#Mind-controlled BMW i3 driven in tron-like car insurance campaign As part of a British car insurance marketing campaign,
and to keep you safe while saving money on your car insurance. Using a modified BMW i3 electric car,
the team of Moneysupermarket has given lucky members of the public the opportunity to be trained brain
and drive the car through an electroencephalography (EEG) headset manufactured by Emotiv. The BMW was fitted with a mechanical rig capable of pressing the pedals and turning the steering wheel on command
while the drivers received an EEG neuro headset to monitor their brain activity while being trained to remotely drive the car.
The driverstraining involved thinking left, right, and about going forward and stopping. However, instead of simply thinking about the actions and movements, the training involves associating a specific mental image with each command.
According to this Dailymail article, the software can be trained to associate a person thinking about a floating balloon with turning left.
Each time the driver thinks of the floating balloon their brain signals are the same, and it is these signals that are ranslatedinto commands.
Those selected to take the driver seat are judged on the track by a series of variables.
This includes statistics fed back by a telematics box in the car reporting on how safely
and accurately they drive, a technology system used to calculate fair premiums and save drivers money on car insurance policies.
Accuracy, smoothness and lap time feeds into a bespoke formula to generate a score that they can take away with them,
along with the pride of being one of the very first mind-control drivers. For those who didn have the chance to drive the mind-controlled BMW on 16 july,
Moneysupermarket has created also a mobile game controlled using facial recognition and gestures using their phone camera n
#Using Thought to Control a Robotic Arm The next generation of neuroprosthetics: More natural, effortless, intuitive movement achieved.
Paralyzed from the neck down after suffering a gunshot wound when he was 21, Erik G. Sorto now can move a robotic arm just by thinking about it
and using his imagination. Through a clinical collaboration between Caltech, Keck Medicine of USC and Rancho Los Amigos National Rehabilitation Center, the now 34-year-old Sorto is the first person in the world to have a neural
prosthetic device implanted in a region of the brain where intentions are made, giving him the ability to perform a fluid handshaking gesture,
the motor cortex, can allow patients with paralysis to control the movement of a robotic limb.
the clinical trial was led by principal investigator Richard Andersen, the James G. Boswell Professor of Neuroscience at Caltech, neurosurgeon Charles Y. Liu, professor of neurological surgery, neurology,
and biomedical engineering at USC, and neurologist Mindy Aisen, chief medical officer at Rancho Los Amigos. Andersen and his colleagues wanted to improve the versatility of movement that a neuroprosthetic can offer to patients by recording signals from a different brain region other than the motor cortex, i e.,
, the posterior parietal cortex (PPC), a high-level cognitive area. In earlier animal studies, the Andersen lab found that it is here
and the details of the movementuch as lift the arm, extend the arm, grasp the cup,
The device was implanted surgically in Sorto brain at Keck Hospital of USC in April 2013
and he since has been training with Caltech researchers and staff at Rancho Los Amigos to control a computer cursor
and a robotic arm with his mind. The researchers saw just what they were hoping for:
The Surgery The surgical team at Keck Medicine of USC performed the unprecedented neuroprosthetic implant in a five-hour surgery on April 17, 2013.
Liu and his team implanted a pair of small electrode arrays in two parts of the posterior parietal cortex,
Each 4-by-4 millimeter array contains 96 active electrodes that in turn, each record the activity of single neurons in the PPC.
The arrays are connected by a cable to a system of computers that process the signals,
to decode the brain intent and control output devices, such as a computer cursor and a robotic arm. hese arrays are very small so their placement has to be exceptionally precise,
and it took a tremendous amount of planning, working with the Caltech team to make sure we got it right,
and associate chief medical officer at Rancho Los Amigos. ecause it was the first time anyone had implanted this part of the human brain,
everything about the surgery was different: the location, the positioning and how you manage the hardware.
Keep in mind that what wee able to dohe ability to record the brain signals and decode them to eventually move the robotic arms critically dependent on the functionality of these arrays,
which is determined largely at the time of surgery. The USC Neurorestoration Center primary mission is to leverage partnerships to create unique opportunities to translate scientific discoveries into effective therapies. e are at a point in human research where we are making huge strides in overcoming a lot of neurologic disease,
says neurologist Christianne Heck, associate professor of neurology at USC and co-director of the USC Neurorestoration Center. hese very important early clinical trials could provide hope for patients with all sorts of neurologic problems
that involve paralysis such as stroke, brain injury, ALS and even multiple sclerosis. The Rehabilitation Sixteen days after his implant surgery, Sorto began his training sessions at Rancho Los Amigos National Rehabilitation Center,
where a computer was attached directly to the ports extending from his skull, to communicate with his brain.
