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A pioneering study conducted by leading researchers at the University of Sheffield has revealed blood types play a role in the development of the nervous system and may cause a higher risk of developing cognitive decline.

The research, carried out in collaboration with the IRCCS San Camillo Hospital Foundation in Venice, shows that people with an ‘O’ blood type have more grey matter in their brain, which helps to protect against diseases such as Alzheimer’s, than those with ‘A’, ‘B’ or ‘AB’ blood types.

Research fellow Matteo De Marco and Professor Annalena Venneri, from the University’s Department of Neuroscience, made the discovery after analysing the results of 189 Magnetic Resonance Imaging (MRI) scans from healthy volunteers.

The researchers calculated the volumes of grey matter within the brain and explored the differences between different blood types.

The results, published in The Brain Research Bulletin, show that individuals with an ‘O’ blood type have more grey matter in the posterior proportion of the cerebellum.

In comparison, those with ‘A’, ‘B’ or ‘AB’ blood types had smaller grey matter volumes in temporal and limbic regions of the brain, including the left hippocampus, which is one of the earliest part of the brain damaged by Alzheimer’s disease.

These findings indicate that smaller volumes of grey matter are associated with non-‘O’ blood types.

As we age a reduction of grey matter volumes is normally seen in the brain, but later in life this grey matter difference between blood types will intensify as a consequence of ageing.

“The findings seem to indicate that people who have an ‘O’ blood type are more protected against the diseases in which volumetric reduction is seen in temporal and mediotemporal regions of the brain like with Alzheimer’s disease for instance,” said Matteo DeMarco.

“However additional tests and further research are required as other biological mechanisms might be involved.”

Professor Annalena Venneri added: “What we know today is that a significant difference in volumes exists, and our findings confirm established clinical observations. In all likelihood the biology of blood types influences the development of the nervous system. We now have to understand how and why this occurs.”

Source: Amy Pullan – University of Sheffield
Image Credit: The image is credited to the researchers and is adapted from the press release
Original Research: Abstract for “‘O’ blood type is associated with larger grey-matter volumes in the cerebellum” by Matteo De Marco and Annalena Venneri in Brain Research Bulletin. Published online June 03 2015 doi:10.1016/j.brainresbull.2015.05.005

Abstract

‘O’ blood type is associated with larger grey-matter volumes in the cerebellum

Recent evidence indicated higher incidence of cognitive deficits in ABO blood-type system ‘AB’ individuals. Since this statistical difference might originate from the lack of protective effects exerted by ‘O’ alleles on the brain via vascular or non-vascular routes, this study investigated volumetric differences in grey matter between ‘O’ and non-‘O’ adults to explore the possibility of a structural endophenotype visible in ‘O’ adults without cognitive impairment or neurodegeneration.

A large sample of cognitively healthy adults who had previously undergone structural MRI for research purposes were contacted telephonically and enquired about their ABO blood type. Out of the 189 individuals who were able to retrieve and communicate this information, ‘O’ (n = 76) and ‘A’ adults (n = 65) were included in Model 1. In Model 2, all non-‘O’ (n = 113) were instead collapsed in a single group. Voxel-Based Morphometry analyses were carried out on three-dimensional T1-weighted scans, and between-sample t tests were run to compare the maps of grey-matter volumes of the subgroups of interest, controlling for major nuisance variables.

In Model 1, ‘O’ adults had larger grey-matter volumes in two symmetrical clusters within the posterior ventral portion of the cerebellum. This was confirmed in Model 2. Additionally, non-‘O’ adults showed lower volume values in temporal and limbic regions, including the left hippocampus.

The cerebellar clusters were located in regions previously found to be part of a network responsible for sensorimotor integration. It is speculated that the structural reductions seen in non-‘O’ adults might result in a susceptibility to down-regulation of this network. This occurrence is likely to intensify along the ageing process and may contribute to foster cognitive decline. Although Model 2 seems to suggest that having a ‘O’ blood type might play a role in protection against those conditions in which temporal and mediotemporal volumetric loss is observed (Alzheimer’s disease), additional supporting evidence is needed.

A number of potential biological processes might sustain these between-group differences, including sensorimotor ontogenesis, hormonal function, and a regional impact of cerebral amyloid angiopathy. These findings identify the cerebellar tissue as a candidate for further studying ABO function, and support a general association between ABO blood type and variance in the development of the nervous system.

