Ours is the first study describing
how brain genes affect food intake and dietary preferences in a group of healthy people.»
Not exact matches
2) As to Neanderthal they did not have the
brain capacity (Steve Olson, Mapping Human History:
Genes, Race, and Our Common Origins (New York: Houghton Mifflin Co., 2002), to wonder, thus not the first Adam 3) Nicodemus went to Jesus in the dark of night and Jesus said «I have spoken to you of earthly things and you do not believe so
how can you believe when I speak of heavenly things».
The
genes in the network are thought to be involved in
how brain cells communicate with each other.
15 years after a
gene defect was found to increase the risk of schizophrenia 30-fold, scientists have figured out
how it might cause the
brain disorder's debilitating symptoms
«The key point here is that we can say something about
how the
gene acts to influence this behavior — that is, is by functioning as a chemical messenger in cells that control this behavior in the
brain.
Now a
gene that causes such disorders has been found, and it may help unravel a deeper mystery:
how it is that the left side of our
brain controls the right side of the body, and vice versa.
The study, which is published in the journal Molecular Psychiatry, describes a possible mechanism for
how the
gene variant produces clinical symptoms by affecting levels of specific proteins in the
brain.
To learn
how the rats»
genes had changed in response to the
brain injury, the researchers analyzed
genes from five animals in each group.
We're funding researchers to investigate
how drugs alter what
genes are activated such that they modify the function of the cells, and
how this, in turn, modifies the functions of
brain circuits, and
how that modifies behavior.
Page and his colleagues, who use animal models to understand
how autism risk factors impact the developing
brain and to identify potential treatments for the condition, have found that animals with mutations in the autism risk
gene phosphatase and tensin homolog (Pten) mimic aspects of autism, including increased
brain size, social deficits and increased repetitive behavior.
But
how did the human
brain get larger than that of our closest living relative, the chimpanzee, if almost all of our
genes are the same?
For them, the discovery of
how an individual becomes gay is likely to shed light on
how sexuality - related
genes build
brains,
how people of any persuasion are attracted to each other, and perhaps even
how homosexuality evolved.
«Enigmatic
gene critical for a healthy
brain: New research has shown
how an unusual
gene is needed for
brain development in young mice.»
Over the past 15 years, the GFP
gene has enabled scientists to watch a plethora of previously murky biological processes in action:
how nerve cells develop in the
brain,
how insulin - producing beta cells form in the pancreas of an embryo,
how proteins are transported within cells, and
how cancer cells metastasize through the body.
The researchers found that adolescents who had a variation of another
gene, which contributes to
how quickly serotonin is recycled in the
brain and which has been linked to hostile behavior in children, were more likely to exhibit signs of psychopathy.
«We used the Allen Human
Brain Atlas data to quantify how consistent the patterns of expression for various genes are across human brains, and to determine the importance of the most consistent and reproducible genes for brain function.&r
Brain Atlas data to quantify
how consistent the patterns of expression for various
genes are across human
brains, and to determine the importance of the most consistent and reproducible
genes for
brain function.&r
brain function.»
The Duke researchers who made this discovery say it may help explain
how a relatively small number of
genes can create the dazzling array of different cell types found in human
brains and the nervous systems in other animals.
Now, an international team of scientists has made inroads to understanding
how genes influence
brain structure and cognitive abilities and
how neural circuits produce language.
DNA studies have zeroed in on various
genes, including the glucocorticoid receptor
gene, that dictate
how intensely our
brains and bodies react to stress.
«Determining the role of ZNF804A is the first step in understanding
how schizophrenia - associated
genes contribute to abnormal
brain development,» said Mao.
Establishing links between
genes, the
brain and human behavior is a central issue in cognitive neuroscience research, but studying
how genes influence cognitive abilities and behavior as the
brain develops from childhood to adulthood has proven difficult.
The newly unmasked
genes play a role in three distinctively different bodily functions, including systems that control inflammation and cholesterol and the regulation of
how brain cells clean up toxic proteins.
Recent research also has illuminated
how the deadly cascade that leads to
brain atrophy is set in motion: The buildup of amyloid plaques, working in tandem with certain
gene mutations, sparks the formation of the renegade tau proteins.
To test this hypothesis, an international team led by evolutionary biologist Philipp Khaitovich of the Shanghai Institutes for Biological Sciences in China and the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, set out to see
how many
brain - related
genes implicated in schizophrenia underwent positive natural selection since humans and chimpanzees diverged from a common ancestor between 5 million and 7 million years ago.