The rehabilitation team of occupational therapists who specialize in helping patients adapt to loss of function in their upper limbs
and edesignthe way patients do tasks with the function they have left, worked with Sorto
and the Caltech team daily to help Sorto visualize what it would be like to move his arm again. t was a big surprise that the patient was able to control the limb on day one he very first day he tried,
Andersen says. his attests to how intuitive the control is when using PPC activity. Although he was able to immediately move the robot arm with his thoughts,
such as controlling a computer cursor; drinking a beverage; making a handshaking gesture; and performing various tasks with the robotic arm.
Aisen, the chief medical officer at Rancho Los Amigos who led the study rehabilitation team, says that advancements in prosthetics like these hold promise for the future of patient rehabilitation. e at Rancho are dedicated to advancing rehabilitation and to restoration of neurologic function through new technologies,
which can be assistive or can promote recovery by capitalizing on the innate plasticity of the human nervous system,
also a clinical professor of neurology at the Keck School of medicine of USC. his research is relevant to the role of robotics and brain-machine interfaces as assistive devices,
We have created a unique environment that can seamlessly bring together rehabilitation, medicine, and science as exemplified in this study.
He says the study has inspired him to continue his education and pursue a master degree in social work. his study has been very meaningful to
Andersen says. hat we have here is a unique window into the workings of a complex high-level brain area,
The implanted device and signal processors used in the Caltech-led clinical trial were the Neuroport Array
and Neuroport Bio-potential Signal Processors developed by Blackrock Microsystems in Salt lake city, Utah. The robotic arm used in the trial was the Modular Prosthetic Limb,
developed at the Applied Physics laboratory at Johns Hopkins. Sorto was recruited to the trial by collaborators at Rancho Los Amigos National Rehabilitation Center and at Keck Medicine of USC.
Keck Medicine of USC team members include Brian Lee, Christianne Heck, Sandra Oviedo, Paul Kim,
researchers at the University of Virginia School of medicine have determined that the brain is connected directly to the immune system by vessels previously thought not to exist.
and treatment of neurological diseases ranging from autism to Alzheimer disease to multiple sclerosis. nstead of asking,
hy do multiple sclerosis patients have the immune attacks? now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels,
said Jonathan Kipnis, Phd, professor in the UVA Department of Neuroscience and director of UVA Center for Brain Immunology and Glia (BIG).
But apparently they have not. ery Well Hidden The discovery was made possible by the work of Antoine Louveau
The vessels were detected after Louveau developed a method to mount a mouse meninges the membranes covering the brain on a single slide
Harris, a Phd, is an assistant professor of neuroscience and a member of the BIG center.
Alzheimer, Autism, MS and Beyond The unexpected presence of the lymphatic vessels raises a tremendous number of questions that now need answers, both about the workings of the brain and the diseases that plague it.
For example, take Alzheimer disease. n Alzheimer, there are accumulations of big protein chunks in the brain,
Kipnis said. e think they may be accumulating in the brain because theye not being removed efficiently by these vessels.
so the role they play in aging is another avenue to explore. And there an enormous array of other neurological diseases, from autism to multiple sclerosis, that must be reconsidered in light of the presence of something science insisted did not exist u
#Growing Eyes From Stem Cells Embryonic stem cells give rise to three-dimensional, multilayered retinal tissue in a dish.
The achievement brings scientists a step closer to growing the most complex component of the eyehe eye neural tissuend could enable doctors to repair damaged eyes with lab-grown retinal tissue.
Yoshiki Sasai, Mototsugu Eiraku and their colleagues from the RIKEN Center for Developmental biology had shown previously that they could coax human
which resides at the boundary between the neural retina and the retinal pigment epithelium. Their stepwise nduction-reversalculture method induces the formation of boundary tissue,
This degree of cellular organization is the closest scientists have yet come to building self-growing retinal tissue from stem cells. ur results are consistent with the current view that the retinal pigment epithelium
and his colleagues could one day be used to culture tissue that can be transplanted into a human retina damaged by conditions such as macular degeneration and retinitis pigmentosa,
which lead to blindness. he protocol developed here allows us to generate retinal tissue that closely resembles the biological retina with high efficiency and stability,
notes lead author Atsushi Kuwahara. t is a step closer to realizing regenerative medicine for retinal disorders. ource:
RIKENIMAGE Credit: The image is credited to Nature Communicationsoriginal Research: Abstract for eneration of a ciliary margin-like stem cell niche from self-organizing human retinal tissueby Atsushi Kuwahara, Chikafumi Ozone, Tokushige Nakano, Koichi Saito, Mototsugu Eirak
First, we developed a culture method for selective NR differentiation by timed MP4 treatment. We then found that inhibiting GSK3
and FGFR induced the transition from NR tissue to retinal pigment epithelium (RPE), and that removing this inhibition facilitated the reversion of this RPE-like tissue back to the NR fate.
