Getting Rid of Old MitochondriaSome neurons turn to neighbors to help take out the trash
It’s broadly assumed that cells degrade and recycle their own old or damaged organelles, but researchers at University of California, San Diego School of Medicine, The Johns Hopkins University School of Medicine and Kennedy Krieger Institute have discovered that some neurons transfer unwanted mitochondria – the tiny power plants inside cells – to supporting glial cells called astrocytes for disposal. 
The findings, published in the June 17 online Early Edition of PNAS, suggest some basic biology may need revising, but they also have potential implications for improving the understanding and treatment of many neurodegenerative and metabolic disorders.
“It does call into question the conventional assumption that cells necessarily degrade their own organelles. We don’t yet know how generalized this process is throughout the brain, but our work suggests it’s probably widespread,” said Mark H. Ellisman, PhD, Distinguished Professor of Neurosciences, director of the National Center for Microscopy and Imaging Research (NCMIR) at UC San Diego and co-senior author of the study with Nicholas Marsh-Armstrong, PhD, in the Department of Neuroscience at Johns Hopkins University and the Hugo W. Moser Research Institute at Kennedy Krieger Institute in Baltimore.
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From idea to published discovery: the whole story
Scientific canon long held that when the tiny energy producers within cells, called mitochondria, became damaged or dysfunctional these tiny organelles were degraded and recycled within the cell that produced them. But recent research shows that damaged mitochondria, particularly in the long axons of the brain’s nerve cells, are instead transferred to nearby glial cells for elimination. This process, in effect, outsources a substantial portion of the neurons’ housekeeping.
A research team made up of scientists from the University of California, San Diego School of Medicine and Johns Hopkins University (JHU) School of Medicine recently reported this new paradigm. It was revealed from careful study of the fate of mitochondria in the axons of retinal ganglion cells in mice. Mice are close enough genetically to humans that they are often used to model disease to better understand underlying mechanisms and explore possible treatment strategies for diseases affecting people, such as glaucoma.
Retinal ganglion neurons are a type of nerve cell that transmits visual information from the eye to the brain. The research team determined that large numbers of damaged mitochondria in retinal ganglion cells were shed at a site right behind the eye in an area called the optic nerve head (ONH), where ganglion neuron axons exit the eye to form the optic nerve, carrying signals from the eye to the brain. The transferred pieces of mitochondria were then absorbed and broken down by lysosomes inside adjacent, specialized glial cells. This surprising result upends the assumption that a cell necessarily degrades its own organelles, particularly its own mitochondria.
The work is the first demonstration of a process, dubbed transmitophagy, used by nerve axons of the visual system. But evidence suggests this outsourcing capacity may be fundamental and exist in other regions of the brain. Hence, this result, with its immediate implications for biomedical research on eye disease, is likely to have a profound impact on studies on other topics related to the brain in general, most particularly age-associated neurodegenerative processes such as those occurring in Parkinson’s and Alzheimer’s disease.
Behind the findings, however, is a another story of how the discovery came to be, one that reveals the critical roles played by diverse research-promoting mechanisms used by foundations and the federal government to cultivate and catalyze interdisciplinary, collaborative approaches needed to address hard questions and produce new understanding of complex biomedical questions.
Scientific discoveries often seem to be reported as isolated, discrete conclusions: Scientist X conducted research Y and obtained conclusion Z. This structure implies a simple linear progression. End of story. Though the impact of these discoveries is often felt, the process that produced these discoveries, like hard scientific questions themselves, tends to be insufficiently understood.
But modern science is complicated and far from linear. It often involves years of traversing switchbacks on the scientific trail; intense technology development and application with successes and failures; and scientific personalities, with different talents and roles, scattered geographically. All of this is true of the story at hand.
To illustrate how such scientific discoveries can be realized, let’s pick up the transmitophagy story mid-stream: Nicholas Marsh-Armstrong, a young Harvard-trained molecular neurobiologist chose to focus his research program on glaucoma, a devastating but common scourge that progressively robs the elderly of sight. His creativity and penchant for studying hard problems using relevant, simple systems in frog or mouse models of disease had been noticed by the Glaucoma Research Foundation and National Institutes of Health, which provided him with support to study a specialized region behind the eye for clues as to the first changes that might be harbingers of glaucoma.
