore, being “in sync” with the group or your direct dance partner may help to improve your health, science says. In a nutshell, a recent study found that synchronizing with others while dancing raised pain tolerance and encouraged people to feel closer to others.

This year, Dr. Burzynska et al., at Colorado State University, separated 174 healthy adults, 60s to 79 years old, who had no signs of memory loss or impairment, into 3 activity groups: walking, stretching and balance training, or dance classes. The activities were carry on for 6 months and three times a week, those in the dance group practiced and learned a country dance choreography. Brain scans were done on all participants and compared with scans taken before the activities began. Not surprisingly, the participants in the dancing group performed better and had less deterioration in their brains than the other groups. Their most recent study published in November: “The Dancing Brain: Structural and Functional Signatures of Expert Dance Training” showed that dancers’ brains differed from non-dancers’ at both functional- and structural-levels. Most of the group differences were skill-relevant and correlated with objective laboratory measures of dance skill and balance. Their results are promising in that long-term, versatile, combined motor and coordination training may induce neural alterations that support performance demands.” (link 2)

Moreover, It is well established that dancing-based therapies are providing outstanding results in the treatment of dementia, autism and Parkinson’s. Indeed, dance therapy improves motor and cognitive functions in patients with Parkinson’s disease. Dancing was suggested to be a powerful tool to improve motor-cognitive dual-task performance in adults. Dance movement therapy has known benefits for cancer patients’ physical and psychological health and quality of lifeAnother study by Domane and collaborators, working with a cohort of overweight and physically inactive women, showed that Zumba fitness is indeed an efficacious health-enhancing activity for adults. Park also concluded that “a 12-week low- to moderate-intensity exercise program appears to be beneficial for obese elderly women by improving risk factors for cardiovascular disease”.

Dancing helps generate positive connections with others and this is one of the evolutionary reasons you are “called” to the dance floor when a song you like starts playing, and probably you will start your dance by coordinating with or copying others. Probably this behavior signaled tribe membership for early humans and also got couples together in a more romantic way, creating emotional bonds. Coordinated dances are as old as music, and distributed in a lot of different cultures, for example, the nowadays Hakka, used by rugby players, was a native group dance that intimidates rival tribes.

Talking about the chemistry of dancing, as any other exercise, it releases endorphins (the hormones of happiness and pain relief). For example, a study from the University of London were anxiety-sufferers enrolled in one of four settings: exercise class, a music class, a math class and a dance class, showed that only the last group displayed “significantly reduced anxiety.”

In the most recent study done in the same London University by Tarr and collaborators, the researchers used pain thresholds as an indirect measure of endorphin realize (more endorphins mean we tolerate pain better) for 264 young people in Brazil. The volunteers were divided into groups of three, and they did either high or low-exertion dancing that was either synchronized or unsynchronized. The high exertion moves were standing, full-bodied movements, on the other hand, in the low-exertion groups did small hand movements sitting down. They measured the before and after feelings of closeness to each other via a questionnaire and their pain threshold by attaching and inflating a blood pressure cuff on their arm, and determining how much pressure they could stand.

Most of the volunteers who did full-bodied exertive dancing had higher pain thresholds compared with those who were in the low-exertion groups. Most importantly, synchronization led to higher pain thresholds, even if the synchronized movements were not exertive. Therefore when the volunteers saw that others were doing the equivalent movement at the same time, their pain thresholds increased.

The results also showed that synchronized activity encouraged bonding and closeness feelings more than unsynchronized dancing. Therefore, “Dance which combined high energy and synchrony had the greatest effects. So the next time you find yourself in an awkward Christmas party or at a wedding wondering whether or not to get up and groove, just do it”, claims Dr. Tarr.

