Posts tagged science
Articles and news from the latest research reports.
Circadian Clock is Key to Firing Up Cell’s Furnace
Clock’s rhythm ensures steady energy supply to cells during times of fasting
Each of our cells has an energy furnace, and it is called a mitochondrion. A Northwestern University-led research team now has identified a new mode of timekeeping that involves priming the cell’s furnace to properly use stored fuel when we are not eating.
The interdisciplinary team has identified the “match” and “flint” responsible for lighting this tiny furnace. And the match is only available when the circadian clock says so, underscoring the importance of the biological timing system to metabolism.
“Circadian clocks are with us on Earth because they have everything to do with energy,” said Joe Bass, M.D., who led the research. “If an organism burns its energy efficiently, it has a better chance of survival. Our results tell us how the circadian clock triggers the cell’s energy-burning process. Cells are most capable of using fuel when the clock is working properly.”
Bass is the Charles F. Kettering Professor and chief of the division of endocrinology, metabolism and molecular medicine at Northwestern University Feinberg School of Medicine and an endocrinologist at Northwestern Memorial Hospital.
Mitochondria regulate the supply of energy to cells when we are at rest, with no glucose available from food. In a study of mice, the researchers found that the circadian clock supplies the match to light the furnace and on the match tip is a critical compound called NAD+. It combines with an enzyme in mitochondria called Sirtuin 3, which acts as the flint, to light the furnace. When the clock in an animal isn’t working, the animal can’t metabolize stored energy and the process doesn’t ignite.
This pathway through which the body clock controls activities within the mitochondria shows how energy generation is tied tightly to the light-dark/activity-rest cycle each day.
The findings, which could be useful in the development of therapies to treat metabolic disorders related to circadian disruption, is published today (Sept. 19) by the journal Science.
The results demonstrate that the circadian clock, a genetic timekeeper that evolved to enable organisms to track the daily transition from light to darkness early in evolution, generates oscillations in mitochondrial energy capacity through rhythmic regulation of NAD+ biosynthesis.
The clock facilitates oxidative rhythms that anticipate an animal’s fasting/feeding cycle that occurs during the transition from light to darkness and wakefulness to sleep each day, and, in so doing, prevents the cell from “starving” during the night.
To understand how mitochondria are affected by circadian clock disorder, the researchers genetically removed the clocks in laboratory mice and compared them to controls. Both groups of mice were studied in a state of fasting; this “stress” test enabled the researchers to pinpoint just how the clock maintains “energy reserves” (akin to stress testing of a bank).
Bass and his research group worked together with Navdeep S. Chandel, a colleague of Bass’ at Feinberg, and John M. Denu, at the University of Wisconsin-Madison. They found the mice lacking clocks had defects in their mitochondria: the mitochondria could not metabolize stored energy and had no reserve to prevent depletion of the main currency, ATP. (Adenosine triphosphate is an energy-bearing molecule found in all living cells.)
Working with Northwestern colleague Milan Mrksich, they went on to show that removal of the clock depletes the necessary ingredient to turn on an enzyme within mitochondria, Sirtuin 3, which activates energy burning during fasting.
The researchers also showed that when the circadian clock was disrupted, resulting in a lack of NAD+, they could provide NAD+ supplements and restore function to the mitochondrion.
The findings expand the understanding of the molecular pathways linking the circadian clock with metabolism and show that the clock provides an essential buffer to stabilize the cell as organisms transition between eating and fasting each day. This knowledge has implications for disease intervention and prevention, including of diabetes, and potentially for states of increased cell demand for metabolism (including inflammation and cancer).
“We have established the chain of events that couples the clock’s control switch with the machinery of the mitochondria,” said Bass, who also is a member of the department of neurobiology at the Weinberg College of Arts and Sciences. “We now have identified an additional link in the supply chain that provides energy to the cell at different phases of our daily sleep-wake cycle. These findings establish a key role for the NAD+ biosynthetic cycle in this process.”
Major senior authors from Northwestern include Chandel, a professor in medicine-pulmonary and cell and molecular biology at Feinberg, and Mrksich, the Henry Wade Rogers Professor of Biomedical Engineering, Chemistry and Cell and Molecular Biology at Feinberg, Weinberg and the McCormick School of Engineering and Applied Science. Chandel and Mrksich are members of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.