#Disruption of Delicate Chemical Balance Implicated as a Cause of Schizophrenia Scientists produce strongest evidence yet of schizophrenia causes.
Researchers discover that risk mutations disrupt a delicate chemical balance in the brain, responsible for brain development and function.
An international team of scientists led by Cardiff University researchers has provided the strongest evidence yet of
what causes schizophrenia a condition that affects around 1%of the global population. Published today in the journal Neuron,
their work presents strong evidence that disruption of a delicate chemical balance in the brain is implicated heavily in the disorder.
the team found that disease-linked mutations disrupt specific sets of genes contributing to excitatory and inhibitory signalling, the balance
The breakthrough builds on two landmark studies led by members of the Cardiff University team, published last year in the journal Nature. ee finally starting to understand what goes wrong in schizophrenia,
says lead author Dr Andrew Pocklington from Cardiff University MRC Centre for Neuropsychiatric Genetics and Genomics. ur study marks a significant step towards understanding the biology underpinning schizophrenia,
which is an incredibly complex condition and has up until very recently kept scientists largely mystified as to its origins. e now have
what we hope is a pretty sizeable piece of the jigsaw puzzle that will help us develop a coherent model of the disease,
while helping us to rule out some of the alternatives. reliable model of disease is needed urgently to direct future efforts in
developing new treatments, which haven really improved a great deal since the 1970s. Professor Hugh Perry, who chairs the Medical Research Council Neuroscience and Mental health Board said:
his work builds on our understanding of the genetic causes of schizophrenia unravelling how a combination of genetic faults can disrupt the chemical balance of the brain. cientists in the UK,
as part of an international consortium, are uncovering the genetic causes of a range of mental health issues, such as schizophrenia. n the future,
this work could lead to new ways of predicting an individual risk of developing schizophrenia
and form the basis of new targeted treatments that are based on an individual genetic makeup.
Researchers studying psychiatric disorders have suspected previously that disruption of this balance contributes to schizophrenia. The first evidence that schizophrenia mutations interfere with excitatory signalling was uncovered in 2011 by the same team,
based at Cardiff University MRC Centre for Neuropsychiatric Genetics and Genomics. This paper not only confirms their previous findings,
but also provides the first strong genetic evidence that disruption of inhibitory signalling contributes to the disorder.
To reach their conclusions scientists compared the genetic data of 11,355 patients with schizophrenia against a control group of 16,416 people without the condition.
They looked for types of mutation known as copy number variants (CNVS), mutations in which large stretches of DNA are deleted
Comparing the CNVS found in people with schizophrenia to those found in unaffected people the team was able to show that the mutations in individuals with the disorder tended to disrupt genes involved in specific aspects of brain function.
The disease-causing effects of CNVS are suspected also to be involved in other neurodevelopmental disorders such as intellectual disability, Autism Spectrum Disorder and ADHD.
Around 635,000 people in the UK will at some stage in their lives be affected by schizophrenia.
The estimated cost of schizophrenia and psychosis to society is around £11. 8 billion a year.
The symptoms of schizophrenia can be extremely disruptive, and have a large impact on a person ability to carry out everyday tasks,
such as going to work, maintaining relationships and caring for themselves or others a
#Deficiency of Specific Protein in Brain Blood vessels Increases Risk for Alzheimer Disease New study finds that PICALM protein regulates removal of toxic plaques from brain.
Sientists at the Keck School of medicine of USC have discovered that a protein known as PICALM regulates removal of toxic plaques from the brain,
which could be a potential therapeutic target for the treatment of Alzheimer disease. In a study that appeared in a recent edition of Nature Neuroscience,
researchers identify this new role for PICALM, which is known a genetic risk factor for Alzheimer disease.
Alzheimer is the most common type of dementia characterized by the loss of memory and other mental abilities linked to an accumulation of amyloid-beta and other toxic compounds in the brain.