Coming back to the dance floor, I had reached out for an opinion about the wellness of dancing to the best Bachata DJ: Brian el Matatan: “I enjoy the dancing for a few reasons. There’s the enjoyment & challenge of using what I’ve learned; socially as well as choreographed performance. Also, there is the rush of endorphins similar to “runner’s high”. There’s also the socializing aspect of dancing. It’s like having a conversation without speaking.” Well said DJ!
He also offered some advice for followers: dance with many different types of leaders if you’d like to improve your following. There are many different leads, and there is an experience to be gained in social dancing that would not be gained via dance class. Also, feel free to ask a leader to dance, & be courteous in how you decline a dance. Most importantly- communicate. Don’t “lead” a leader into thinking their lead is better than what it really is- for your sake & that of your fellow followers. For example, if he almost ended your life with that risky move, let him know so that he doesn’t try it on you or anyone else again (at least not without figuring out how to do the move properly). And some advice for leaders: be VERY  courteous in how you ask for a dance, try to not take rejection personally, be patient with follows who may not be on the same skill level as you, & don’t almost end her life with risky moves.

Lastly, I asked for the most sensual dancer, scientist, and project manager –  Debbie McCabe – for her advice for followers. She commented “The lady’s job is to surrender and connect to her partner…it is a 3-minute love affair and energy exchange. I love Bachata because I can get out of my head and just feel, express my sensuality, be playful and connect… it balances out my left brained day job.”

More than 20 years ago, scientists found a connection between music and enhancement of performance or changing of neuropsychological activity involving Mozart’s music from which the theory of “The Mozart Effect” was derived. The basis of The Mozart Effect lies at the super-organization of the cerebral cortex that might resonate with the superior architecture of Mozart’s music. Basically listening to Mozart K.448 enhances performance on spatial tasks for a period of approximately 20 min.

So dear reader, please stop complaining and making excuses and just dance! Or at least listen to music, as the outstanding jazz singer Tamar Korn once told me when I was in distress “music heals”.


This post was originally published on Dec 30, 2015 and was updated with new research on Dec 12, 2016 and on Dec 19, 2017.

Is the Fountain of Youth in the Blood of Youth?


By Elaine To

Although the rumors of the Countess of Bathory bathing in virgin blood to restore her beauty are unfounded, there may actually be scientific merit in the myth. In two separate publications in the same issue of Science, researchers investigating aging have shown that blood, brain, and muscle tissues in elderly mice can be regenerated by the GDF11 protein found in the blood of young mice.

The researchers begin by creating parabiotic pairs of mice who are joined surgically to share a circulatory system. Pairs were created between mice of the same age (isochronic) or different ages (heterochronic), resulting in young-young (Iso-Y), old-old (Iso-O), or young-old pairs (Het-Y and Het-O). The young mice were 2 months of age and the old mice were 15 months old. After 5 weeks of being surgically joined, the mice were separated and their characteristics analyzed for the hallmarks of aging. Throughout the study, the Iso-O mice are compared to the Iso-Y and Het-Y to understand the effects of aging. Then the Het-O mice are compared to the other three and they are found to consistently resemble the Iso-Y and Het-Y mice more closely than the Iso-O mice.

In the first publication, the researchers focus on effects on neural and vascular cell and tissue regeneration. Neural progenitor cells identified by Ki67, Sox2, and Olig2 markers are noticeably decreased in the Iso-O mice, and Het-O mice recover these cell populations. Examining the olfactory bulb revealed that Iso-O mice have fewer newborn neurons, and Het-O mice have more than the Iso-O mice, though they don’t quite recapitulate neuron counts of the Het-Y and Iso-Y mice. When mice were exposed to small amounts of an aroma, the Iso-O mice ignored the stimulus while both the Het-O and Iso-Y mice spent time exploring the scent. This indicates that the Het-O and Iso-Y mice had greater sensitivity towards the smell.

Examining vasculature in the brain showed that Iso-O mice had lower blood vessel volume than Iso-Y and Het-Y mice, whereas Het-O mice were similar to Iso-Y and Het-Y. Iso-O mice also have much decreased cerebral blood flow versus Iso-Y, which is equal between Het-O and Iso-Y mice.

It became clear that the regeneration factor was in the blood serum, and GDF11 was identified as the responsible protein. 21-month old mice treated with GDF11 had increased blood vessel volume and Sox2 progenitor cells versus the untreated controls. GDF11 also increased the number of phosphor-SMAD2/3+ cells, showing that GDF11 acts through the SMAD/TGF beta signaling pathway.