The co-first authors are Clara Bien Peek, a postdoctoral fellow, and Alison H. Affinati, an M.D./Ph.D. candidate, both working in Bass’ lab. They have literally worked around the clock on the research, which builds on the earlier work of co-author Kathryn Moynihan Ramsey. In 2009, she and colleagues reported in Science that the compound NAD, together with the enzyme SIRT1, functions as a molecular “switch” to coordinate the internal clock with metabolic systems.
The current research team combined Northwestern expertise in basic circadian clock research, chemistry and physiology with outside collaborators who were able to verify the Northwestern findings.
Co-author Eric Goetzman, from the University of Pittsburgh School of Medicine, an expert in the rare children’s disease called metabolic myopathy, was able to confirm that the pattern the researchers observed in mice was the same as that seen in these children. Fasting can be life-threatening for children with this disorder because they can’t metabolize stored energy due to defects in their mitochondria.
Analyses by co-author Christopher B. Newgard at Duke University Medical Center identified a signature profile of the metabolic myopathy in mice with altered circadian clock genes.
(Source: northwestern.edu)
A Brake in the Head: German researchers gain new insights into the working of the brain
Scientists of the Charité – Universitätsmedizin Berlin and the German Center for Neurodegenerative Diseases (DZNE) have managed to acquire new insights into the functioning of a region in the brain that normally is involved in spatial orientation, but is damaged by the Alzheimer’s disease. They investigated how nerve signals are suppressed inside the so-called entorhinal cortex. According to the researchers, this neuronal inhibition leads nerve cells to synchronize their activity. The results of this study are now published in Neuron.
The entorhinal cortex is a link between the brain’s memory centre, the hippocampus, and the other areas of the brain. It is, however, more than an interface that only transfers nervous impulses. The entorhinal cortex also has an independent role in learning and thinking processes. This is particularly applicable for spatial navigation. “We know precious little about how this happens,” says Prof. Dietmar Schmitz, a researcher at the Cluster of Excellence NeuroCure at the Charité – Universitätsmedizin Berlin and Site Speaker for the DZNE in Berlin. “This is why we are investigating in animal models how the nerve cells within the entorhinal cortex are connected with each other.“
Signals wander inside the brain as electrical impulses from nerve cell to nerve cell. In general, signals are not merely forwarded. Rather, operation of the brain critically depends on the fact that the nerve impulses in some situations are activated and in other cases suppressed. A correct balance between suppression and excitation is decisive for all brain processes. “Until now research has mainly concentrated on signal excitation within the entorhinal cortex. This is why we looked into inhibition and detected a gradient inside the entorhinal cortex,” explains Dr. Prateep Beed, lead author of the study. “This means that nerve signals are not suppressed equally. The blockage of the nerve signals is weaker in certain parts of the entorhinal cortex and stronger in others. The inhibition has, so to speak, a spatial profile.”
When the brain is busy, nerve cells often coordinate their operation. In an electroencephalogram (EEG) – a recording of the brain’s electrical activity – the synchronous rhythm of the nerve cells manifests as a periodic pattern. “It is a moot question as to how nerve cells synchronize their behavior and how they bring about such rhythms,” says Beed. As he explains, it is also unclear whether these oscillations are only just a side effect or whether they trigger other phenomena. “But it has been demonstrated that neuronal oscillations accompany learning processes and even happen during sleep. They are a typical feature of the brain’s activity,” describes the scientist. “In our opinion, the inhibitory gradient, which we detected, plays an important role in creating the synchronous rhythm of the nerve cells and the related oscillations.”
In the case of Alzheimer’s, the entorhinal cortex is among the regions of the brain that are the first to be affected. “In recent times, studies related to this brain structure have increased. Here, already in the early stages of Alzheimer’s, one finds the protein deposits that are typical of this disease,” explains Schmitz, who headed the research. “It is also known that patients affected by Alzheimer’s have a striking EEG. Our studies help us to understand how the nerve cells in the entorhinal cortex operate and how electrical activities might get interrupted in this area of the brain.”
Coma: researchers observe never-before- detected brain activity
Researchers from the University of Montreal and their colleagues have found brain activity beyond a flat line EEG, which they have called Nu-complexes (from the Greek letter n). According to existing scientific data, researchers and doctors had established that beyond the so-called “flat line” (flat electroencephalogram or EEG), there is nothing at all, no brain activity, no possibility of life. This major discovery suggests that there is a whole new frontier in animal and human brain functioning.