The study found that a deficiency in PICALM in cerebral blood vessels and in PICALM-related gene variants associated with increased risk for Alzheimer,
disable amyloid-beta from being cleared out of the brain across a region known as the blood-brain barrier. here have been many new genes discovered to be associated with Alzheimer disease,
but the biology of these genes are understood poorly, said the study principal investigator Berislav Zlokovic, director of the Zilkha Neurogenetic Institute and holder of the Mary Hayley and Selim Zilkha chair for Alzheimer Disease research at the Keck School of medicine. ur new study shows that a deficiency in PICALM in blood vessels
and its variants associated with increased risk for the disease inactivate amyloid-beta clearance from the brain,
leading to its accumulation and cognitive impairment. This new study provides fundamental new information about PICALM
and brings to light novel potential therapeutic targets for increasing amyloid-beta clearance in Alzheimer disease.
Autopsies from Alzheimer patients and recent research in experimental models have shown the importance of brain blood vessels in the disease initiation and progression.
Molecular mechanisms For more than two decades Zlokovic and his research team have studied the cellular and molecular mechanisms of brain blood vessels that maintain normal cognition with hopes of developing new treatments for Alzheimer and other neurodegenerative diseases.
One focus of their lab at the Zilkha Neurogenetic Institute is on PICALM, or phosphatidylinositol binding clathrin assembly protein,
which in humans is encoded by the PICALM gene. By performing a neuropathological study in humans with Alzheimer
and using transgenic animals to model the disease, the group found that low levels of PICALM in brain endothelial cells lead to amyloid-beta accumulation in the brain.
Genetic variants associated with the PICALM gene have been shown to increase the risk of Alzheimer disease.
The researchers also generated human endothelial cells from induced pluripotent stem cells to examine the consequences of a known PICALM variant associated with increased risk for Alzheimer;
they found that this genetic alteration disrupted amyloid-beta clearance by cerebral blood vessels. These new findings have prompted Zlokovic to address new questions about the role of PICALM in Alzheimer.
Future studies will explore how genetic flaws in the PICALM gene influence its expression levels
and clearance function at the blood-brain barrier and the general health of cerebral blood vessels. The team also will work on developing therapeutic strategies,
including gene therapy, and screening for new drugs to overcome PICALM deficiency e
#DNA Breakage Underlies Learning and Age Related Neurodegeneration The process that allows our brains to learn
and generate new memories also leads to degeneration as we age, according to a new study by researchers at MIT.
The finding, reported in a paper published today in the journal Cell, could ultimately help researchers develop new approaches to preventing cognitive decline in disorders such as Alzheimer disease.
Each time we learn something new, our brain cells break their DNA, creating damage that the neurons must immediately repair, according to Li-Huei Tsai, the Picower Professor of Neuroscience and director of the Picower Institute for Learning and Memory at MIT.
This process is essential to learning and memory. ells physiologically break their DNA to allow certain important genes to be expressed,
Tsai says. n the case of neurons, they need to break their DNA to enable the expression of early response genes,
which ultimately pave the way for the transcriptional program that supports learning and memory, and many other behaviors.
Slower DNA repair However, as we age, our cellsability to repair this DNA damage weakens, leading to degeneration,
Tsai says. hen we are young, our brains create DNA breaks as we learn new things,
Tsai says. ut during aging, and particularly with some genetic conditions, the efficiency of the DNA repair system is compromised, leading to the accumulation of damage,
and in our view this could be very detrimental. In previous research into Alzheimer disease in mice, the researchers found that even in the presymptomatic phase of the disorder,
neurons in the hippocampal region of the brain contain a large number of DNA lesions, known as double strand breaks.
To determine how and why these double strand breaks are generated, and what genes are affected by them,
They applied a toxic agent to the neurons known to induce double strand breaks and then harvested the RNA from the cells for sequencing.
according to the paper lead author Ram Madabhushi, a postdoc in Tsai laboratory. hen we knocked down this enzyme,
even though conventional wisdom dictates that DNA lesions are very bad as this amagecan be mutagenic
and sometimes lead to cancer it turns out that these breaks are part of the physiological function of the cell,
Previous research has shown that the expression of genes involved in learning and memory is reduced as people age.