The second publication focused on muscular degeneration in elderly mice. The stem cells responsible for muscle regeneration, especially after injury, are known as satellite cells. The Iso-Y, Het-Y, and Het-O mice had greater amounts of satellite cells than the Iso-O. Aging satellite cells were also associated with increased DNA damage and phosphorylation of histone H2AX. The Het-Y, Iso-Y, and Het-O mice had much less of both as compared to the Iso-O mice.

Treating elderly mice with GDF11 increased the frequency of satellite cells and decreased their DNA damage versus the untreated mice. There were also more regenerating muscle fibers after an injury. Electron micrographs of muscles showed fewer swollen mitochondria and more regular muscle fiber patterning in the GDF11 treated mice. There were greater amounts of PGC-1alpha, a regulator of mitochondrial biogenesis, and a greater LC3-II over LC3-I ratio, indicating enhanced autophagy. Lastly, the GDF11 treated mice had greater endurance while running and demonstrated greater grip strength.

This collection of papers provides strong evidence for GDF11’s ability to regenerate neurons, blood vessels, and muscles. While it may have potential to greatly improve quality of life for elderly individuals, further studies must first prove that these effects occur in humans as well and examine long term effects.

Disclaimer: we do not condone bathing in the blood of virgins, or anyone else for that matter!


Yoda and the Science of Aging in the Star Wars Universe


By Evelyn Litwinoff


The first time I saw the Star Wars movies, I could not take Yoda seriously. Having grown up watching and loving the muppets, Yoda sounded too much like Fozzy Bear to be a Jedi Master. I kept waiting for him to add “wakka wakka” to the end of his nonsensical sentences and break out into song and dance.


If you think about it, Yoda is certainly an interesting creature. His species is never defined, we don’t know much about his childhood background, he has a crazy long lifespan, and he’s two feet tall yet a powerful fighter. So as homage to Yoda from a scientist’s perspective, I’d like to play a game with you. Let’s pretend Yoda lives in our universe and use our science prowess to figure out how on earth, excuse me, on Dagobah, he lived to be 900 years old without getting cancer.


When thinking about mechanisms behind aging, the first thing that comes to mind is telomeres. A telomere is a non-coding DNA sequence that serves as a protective “cap” on the end of a chromosome. (A chromosome is essentially a condensed string of DNA.) Every time a cell replicates it makes a copy of its DNA to pass on to the new cell. However during the process of replication, the new DNA copy loses some of the sequence on the end of the chromosome. In order to prevent losing important DNA sequence, the telomere sequence comes after the important DNA sequence so it is the telomere sequence that gets shorter with each replication. When telomeres become too short, which is usually by the end of the organisms’ lifespan, the cells are considered old and will die, eventually resulting in the death of the whole organism.


This leads us to idea #1: Yoda must have super long telomeres so it would take centuries for these telomeres to shorten and cause death. This issue with this hypothesis is that absolute length of telomeres does not necessarily correlate with longer lifespan. For instance, mice telomeres are longer than humans telomeres, but mice have a lifespan of 3-5 years, which is way shorter than human lifespan. Vera et al suggested that instead of telomere length, rate of telomere shortening more accurately correlates with lifespan, i.e., the slower the rate of telomere shortening, the longer the lifespan. So let’s alter idea #1 to idea #2: Yoda had super long telomeres with a super slow rate of telomere shortening.


Now telomeres can be elongated by the enzyme telomerase. So it would be possible that in addition to having long telomeres with a slow shortening rate, Yoda could also have high levels of telomerase. However, overexpressing telomerase in mice leads to the development of cancer, and as far as I know, Yoda didn’t have any tumors or chemotherapy during his lifetime. Interestingly, there is a body of literature on telomerase in cancer resistant mice. How fascinating is that! These cancer resistant mice have a mutated tumor suppressor gene, p53, which prevents development of cancer cells. In this cancer resistant environment, telomerase overexpression leads to a longer, healthier lifespan.