“‘O’ blood type is associated with larger grey-matter volumes in the cerebellum” by Matteo De Marco and Annalena Venneri in Brain Research Bulletin. Published online June 03 2015 doi:10.1016/j.brainresbull.2015.05.005

Summary: Yesterday, the Nobel Assembly at the Karolinska Institute announced the 2017 Nobel Prize for Physiology or Medicine is to be awarded jointly to Jeffrey C. Hall, Michael Rosbash and Michael W. Young for their work unraveling the molecular mechanisms behind circadian rhythm.

Source: NobelPrize.org.

The Nobel Assembly at Karolinska Institutet has today decided to award the 2017 Nobel Prize in Physiology or Medicine jointly to Jeffrey C. Hall, Michael Rosbash and Michael W. Young for their discoveries of molecular mechanisms controlling the circadian rhythm.

Life on Earth is adapted to the rotation of our planet. For many years we have known that living organisms, including humans, have an internal, biological clock that helps them anticipate and adapt to the regular rhythm of the day. But how does this clock actually work? Jeffrey C. Hall, Michael Rosbash and Michael W. Young were able to peek inside our biological clock and elucidate its inner workings. Their discoveries explain how plants, animals and humans adapt their biological rhythm so that it is synchronized with the Earth’s revolutions.

Using fruit flies as a model organism, this year’s Nobel laureates isolated a gene that controls the normal daily biological rhythm. They showed that this gene encodes a protein that accumulates in the cell during the night, and is then degraded during the day. Subsequently, they identified additional protein components of this machinery, exposing the mechanism governing the self-sustaining clockwork inside the cell. We now recognize that biological clocks function by the same principles in cells of other multicellular organisms, including humans.

With exquisite precision, our inner clock adapts our physiology to the dramatically different phases of the day. The clock regulates critical functions such as behavior, hormone levels, sleep, body temperature and metabolism. Our wellbeing is affected when there is a temporary mismatch between our external environment and this internal biological clock, for example when we travel across several time zones and experience “jet lag”. There are also indications that chronic misalignment between our lifestyle and the rhythm dictated by our inner timekeeper is associated with increased risk for various diseases.

Our inner clock

Most living organisms anticipate and adapt to daily changes in the environment. During the 18th century, the astronomer Jean Jacques d’Ortous de Mairan studied mimosa plants, and found that the leaves opened towards the sun during daytime and closed at dusk. He wondered what would happen if the plant was placed in constant darkness. He found that independent of daily sunlight the leaves continued to follow their normal daily oscillation. Plants seemed to have their own biological clock.

Other researchers found that not only plants, but also animals and humans, have a biological clock that helps to prepare our physiology for the fluctuations of the day. This regular adaptation is referred to as the circadian rhythm, originating from the Latin words circa meaning “around” and dies meaning “day”. But just how our internal circadian biological clock worked remained a mystery.

Identification of a clock gene

During the 1970’s, Seymour Benzer and his student Ronald Konopka asked whether it would be possible to identify genes that control the circadian rhythm in fruit flies. They demonstrated that mutations in an unknown gene disrupted the circadian clock of flies. They named this gene period. But how could this gene influence the circadian rhythm?

This year’s Nobel Laureates, who were also studying fruit flies, aimed to discover how the clock actually works. In 1984, Jeffrey Hall and Michael Rosbash, working in close collaboration at Brandeis University in Boston, and Michael Young at the Rockefeller University in New York, succeeded in isolating the period gene. Jeffrey Hall and Michael Rosbash then went on to discover that PER, the protein encoded by period, accumulated during the night and was degraded during the day. Thus, PER protein levels oscillate over a 24-hour cycle, in synchrony with the circadian rhythm.

A self-regulating clockwork mechanism

The next key goal was to understand how such circadian oscillations could be generated and sustained. Jeffrey Hall and Michael Rosbash hypothesized that the PER protein blocked the activity of the period gene. They reasoned that by an inhibitory feedback loop, PER protein could prevent its own synthesis and thereby regulate its own level in a continuous, cyclic rhythm.