The researchers observed a human patient in an extreme deep hypoxic coma under powerful anti-epileptic medication that he had been required to take due to his health issues. “Dr. Bogdan Florea from Romania contacted our research team because he had observed unexplainable phenomena on the EEG of a coma patient. We realized that there was cerebral activity, unknown until now, in the patient’s brain,” says Dr. Florin Amzica, director of the study and professor at the University of Montreal’s School of Dentistry.
Dr. Amzica’s team then decided to recreate the patient’s state in cats, the standard animal model for neurological studies. Using the anesthetic isoflurane, they placed the cats in an extremely deep—but completely reversible—coma. The cats passed the flat (isoelectric) EEG line, which is associated with silence in the cortex (the governing part of the brain). The team observed cerebral activity in 100% of the cats in deep coma, in the form of oscillations generated in the hippocampus, the part of the brain responsible for memory and learning processes. These oscillations, unknown until now, were transmitted to the master part of the brain, the cortex. The researchers concluded that the observed EEG waves, or Nu-complexes, were the same as those observed in the human patient.
Dr. Amzica stresses the importance of understanding the implications of these findings. “Those who have decided to or have to ‘unplug’ a near-brain-dead relative needn’t worry or doubt their doctor. The current criteria for diagnosing brain death are extremely stringent. Our finding may perhaps in the long term lead to a redefinition of the criteria, but we are far from that. Moreover, this is not the most important or useful aspect of our study,” Dr. Amzica said.
From Nu-complexesto therapeutic comas
The most useful aspect of this finding is the therapeutic potential, the neuroprotection, of the extreme deep coma. After a major injury, some patients are in such serious condition that doctors deliberately place them in an artificial coma to protect their body and brain so they can recover. But Dr. Amzica believes that the extreme deep coma experimented on the cats may be more protective.
“Indeed, an organ or muscle that remains inactive for a long time eventually atrophies. It is plausible that the same applies to a brain kept for an extended period in a state corresponding to a flat EEG,” says Professor Amzica. “An inactive brain coming out of a prolonged coma may be in worse shape than a brain that has had minimal activity. Research on the effects of extreme deep coma during which the hippocampus is active, through Nu-complexes. is absolutely vital for the benefit of patients.”
“Another implication of this finding is that we now have evidence that the brain is able to survive an extremely deep coma if the integrity of the nervous structures is preserved,” said lead author of the study, Daniel Kroeger. “We also found that the hippocampus can send ‘orders’ to the brain’s commander in chief, the cortex. Finally, the possibility of studying the learning and memory processes of the hippocampus during a state of coma will help further understanding of them. In short, all sorts of avenues for basic research are now open to us.”
Fluorescent compounds allow clinicians to visualize Alzheimer’s disease as it progresses
What if doctors could visualize all of the processes that take place in the brain during the development and progression of Alzheimer’s disease? Such a window would provide a powerful aid for diagnosing the condition, monitoring the effectiveness of treatments, and testing new preventive and therapeutic agents. Now, researchers reporting in the September 18 issue of the Cell Press journal Neuron have developed a new class of imaging agents that enables them to visualize tau protein aggregates, a pathological hallmark of Alzheimer’s disease and related neurodegenerative disorders, directly in the brains of living patients.
In the brains of patients with Alzheimer’s disease, tau proteins aggregate together and become tangled, while fragments of another protein, called amyloid beta, accumulate into deposits or plaques. Tau tangles are not only considered an important marker of neurodegeneration in Alzheimer’s disease but are also a hallmark of non-Alzheimer’s neurodegenerative disorders, tauopathies that do not involve amyloid beta plaques. While imaging technologies have been developed to observe the spread of amyloid beta plaques in patients’ brains, tau tangles were previously not easily monitored in the living patient.
In this latest research in mice and humans, investigators developed fluorescent compounds that bind to tau (called PBBs) and used them in positron emission tomography (PET) tests to correlate the spread of tau tangles in the brain with moderate Alzheimer’s disease progression. “PET images of tau accumulation are highly complementary to images of senile amyloid beta plaques and provide robust information on brain regions developing or at risk for tau-induced neuronal death,” says senior author Dr. Makoto Higuchi, of the National Institute of Radiological Sciences in Japan. “This is of critical significance, as tau lesions are known to be more intimately associated with neuronal loss than senile plaques.”