This led me to wonder, do any species have naturally occurring mutations that make them resistant to cancer (and would this species be similar to Yoda)? Scizzle to the rescue! Apparently, naked mole rats have fibroblasts (cells that produce fibers such as collagen) that secrete cancer killing signaling molecules, which makes these mole rats resistant to cancer! (For those interested, they took the media from cultured naked mole rat fibroblasts and used it to culture breast cancer and liver cancer cells. These cancer cells were unable to survive with the mole rat fibroblast media, although they did survive with media from cultured mouse fibroblasts.) So what is different about these naked mole rat fibroblasts? Although the mechanism of cancer resistance is not fully worked out, it is known that there are mutations in the naked mole rat p53 gene that increase DNA repair mechanisms and cell cycle arrest, but promote apoptosis (cell death). These mutations are believed to have evolved to promote survival in hypoxic (low oxygen) environments, where naked mole rats live.


Let’s bring this back to Yoda. If Yoda’s lifespan is due to long telomeres with a slow rate of telomere shortening, it is possible that Yoda has constitutively active telomerase in order to keep the telomeres in tact. However, if he had high levels of telomerase and no signs of cancer, he must also be cancer resistant. Since we just learned that naked mole rats are naturally cancer resistant and this may be related to their hypoxic environment, could Yoda’s environment make him cancer resistant? Towards the end of his life, Yoda lives in a swamp: definitely not a hypoxic environment. Furthermore his end of life environment wouldn’t explain how he survived all those years before arriving to Dagobah. Since we don’t know all that much about Yoda’s childhood, let’s get creative here. We do know that Yoda lives and breathes with the force just like the rest of his species. So maybe the force is a stream of hypoxic energy that altered his species’ genes to make them cancer resistant. This fits well with the fact that all members of his species we know about are Jedi, and Jedi are known to have longer lifespans.


Our study of Yoda and telomeres gives us an idea of how Yoda lived to be 900 years old without developing cancer. Of note, this discussion is based on the major motion pictures, not the Expanded Universe. But, if you are well versed in this expanded media franchise, I’d love to hear your scientific take on aging in the Star Wars universe!




Mitochondrial Clues for a Long Life


By Thalyana Smith-Vikos

Biological clocks that can predict an individual’s lifespan more accurately than chronological time alone have been proposed in multiple molecular, cellular and genetic contexts, but a single clock has yet to be identified. Mitochondria, however, have been identified as promising candidates for a biological aging clock in many organisms. Dong and colleagues report that mitochondrial function in Caenorhabditis elegans young adults provides a highly accurate predictive measure of eventual longevity of individual nematodes.

By visualizing quantal mitochondrial flashes, or mitoflashes, in vivo, the authors were able to show that this optical readout was specific to free-radical production and metabolic rate at the single-mitochondrion level. These mitoflashes exhibited a strong correlation with C. elegans aging and had similar attributes in a mammalian system. Mitoflash measurements in pharyngeal muscles peaked during active reproduction and when the first nematodes began dying off. The mitoflash activity on day 3 of adulthood during active reproduction explained up to 59% of lifespan variation. Day 3 mitoflash frequency was negatively correlated with future lifespan of individual C. elegans, and this negative correlation persisted in the face of various genetic and environmental alterations that extend or shorten lifespan. The authors further showed that day 3 mitoflash frequency was due to glyoxylate cycle activity, and they propose that mitochondrial activity not only predicts but also determines lifespan, as the lifespan of long-lived insulin receptor mutants was at least partially explained by decreased mitochondrial production of superoxide.

These findings indicate that mitochondria can function as a biological clock that predicts lifespan of individual C. elegans in various contexts. Importantly, this clock has already begun ticking very early in life, as mitochondrial flashes in early adulthood during active reproduction have been shown to be most potent predictors of future longevity.


Forever Young?


Sally Burn

Embryos and the young can repair tissue injuries faster than adults in many different species. Wolverine, the lupine superhero of Marvel Comics, is a mutant who has harnessed this regenerative power, allowing him to rapidly heal any wound and also to age slower than mere mortals. While this may be the stuff of comic books, a new Cell paper from the lab of George Daley at Harvard University has reported a mouse mutant with uncannily similar traits.