a professor of genetics and neurology at Harvard Medical school who was involved not in the research. he work elegantly links DNA strand break formation by the enzyme topoisomerase IIß to the temporal control of transcription,
providing the most compelling evidence to date that this is a core transcriptional control mechanism, he says. anticipate that this advance will have broad implications ranging from the basic biology of transcription to pathological mechanisms involved in diseases such as Alzheimer disease
#Reprogramming of DNA Obeserved in Human Germ cells for First time A team of researchers led by the University of Cambridge has described for the first time in humans how the epigenome the suite of molecules attached to our DNA that switch our genes on and off is erased comprehensively in early primordial germ cells prior to the generation of egg
and sperm. However, the study, published today in the journal Cell, shows some regions of our DNA including those associated with conditions such as obesity
and schizophrenia resist complete reprogramming. A team of researchers led by the University of Cambridge has described for the first time in humans how the epigenome the suite of molecules attached to our DNA that switch our genes on
and off is erased comprehensively in early primordial germ cells prior to the generation of egg and sperm.
and schizophrenia resist complete reprogramming. Although our genetic information the ode of lifeis written in our DNA,
our genes are turned on and off by epigenetic witches For example, small methyl molecules attach to our DNA in a process known as methylation
and contribute to the regulation of gene activity, which is important for normal development. Methylation may also occur spontaneously or through our interaction with the environment for example
periods of famine can lead to methylation of certain genes and some methylation patterns can be potentially damaging to our health.
Almost all of this epigenetic information is erased, however in germ cells prior to transmission to the next generation.
Professor Azim Surani from the Wellcome Trust/Cancer Research UK Gurdon Institute at the University of Cambridge, explains:
It like erasing a computer disk before you add new data. hen an egg cell is fertilised by a sperm,
Within the blastocyst, some cells are reset to their master state becoming stem cells, which have the potential to develop into any type of cell within the body.
Professor Surani and colleagues showed that a process of reprogramming the epigenetic information contained in these primordial germ cells is initiated around two weeks into the embryo development
These scapeeregions of the genome contain some genes that are particularly active in neuronal cells,
However, data analysis of human diseases suggests that such genes are associated with conditions such as schizophrenia, metabolic disorders and obesity.
Walfred Tang, a Phd student who is the first author on the study, adds: ur study has given us a good resource of potential candidates of regions of the genome where epigenetic information is passed down not just to the next generation but potentially to future generations, too.
We know that some of these regions are the same in mice, too, which may provide us with the opportunity to study their function in greater detail. pigenetic reprogramming also has potential consequences for the so-called ark matterwithin our genome.
As much as half of human DNA is estimated to be comprised of etroelements regions of DNA that have entered our genome from foreign invaders including bacteria and PLANT DNA.
Some of these regions can be beneficial and even drive evolution for example some of the genes important to the development of the human placenta started life as invaders.
says Professor Surani. In fact, the researchers found that a notable fraction of the retroelements in our genome are scapeesand retain their methylation patterns particularly those retroelements that have entered our genome in our more recent evolutionary history.
This suggests that our body defence mechanism may be keeping some epigenetic information intact to protect us from potentially detrimental effects.
Source: Craig Brierley University of Cambridgeimage Credit: The image is credited to the researchers/Celloriginal Research:
Full open access research for Unique Gene Regulatory Network Resets the Human Germline Epigenome for Developmentby Walfred W c. Tang, Sabine Dietmann, Naoko Irie, Harry
and chromatin reorganization volutionarily young and hazardous retrotransposons remain partially methylated ome demethylation resistant loci are candidates for epigenetic inheritancesummary Resetting of the epigenome in human primordial germ cells (hpgcs) is critical
revealing potential for transgenerational epigenetic inheritance that may have phenotypic consequences. We provide comprehensive insight on early human germline transcriptional network
and epigenetic reprogramming that subsequently impacts human development and disease. Unique Gene Regulatory Network Resets the Human Germline Epigenome for Developmentby Walfred W c. Tang
#Researchers Discover Initiation Mechanism for Dendritic Spines Researchers from the University of Helsinki, ETH Zürich,
Aix-Marseille and the German Mouse Clinic teamed up to investigate the initiation process of dendritic spines.
In many central nervous system diseases, the dendritic spine density is altered. nderstanding of the molecular mechanisms underlying the initiation process of dendritic spines enables us to manipulate their initiation rate and density.
this knowledge can be helpful in the development of therapeutic interventions for neurological diseases underlined by altered dendritic spine density, such as autism spectrum disorder, Schizophrenia or Alzheimer's disease.
Furthermore, this will help us to understand the molecular basis of learning, as new spines are initiated readily during learning,
says project leader Pirta Hotulainen from the Neuroscience Center of the University of Helsinki. This research has been collaboration between many distinct research groups combining cell biology to neuroscience. o sole research group could have achieved such a comprehensive view of the dendritic spine initiation mechanism and show its importance for the brain function
says Pirta Hotulainen
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