The advance may also be helpful for diagnosing, monitoring, and treating other neurological conditions because tau tangles are not limited to Alzheimer’s disease but also play a role in various types of dementias and movement disorders.
Smithsonian experts find e-readers can make reading easier for those with dyslexia
As e-readers grow in popularity as convenient alternatives to traditional books, researchers at the Smithsonian have found that convenience may not be their only benefit. The team discovered that when e-readers are set up to display only a few words per line, some people with dyslexia can read more easily, quickly and with greater comprehension. Their findings are published in the Sept. 18 issue of the journal PLOS ONE.
An element in many cases of dyslexia is called a visual attention deficit. It is marked by an inability to concentrate on letters within words or words within lines of text. Another element is known as visual crowding—the failure to recognize letters when they are cluttered within the word. Using short lines on an e-reader can alieviate these issues and promote reading by reducing visual distractions within the text.
"At least a third of those with dyslexia we tested have these issues with visual attention and are helped by reading on the e-reader," said Matthew H. Schneps, director of the Laboratory for Visual Learning at the Smithsonian Astrophysical Observatory and lead author of the research. "For those who don’t have these issues, the study showed that the traditional ways of displaying text are better."
An earlier study by Schneps tracked eye movements of dyslexic students while they read, and it showed the use of short lines facilitated reading by improving the efficiency of the eye movements. This second study examined the role the small hand-held reader had on comprehension, and found that in many cases the device not only improved speed and efficiency, but improved abilities for the dyslexic reader to grasp the meaning of the text.
The team tested the reading comprehension and speed of 103 students with dyslexia who attend Landmark High School in Boston. Reading on paper was compared with reading on small hand-held e-reader devices, configured to lines of text that were two-to-three words long. The use of an e-reader significantly improved speed and comprehension in many of the students. Those students with a pronounced visual attention deficit benefited most from reading text on a handheld device versus on paper, while the reverse was true for those who did not exhibit these issues. The small screen on a handheld device displaying few words (versus a full sheet of paper) is believed to narrow and concentrate the reader’s focus, which controls visual distraction.
"The high school students we tested at Landmark had the benefit of many years of exceptional remediation, but even so, if they have visual attention deficits they will eventually hit a plateau, and traditional approaches can no longer help," said Schneps. "Our research showed that the e-readers help these students reach beyond those limits."
These findings suggest that this reading method can be an effective intervention for struggling readers and that e-readers may be more than new technological gadgets: They also may be educational resources and solutions for those with dyslexia.
A genetic mutation, known as GBA, that leads to early onset of Parkinson’s disease and severe cognitive impairment (in about 4 to 7 percent of all patients with the disease) also alters how specific lipids, ceramides and glucosylceramides are metabolized. Mayo Clinic researchers have found that Parkinson’s patients who do not carry the genetic mutation also have higher levels of these lipids in the blood. Further, those who had Parkinson’s and high blood levels were also more likely to have cognitive impairment and dementia. The research was recently published online in the journal PLOS ONE.
The discovery could be an important warning for those with Parkinson’s disease. Parkinson’s is the second most common neurodegenerative disease after Alzheimer’s disease. There is no biomarker to tell who is going to develop the disease — and who is going to develop cognitive impairment after developing Parkinson’s, says Michelle Mielke, Ph.D., a Mayo Clinic researcher and first author of the study.
Cognitive impairment is a frequent symptom in Parkinson’s disease and can be even more debilitating for patients and their caregivers than the characteristic motor symptoms. The early identification of Parkinson’s patients at greatest risk of developing dementia is important for preventing or delaying the onset and progression of cognitive symptoms. Changing these blood lipids could be a way to stop the progression of the disease, says Dr. Mielke.
There is a suggestion this blood lipid marker also could help to predict who will develop Parkinson’s disease and this research is ongoing.
"There is currently no cure for Parkinson’s, but the earlier we catch it — the better chance we have to fight it," says Dr. Mielke. "It’s particularly important we find a biomarker and identify it in the preclinical phase of the disease, before the onset even begins."
Dr. Mielke’s lab is researching blood-based biomarkers for Parkinson’s disease because blood tests are less invasive and cheaper than a brain scan or spinal tap — other tools used to research the disease.