Researchers in Daley’s lab genetically engineered mice to post-natally produce Lin28a, an RNA-binding protein usually only active in embryos, where it is involved in tissue repair. The effects of postnatal retention of this protein were breathtaking. Much like Wolverine the mice were huge, hairy, and with an increased healing capacity. The authors got a massive shock when they carried out ear and toe clipping (both standard identification procedures): the tissue grew back. Regenerative ability varied between tissues though, indicating that Lin28a has tissue-dependent effects. Excessive hair growth was evident throughout life, and shaved mutant mice regrew hair faster than unmodified mice. Tissue removed during ear clipping also grew back in adults, whereas toe regrowth was only enhanced in juveniles; once they reached adulthood they lost their ability to regenerate toes. Cardiac tissue, however, could never be restored by reactivating Lin28a, suggesting that the heart may have mechanisms to resist regeneration.

Lin28a was already known to be expressed in embryonic stem cells and to play roles in cancer development. This new study shows that it is also a regulator of the ability to repair tissue damage. This ability lessens with age, as does production of Lin28a. Adults genetically modified to produce Lin28a retain an embryonic-like ability to heal, suggesting that the biological age of their cells has somehow been reset. The mechanism for resetting is not absolutely clear but the authors show that metabolism is increased in the Lin28a-producing cells, as indicated by heightened levels of oxidative enzymes required for mitochondrial function. Adult cells in which Lin28a is reactivated appear to revert to a juvenile bioenergetic state.

Harnessing Lin28a activity for therapeutic purposes in the injured or elderly is unlikely to be straightforward. Lin28a is involved in many cellular processes and increasing levels would produce many side-effects. Directly targeting the metabolic processes downstream of Lin28a may therefore be a better option. Indeed, the authors found that taking this approach in non-mutant mice replicated the effects seen in the Lin28a-producing mice. The giants of the cosmetics industry are probably now falling over themselves to target these pathways in a bid to make the ultimate anti-aging cream. Let’s just hope they iron out the excessive hair growth effects before any product hits the market…


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From Trials to Practice – Improving Health Outcomes of the Elderly


Thalyana Smith-Vikos


Disabilities that limit mobility diminish quality of life for many seniors and represent a major burden on the healthcare system. The Yale Claude D. Pepper Older Americans Independence Center

is investigating whether physical activity and exercise can prevent these disabilities as part of the largest clinical trial of its kind.

The trial is just the latest in more than two decades of research by the Pepper Center, which is dedicated to improving the lives of the elderly by studying the complex issues they face.

“This is a landmark study that could provide the evidence needed to establish exercise programs more widely throughout the country, in senior centers, YMCAs and other community settings,” stated Pepper Center Director Dr. Thomas Gill.

The Pepper Center, along with the Yale Program on Aging, has enrolled 200 participants and is one of eight LIFE Study sites around the country. Each of the participants has been enrolled for a minimum of two years, with some individuals receiving continuous exercise training or health education for four years.

The physical activity intervention primarily focuses on moderate-paced walking, but also addresses methods for improving gait, balance and muscle strengthening. The major assessment has been to observe improvements in mobility every six months by asking each participant to walk without assistance around a ¼ mile-long course.

Participants have been using exercise facilities at Southern Connecticut State University or Choate Rosemary Hall in Wallingford, CT, while the health education classes occur at either Albertus Magnus College or Ashlar Village in Wallingford.  The Program on Aging evaluates changes in participants’ cognition, risk of injury from falling, and risk of hospitalization due to myocardial infarction, congestive heart failure or other serious health conditions.

In total, the LIFE Study has been following 1635 men and women aged 70-89, who are receiving either a physical activity intervention or a health education intervention. The LIFE Study is in its third year, and Gill expects that the trial will be completed by the end of 2013. The research is funded by the National Institute on Aging (NIA) and the National Heart, Lung and Blood Institute (NHLBI).

The Operations Core reached out to participants through mailing lists for persons 70 years or older in the Greater New Haven, CT area.

“We received an excellent response for participation in the LIFE Study; in fact, we completed recruitment about one month earlier than expected,” Gill said. “Not only do we have an outstanding field operation to recruit people to the LIFE Study, but we have also had very few dropouts and are by far the top performing site out of the eight research sites. This is truly a testament to the Program on Aging’s dedicated research staff.”