The observation could explain
how a
gene that specifies a particular behavior can adapt to accommodate changes in
brain circuitry that happen over evolutionary time.
The researchers investigated 16 groups of female and male mice offspring exposed to maternal diet - induced obesity and male hormone excess and studied
how these environmental factors affected the mice's behaviour as well as
gene expression in the
brain.
How do brains grow, how do genes build complicated nervous syste
How do
brains grow,
how do genes build complicated nervous syste
how do
genes build complicated nervous systems?
Researchers say that future studies could look at
how changes in these
genes may bring about this risk of — or resilience — to
brain injury.
When multiple maps are overlaid, patterns begin to emerge that show
how different regions of the
brain activate specific and often discrete complements of
genes.
How do these imprinted
genes related to
brain function fit into the scheme of intersexual warfare?
Researchers have identified a group of immune system
genes that may play a role in
how long people can live after developing a common type of
brain cancer called glioblastoma multiforme, a tumor of the glial cells in the
brain.
Led by Matthew P. Anderson, MD, PhD, Director of Neuropathology at BIDMC, the scientists determined
how a
gene linked to one common form of autism works in a specific population of
brain cells to impair sociability.
«They help us to understand
how the FOXP2
gene might have been important in the evolution of the human
brain and direct us towards neural mechanisms that play a role in speech and language acquisition.»
For example, one
gene might determine
how quickly the gut lets the
brain know that it is full.
«In this study, we wanted to determine where in the
brain this social behavior deficit arises and where and
how increases of the UBE3A
gene repress it,» said Anderson, who is also an Associate Professor in the Program in Neuroscience at Harvard Medical School and Director of Autism BrainNET Boston Node.
It also remains unclear
how knocking down expression of certain
genes in zygotes via sperm miRNA leads to altered stress response in adult animals and altered
gene expression in the
brain.
It was just a decade ago that Hariri and colleagues at the National Institutes of Health published what is widely considered the first study linking a particular
gene to
how our
brains work.
Scientists have begun to leverage new methods to decipher
how mutations in these disparate
genes might converge to exert their effects in the developing
brain.
But specifically
how human variants of such
genes shape our
brain in development — and
how they drove its evolution — have remained largely mysterious.
Researchers believe they have learned
how mutations in the
gene that causes Huntington's disease kill
brain cells, a finding that could open new opportunities for treating the fatal disorder.
At a symposium at The American Society of Human Genetics here last month, they reported zooming in on the
genes expressed in a single
brain cell, as well as panning out to understand
how genes foster connections among far - flung
brain regions.
The newly created Paul G. Allen Frontiers Group has selected four initial researchers — Jennifer Doudna of the University of California (UC), Berkeley, Ethan Bier of UC San Diego, James Collins of the Massachusetts Institute of Technology in Cambridge, and Bassem Hassan of the
Brain and Spine Institute in Paris — to receive $ 1.5 million each to study topics ranging from novel techniques for
gene editing,
how shapes and forms arise over the course of evolution, and
how synthetic biology can create microbes that trap and kill dangerous bacteria.
I was fascinated to read
how the double duplication of the SRGAP2
gene, which helps drive development of the
brain's neocortex, appears to have propelled our ancestors» development at two distinct times during the past few million years (12 May, p 10).
To understand
how DIXDC1 mutations put normal
brain function at risk, Cheyette's team turned to mutant mice that lacked a functioning copy of the
gene.
Over the past decade, Michael Meaney, a neurobiologist at McGill University, and his colleagues have been producing one of the most detailed studies of
how experience can reprogram the
brain's
genes.
For example, scientists have not been able to resolve what function the HTT
gene serves normally, or
how its mutation creates problems in the
brain.
In his talk, Wieland Huttner, a molecular cell biologist and developmental neurobiologist at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI - CBG) in Dresden, Germany, explained
how his team searched databases for proteins and other
gene products expressed in the human
brain in these earliest phases of development.
They then exposed the mice to light and studied
how it affected
genes within the
brain.
Using novel technologies developed at HMS, the team looked at
how a single sensory experience affects
gene expression in the
brain by analyzing more than 114,000 individual cells in the mouse visual cortex before and after exposure to light.
Howard Hughes Medical Institute (HHMI) scientists have profiled key features of the genetic material inside three types of
brain cells and found vast differences in the patterns of chemical modifications that affect
how the
genes in each type of neuron are regulated.