Study helps deconstruct estrogen’s role in memory
The loss of estrogens at menopause increases a woman’s risk of dementia and Alzheimer’s disease, yet hormone replacement therapy can cause harmful side effects.
Knowing the exact mechanism of estrogen activation in the brain could lead to new targets for drug development that would provide middle-aged women the cognitive benefits of hormone replacement therapy without increasing their risk for cardiovascular disease or breast cancer.
In a new study, Karyn Frick, professor of psychology at the University of Wisconsin-Milwaukee, uncovers details about estrogen’s role in the complex cellular communication system underlying memory formation.
“The receptor mechanisms that regulate estrogen’s ability to enhance memory are still poorly understood,” says Frick. “With this study, we’ve begun to sort out several of the key players needed for estrogens to mediate memory formation.”
The research, published in the The Journal of Neuroscience today, focused on estrogen effects in a brain region called the hippocampus, which deteriorates with age or Alzheimer’s disease. The researchers found that each of the two known estrogen receptors rapidly activate a specific cellular pathway necessary for memory formation in the hippocampus of female mice, but only if they interact with a certain glutamate receptor, called mGluR1.
The study revealed that when this glutamate receptor is blocked, the cell-signaling protein ERK cannot be activated by the potent estrogen, 17β-estradiol. Because ERK activation is necessary for memory formation, estradiol failed to enhance memory among mice in which mGluR1 was blocked.
Frick’s team also found evidence that estrogen receptors and mGluR1 physically interact at the cell membrane, allowing estradiol to influence memory formation within seconds to minutes. Collectively, the data provide the first evidence that the rapid signaling initiated by such interactions is essential for estradiol to enhance memory regulated by the hippocampus.
“Our data suggesting that interactions between estrogen receptors and mGluR1 at the cell membrane are critical for estradiol to enhance memory provides important new information about how estrogens regulate memory formation,” Frick says. “Because membrane proteins are better targets for drug development than proteins inside the cell, these data could lead to a new generation of therapies that provide the cognitive benefits of estrogens without harmful side effects.”
Motor Control Development Continues Longer Than Previously Believed
Research opens up longer therapy window for children with neurodevelopmental disorders
The development of fine motor control – the ability to use your fingertips to manipulate objects – takes longer than previously believed, and isn’t entirely the result of brain development, according to a pair of complementary studies.
The research opens up the potential to use therapy to continue improving the motor control skills of children suffering from neurodevelopmental disorders such as cerebral palsy, a blanket term for central motor disorders that affects about 764,000 children and adults nationwide.
“These findings show that it’s not only possible, but critical to continue or begin physical therapy in adolescence,” said Francisco Valero-Cuevas, corresponding author of two studies on the matter – one appearing in the Journal of Neurophysiology and the other in the Journal of Neuroscience.
“We find we likely do not have a narrow window of opportunity in early childhood to improve manipulation skills, as previously believed, but rather developmental plasticity lasts much longer and provides opportunity throughout adolescence” he said. “This complements similarly exciting findings showing brain plasticity in adulthood and old age.”
Researchers had previously been able to detect improvements in fine motor control of the hand only until around ages 8-10. However, Valero-Cuevas – a professor of biomedical engineering and of biokinesiology and physical therapy – invented a tool that allows for more precise measurement of fine motor control.
The tool is simple – springs of varying stiffness and length set between plastic pads which Valero-Cuevas has patented. Motor skill is then determined by the individual’s ability to compress the increasingly awkward spring devices. Sudarshan Dayanidhi, during his PhD studies at USC with Valero-Cuevas, developed and applied clinically useful versions of this technology with great success.
With this new tool, and in collaboration with Åsa Hedberg and Hans Forssberg of the Astrid Lindgren Children’s Hospital in Stockholm, they tested 130 children with typical development between 4-16 years of age, and demonstrated that even the 16-year-olds were continuing to hone their fine motor skills. Their findings will appear in the Journal of Neurophysiology on Oct. 1.
To further this study, Dayanidhi and Valero-Cuevas joined forces with Assistant Professor of biokinesiology and physical therapy Jason Kutch (also of USC), to explore if this longer developmental timeline for dexterity was tied not just to brain maturation, but also to muscular development.