Field research by the Operations Core is by far the largest component of the Program on Aging and the Pepper Center. As many as 60 researchers may be collecting data at any one time in a variety of field sites, although this fluctuates with the number of projects being simultaneously funded.

A large percentage of the research staff is composed of nurses who have an extensive background in clinical research. They are responsible for collecting data in many different venues, such as hospitals, nursing homes, participants’ homes, flu clinics, and a clinic assessment space in the Temple Medical Building. With direction from Peter Charpentier, data from dozens of studies are organized and delivered to the Biostatistics Core to be analyzed.

The Yale Pepper Center was first established in 1992 to investigate complex geriatric conditions. Researchers employ laboratory and clinical findings to discover root causes of geriatric conditions. The goal is to develop and test preventative treatments and to help doctors make better decisions when dealing with elderly patients.

The Pepper Center has been at the forefront of advancing the field of aging research, by instituting interdepartmental collaborations and publishing breakthrough research that has directly affected health outcomes of older individuals. True to its success, the Yale Pepper Center, currently one of 13 sites across the country, has been continuously funded by the National Institutes of Health (NIH) since its inception. Effective on June 1, the Pepper Center began its fifth consecutive renewal cycle from 2013-2018.

The new funding cycle will mark the beginning of an initiative to translate research findings from the Pepper Center into everyday practices to improve the welfare of older Americans. This research initiative, directed by Dr. Mary Tinetti, who also led the Pepper Center for its first 19 years, will focus on analyzing the findings generated by various field studies and applying these results to “real world” practices in the community, hospitals and nursing homes, so they can be of use for physicians, patients and their families.

Tinetti has extensive experience in implementing clinical findings into real world practice. An international expert on fall prevention research in older persons, Tinetti previously investigated the risk factors and precipitants that contribute to falls, and developed and tested interventions which successfully reduced falls in older persons participating in a clinical trial. Together with Dr. Dorothy Baker and other researchers, she then worked to incorporate these interventions into a variety of settings in the Greater Hartford, CT area, which resulted in significantly reducing the likelihood of serious fall injuries in these individuals.

“We are well-positioned based on Dr. Tinetti’s previous studies and expertise to develop an outstanding Dissemination and Implementation Core, which will distinguish the Yale Pepper Center from the 12 other Pepper Centers across the country,” Gill commented. “The other trials being conducted here will follow the model Dr. Tinetti has in place to translate research from traditional randomized clinical trials into real world clinical practice.”




Leafing Through The Literature

Thalyana Smith-Vikos

Highlighting recently published articles in molecular biology, genetics, and other hot topics


Aging is inherited maternally


Credit: Bob AuBuchon (Flickr)
Credit: Bob AuBuchon (Flickr)

Ross and colleagues investigated how mitochondrial DNA (mtDNA) mutations, which are exclusively maternally inherited, can contribute to aging. The researchers found that these mutations result in mild aging in otherwise wild-type mice, while decreasing fertility and accelerating premature aging in respectively heterozygous and homozygous PolgA mutants with increased mtDNA mutations. Additionally, maternal and somatic mtDNA mutations also resulted in brain developmental disorders. The authors posit that aging tissues may arise from the rapid expansion of mutated respiratory chain factors as mutated mtDNA replicates.


MicroRNAs regulate micro food portions

Vora et al. have identified a conserved microRNA (miRNA), miR-80, which regulates dietary restriction in C. elegans. Similar to dietary restriction-mediated effects, these mir-80 mutant worms are long-lived and maintain a healthy state for a prolonged period, regardless of the presence of food. Transcription factors DAF-16 and HSF-1 and transcription co-factor CBP-1 are required for these mir-80 mutant phenotypes. Expression of this miRNA is decreased when worms are subjected to a restricted diet, resulting in increased levels of CBP-1.


A fatty reward

Credit: Quinn Dombrowski (Flickr)
Credit: Quinn Dombrowski (Flickr)

Researchers have proposed that lowered dopaminergic function from a high-fat diet leads to obesity by promoting excessive food intake to restore this food-reward relationship. Tellez et al. further investigated how a high-fat diet can affect dopamine levels. The authors identified an intestinal lipid messenger, oleoylethanolamine, which is normally suppressed under a high-fat diet but can restore dopamine release upon administration. Additionally, administration of oleoylethanolamine increased consumption of low-fat foods, indicating that this signaling molecule may be responsible for promoting reward of low-fat foods.