The model was tantalizing, but a few pieces of the puzzle were missing. To block the activity of the period gene, PER protein, which is produced in the cytoplasm, would have to reach the cell nucleus, where the genetic material is located. Jeffrey Hall and Michael Rosbash had shown that PER protein builds up in the nucleus during night, but how did it get there? In 1994 Michael Young discovered a second clock gene, timeless, encoding the TIM protein that was required for a normal circadian rhythm. In elegant work, he showed that when TIM bound to PER, the two proteins were able to enter the cell nucleus where they blocked period gene activity to close the inhibitory feedback loop.

Such a regulatory feedback mechanism explained how this oscillation of cellular protein levels emerged, but questions lingered. What controlled the frequency of the oscillations? Michael Young identified yet another gene, doubletime, encoding the DBT protein that delayed the accumulation of the PER protein. This provided insight into how an oscillation is adjusted to more closely match a 24-hour cycle.

The paradigm-shifting discoveries by the laureates established key mechanistic principles for the biological clock. During the following years other molecular components of the clockwork mechanism were elucidated, explaining its stability and function. For example, this year’s laureates identified additional proteins required for the activation of the period gene, as well as for the mechanism by which light can synchronize the clock.

Keeping time on our human physiology

The biological clock is involved in many aspects of our complex physiology. We now know that all multicellular organisms, including humans, utilize a similar mechanism to control circadian rhythms. A large proportion of our genes are regulated by the biological clock and, consequently, a carefully calibrated circadian rhythm adapts our physiology to the different phases of the day (Figure 3)nd highly dynamic research field, with implications for our health and wellbeing.

Source: ACES/University of Illinois.

For most preschool-age children, picky eating is just a normal part of growing up. But for others, behaviors such as insisting on only eating their favorite food item–think chicken nuggets at every meal–or refusing to try something new might lead to the risk of being over- or underweight, gastrointestinal distress, or other eating disorders later in childhood.

Parents and other caregivers often deem children as being “picky eaters” for a variety of reasons, but there is not a hard-fast definition in place for research. Nutrition and family studies researchers at the University of Illinois have collaborated for the last 10 years to understand the characteristics of picky eaters and to identify possible correlations of the behavior.

In a new study, the researchers wanted to see if chemosensory genes might have a possible relationship to picky eating behavior in young children. They found that certain genes related to taste perception may be behind some of these picky eating habits.

“For most children, picky eating is a normal part of development,” says Natasha Cole, a doctoral student in the Division of Nutritional Sciences at U of I and lead author of the study. “But for some children, the behavior is more worrisome.” Cole, also part of the Illinois Transdisciplinary Obesity Prevention Program at U of I, hopes the research can help identify the determinants of picky eating behavior in early childhood.

Leading up to the taste perception genes study, the U of I researchers identified common characteristics of picky eaters, ages 2 to 4 years, and divided these “types” of picky eaters into distinct groups. Further research from the team looked at how parenting styles may affect picky eating behavior and whether children exhibit picky eating behavior both at home and in childcare–homecare or center-based–situations.

“This has kind of been an evolution of the research, seeing an interaction rather than just seeing the child as on its own, which, when we first started trying to define a picky eater, we were just looking at the child,” explains Soo-Yeun Lee, a professor in the Department of Food Science and Human Nutrition at U of I. “As we were moving into different parts of the research we realized, it’s not just the child, it’s the caregiver and the environment, as well.”

Now, they are looking at the influence of “nature and nurture” on a child’s picky eating behavior.

“Natasha is actually taking a deeper look at the child and genetic predisposition,” Lee says. “She is looking at sensory taste genes and also at some of the behavioral genes that have been highlighted in the literature. She has been looking at the whole field of picky eating research, and classifying it based on ‘nature vs. nurture.’ Nature is the genetic disposition and nurture is the environment and the caregivers.”

The idea, Lee explains, is based on an orchid/dandelion hypothesis. “There are some genes–the behavioral genes–that make the child more prone and more sensitive to being more behaviorally problematic when external influences are present that may not work out their way. That’s the orchid concept. This may be a sensitive child who may not be as resilient with negative feedback or negative mealtime strategies given by parents, versus a dandelion child who is very robust and resistant to whatever, nurture or not, is given to them.

“There is that fine line, and it’s not just the nurture, the environment, that’s influencing that, but it’s the child’s susceptibility to the environmental cues as well,” she adds.