It has long been thought that improved dexterity involved only brain development and muscle growth – where muscles only got bigger and stronger – but did not add to dexterous skills since they are performed at low forces. The research by Dayanidhi, Kutch and Valero-Cuevas indicates otherwise.
“Combining our metrics of dexterity from Dayanidhi’s PhD work, with novel and noninvasive measures of muscle contraction time developed by Prof. Kutch, we were able to show a previously unknown strong association between gains in dexterity with improvement in low force muscle contraction time,” Valero-Cuevas said.
This second facet of the research showing how both dexterity and muscle function improve in children will appear in the Journal of Neuroscience on Sept. 18.
(Source: pressroom.usc.edu)
Shining light on neurodegenerative pathway
University of Adelaide researchers have identified a likely molecular pathway that causes a group of untreatable neurodegenerative diseases, including Huntington’s disease and Lou Gehrig’s disease.
The group of about 20 diseases, which show overlapping symptoms that typically include nerve cell death, share a similar genetic mutation mechanism ‒ but how this form of mutation causes these diseases has remained a mystery.
"Despite the genes for some of these diseases having been identified 20 years ago, we still haven’t understood the underlying mechanisms that lead to people developing clinical symptoms," says Professor Robert Richards, Head of Genetics in the University’s School of Molecular and Biomedical Sciences.
"By uncovering the molecular pathway for these diseases, we now expect to be able to define targets for intervention and so come up with potential therapies. Ultimately this will help sufferers to reduce the amount of nerve cell degeneration or slow its progression."
In an article published in Frontiers in Molecular Neuroscience, Professor Richards and colleagues describe their innovative theory and new evidence for the key role of RNA in the development of the diseases. RNA is a large molecule in the cell that copies genetic code from the cell’s DNA and translates it into the proteins that drive biological functions.
People with these diseases all have expanded numbers of copies of particular sequences of the ‘nucleotide bases’ which make up DNA.
"In most cases people with these diseases have increased numbers of repeat sequences in their RNA," says Professor Richards. "The disease develops when people have too many copies of the repeat sequence. Above a certain threshold, the more copies they have the earlier the disease develops and the more severe the symptoms. The current gap in knowledge is why having these expanded repeat sequences of genes in the RNA translates into actual symptoms."
Professor Richards says evidence points towards a dysfunctional RNA and a pivotal role of the body’s immune system in the development of the disease.
"Rather than recognising the ‘expanded repeat RNA’ as its own RNA, we believe the ‘expanded repeat RNA’ is being seen as foreign, like the RNA in a virus, and this activates the innate immune system, resulting in loss of function and ultimately the death of the cell," he says.
The University of Adelaide laboratory modelled and defined the expanded repeat RNA disease pathway using flies (Drosophila). Other laboratories have reported tell-tale, but previously inexplicable, signs characteristic of this pathway in studies of patients with Huntington’s disease and Myotonic Dystrophy.
"This new understanding, once proven in each of the relevant human diseases, opens the way for potential treatments, and should give cause for hope to those with these devastating diseases," Professor Richards says.
(Source: adelaide.edu.au)
Nanoscale neuronal activity measured for the first time
A new technique that allows scientists to measure the electrical activity in the communication junctions of the nervous systems has been developed by a researcher at Queen Mary University of London.
The junctions in the central nervous systems that enable the information to flow between neurons, known as synapses, are around 100 times smaller than the width of a human hair (one micrometer and less) and as such are difficult to target let alone measure.
By applying a high-resolution scanning probe microscopy that allows three-dimensional visualisation of the structures, the team were able to measure and record the flow of current in small synaptic terminals for the first time.
“We replaced the conventional low-resolution optical system with a high-resolution microscope based on a nanopipette,” said Dr Pavel Novak, a bioengineering specialist from Queen Mary’s School of Engineering and Materials Science.
“The nanopipette hovers above the surface of the sample and scans the structure to reveal its three-dimensional topography. The same nanopipette then attaches to the surface at selected locations on the structure to record electrical activity. By repeating the same procedure for different locations of the neuronal network we can obtain a three-dimensional map of its electrical properties and activity.”
The research, published (Wednesday 18 September) in Neuron, opens a new window into the neuronal activity at nanometre scale, and may contribute to the wider effort of understanding the function of the brain represented by the Brain Activity Map Project (BRAIN initiative), which aims to map the function of each individual neuron in the human brain.
(Source: qmul.ac.uk)