Pathogen-host relationship therapy

C. albicans can exist as part of the non-pathogenic gastrointestinal microbiota or can be pathogenic to mammals. Pande and colleagues report that, while this pathogenic switch is due to the host’s suppressed immune system, a microbial genetic program is also at play. The researchers found that passage of C. albicans through the gut results in a switch to commensalism, driven by the transcription factor Wor1. These C. albicans cells that have transitioned into a commensal state are phenotypically different and express a unique transcriptome. The findings suggest that disrupting this genetic program results in reversion to a pathogenic state.


Breakthrough in wheat stem rust resistance

A highly resistant race of wheat stem rust, Ug99, has been plaguing wheat production areas all over the world for a number of years. Saintenac et al. report that the Sr35 gene cloned from T. monococcum provides near resistance to Ug99 and similar races, and the gene can be successfully transferred to polyploidy wheat. Periyannan et al. similarly identified a resistance gene, Sr33, which was cloned from another wild relative, A. tauschii. Both Sr33 and Sr35 encode coiled-coil, nucleotide-binding, leucine-rich repeat proteins that resemble other pathogen resistance proteins.


Transcribing autism genes

King and colleagues have provided a link to a recent correlation between mutated topoisomerases in individuals with autism and other autism spectrum disorders (ASDs). The researchers showed that a topoisomerase inhibitor, topotecan, reduces the expression of ASD-associated genes in a dose-dependent manner. Intriguingly, these ASD candidate genes are substantially longer than other genes on average. Topectan specifically prevents transcriptional elongation of extremely long genes (>200 kb), which was also achieved by knocking down topoisomerase 1 or 2b in neurons.

Can Protein Synthesis Protect Against Alzheimer’s?

Celine Cammarata

For many, the name Alzheimer’s Disease brings to mind plaques, tangles, and a vague knowledge that these somehow sicken neurons to cause a crippling dementia.  This week, Ma et al. demonstrated that part of that “somehow” lies in dysregulation of protein synthesis.  It makes sense: long term memory requires synthesis of new proteins, while Alzheimer’s Disease (AD)  involves deficits in memory.  Earlier work supports the idea.  The protein eukaryotic initiation factor 2 α (eIF2α) is a general regulator of translation, and when eIF2α is phosphorylated most translation is inhibited.  AD in human patients has been associated with increased eIF2α phosphorylation.  Thus, the researchers reasoned, inhibiting some of the proteins that phosphorylate eIF2α might help alleviate some of the diseases effects.

The investigators chose the protein PERK, one of several able to phosphorylate eIF2α, and bred Continue reading “Can Protein Synthesis Protect Against Alzheimer’s?”

A Marvelous Month of Science

Stephanie Swift

Taking vitamin supplements might not be as healthy as you think

Antioxidant vitamins, like vitamin C and E, are thought to boost health by reducing the creation of DNA-damaging free radicals that can contribute to the ageing process. In lab mice, there is some suggestion that vitamin supplements can extend lifespan, but since laboratory-bred mice are genetic clones, such studies may bear little relevance to a hugely genetically diverse human population.

Giving wild animals, such as the short-tailed field vole, either vitamin C or E supplements has now been shown to have a less positive impact on health. Continue reading “A Marvelous Month of Science”

Leafing through the Literature

Thalyana Smith-Vikos

Avian Influenza Transmission in Mammals

Avian influenza viruses can reassort their genomes to infect mammals. To investigate how this is done, Zhang et al. generated all possible 127 reassorted viruses by combining the hemagglutinin gene of an avian H5N1 influenza virus with an H1N1 virus capable of infecting humans. The researchers examined the virulence of these viruses in mice, as well as their ability to transmit in guinea pigs, which, like certain livestock, have both avian and mammalian airway receptors. Certain H1N1 genes allowed the H5N1 virus to transmit between guinea pigs. The virus was transferred by respiration between guinea pigs without killing them, indicating that livestock could be carriers of this virus without the farmer even knowing. Continue reading “Leafing through the Literature”