For the study, the researchers collected information about breastfeeding history and picky eating behaviors, such as limited food variety, food refusals, and struggles for control, for 153 preschoolers, as reported by their caregivers. Saliva samples were also taken for DNA extraction and genotyping.

The researchers looked at genetic variation in single nucleotide polymorphisms (SNPs, pronounced “snips”) from five candidate genes related to taste perception. Of the five, they found that two had an association with picky eating behaviors in the preschoolers. One (TAS2R38) was associated with limited dietary variety, and the other (CA6) with struggles for control during mealtime.

Interestingly, both the TAS2R38 and CA6 genes are possibly related to bitter taste perception. So it is not surprising that the children who are genetically “bitter-sensitive” may be more likely to be picky eaters (i.e. turning down Brussel sprouts or broccoli). Other chemosensory factors, such as odor, color, and texture, may affect eating behaviors as well. Further studies are needed to see how children’s food preferences are affected by the look or smell of their food.

Along with continuing to look at genetic associations with picky eating, Cole is also interested in understanding how picky eating behaviors start even in children before 2 years of age. Most picky eating research has focused on children over 2 years, but eating habits begin to form before then. She and the research team recently published another study that reviews the research literature on picky eating in children younger than 2 years. The study discusses picky eating associations from an ecological model, starting with the child, and moving out to the child’s environment.

“By two years, children know how to eat and have pretty set habits,” Cole says. “There is a huge gap in the research when children transition from a milk-based diet to foods that the rest of the family eats.”

Cole adds that the research involving children under 2 years shows that 22 percent of those children are perceived as picky eaters by their parents or caregivers. Surprisingly, she also found that each additional month of the child’s age was associated with an increase in food-related fussiness. “So a child could go from rarely being a picky eater to being a frequent picky eater in less than a year,” she says.

Collecting and integrating this comprehensive information from “Cell to Society” is critical to better understand nature-nurture interactions, as many questions in this area remain unsolved, explains Margarita Teran-Garcia, an assistant professor in nutritional sciences, human development and family studies, and the Carle Illinois College of Medicine at the U of I, and co-author of the paper.

Funding: Funding provided by NIH/National Institute of Food and Agriculture, US Department of Agriculture, Illinois Council for Agriculture Research, University of Illinois Health and Wellness Initiative.

Source: Stephanie Henry – ACES/University of Illinois
Image Source: NeuroscienceNews.com image is credited to ACES/University of Illinois.
Original Research: Abstract for “Variants in Chemosensory Genes Are Associated with Picky Eating Behavior in Preschool-Age Children” by Cole N.C., Wang A.A., Donovan S.M., Lee S.-Y., Teran-Garcia M., and the STRONG Kids Team in Journal of Nutrigenetics and Nutrigenomics. Published online October 2017 doi:10.1159/000478857

Abstract

Variants in Chemosensory Genes Are Associated with Picky Eating Behavior in Preschool-Age Children

Background/Aims: Picky eating is prevalent among preschoolers and is associated with risk of both underweight and overweight. Although differences in taste perception may be due to genetic variation, it is unclear whether these variations are related to picky eating behavior. The aim of this study was to investigate the association of 6 single nucleotide polymorphisms (SNPs) in 5 candidate genes related to chemosensory perception with picky eating behavior and adiposity in a cohort of preschool-aged children.

Methods: Parents of 2- to 5-year-old non-Hispanic white preschoolers (n = 153) responded to survey questions on demographics, and information regarding their child’s breastfeeding history and picky eating behavior. Height and weight were measured to calculate body mass index (BMI) z-scores using standard growth charts, and saliva was collected for genotyping. Generalized linear models were used to examine associations between picky eating behavior and BMI z-scores with genetic variation.

Results: When controlling for child age, sex, breastfed status, and parent education level, SNPs in TAS2R38 (rs713598) and CA6 (rs2274327) were associated with picky eating behavior in children. There was no association between SNPs and BMI z-scores.

Conclusion: Genes related to chemosensory perception may play a role in children’s picky eating behavior.

“Variants in Chemosensory Genes Are Associated with Picky Eating Behavior in Preschool-Age Children” by Cole N.C., Wang A.A., Donovan S.M., Lee S.-Y., Teran-Garcia M., and the STRONG Kids Team in Journal of Nutrigenetics and Nutrigenomics. Published online October 2017 doi:10.1159/000478857