Like others before him, he sought answers to what cellular and molecular events initiated the  process that ultimately leads to the breakdown of the nerve axons belonging to the retinal ganglion cells which, once lost, lead to glaucoma.
Based on work supported by a Glaucoma Research Foundation catalyst program, Marsh-Armstrong believed the early events might extend back into the optic nerve through the entire initial region, all the way to where a special form of glia started the job of providing insulation (fatty myelin layers) to help the electric signal propagate rapidly to the brain – the ONH.
At the time, the glaucoma research community was beginning to recognize data pointing to a specialized type of glia, the astrocyte, as having a role in activities associated with inflammation of the ONH in glaucoma. Growing suspicion that there might be more to this story helped motivate a series of small meetings, sponsored by The International Retina Research Foundation, the Lasker Foundation, and the Howard Hughes Medical Institute, which brought together 50 scientists from around the United States to discuss possible new strategies and collaborations that would accelerate progress resulting from glaucoma research.
Marsh-Armstrong attended this meeting where he met Ellisman, a professor of neuroscience and bioengineering at UC San Diego and director of the National Center for Microscopy and Imaging Research (NCMIR). Ellisman specializes in advanced imaging technology development and applications. He is also an expert on the structure and function of the astrocyte.
A decade earlier, Ellisman and colleagues, using high-resolution imaging technology, determined that the astrocyte, which had been thought to be a simple, star-shaped glial cell, was actually much more complicated. In fact, some 85 percent of the cell’s shape had been previously overlooked.
Scientists had been seeing the forest but missing the trees or in this case, the leaves. Ellisman’s team also determined that rather than being intertwined, the branches of astrocytes occupied their own unique spaces or “tiles” in the brain. He was invited to the meeting because the glaucoma research community was interested in understanding the role of astrocytes in the ONH more fully, and the imaging strategies of his group at NCMIR were thought to be a key to addressing this knowledge gap.
During the three-day meeting, Ellisman and Marsh-Armstrong discussed how to apply recently developed imaging technologies to study. In particularly, Marsh-Armstrong wanted to look at the released substances behind the eye in greater detail. The International Retina Research Foundation offered small short-term grants to support creative ideas that emerged from the meeting. Marsh-Armstrong and Ellisman applied and received support. Their plan was for Ellisman’s group to apply a new high-resolution, volume-imaging strategy that uses a scanning electron microscope in a highly automated manner to reconstruct large portions of the ONH in a mouse model to determine more precisely where the first signs of glaucoma appear.
Before they began working with samples from the model, however, Ellisman spotted what he interpreted were static images of transfer between the retinal ganglion neuron axons and associated astrocytes, remarking to his colleague that it looked like they were passing off parts of mitochondria.
At the time, these observations were kept muted. They were very controversial. More analysis and careful assessment would be required to determine if this surprising observation and predictive interpretation would hold up under scrutiny from the community.
The two researchers and their respective teams wrote up this preliminary study and published one scientific paper showing the location of the transfer of material—without identifying it specifically as axonal mitochondria.
The preliminary results proved sufficient to support a successful request for a small grant from the NIH’s National Eye Institute. From that point, it took two to three years and many creative strategies from both labs to gather sufficient data to determine if their interpretation of static images, representing the dynamic transfer of mitochondria, was correct. They reasoned that this would be required before they could publish the work in a peer-reviewed journal.
This is an instructive tale for many reasons. First, it demonstrates a relationship between philanthropic foundations and federal funding agencies in supporting the continuum of the scientific enterprise. Both types of organizations sponsor exclusive topical meetings and invite experts across a range of disciplines to discuss and identify the frontiers—and the intersection of those frontiers—where science can be advanced. The foundation provides seed funding to stimulate new research directions. This seed funding enables scientists to conduct research, demonstrate preliminary progress (proof of concept) on a topic and get some papers published, all of which serves as the basis for pursuing a grant from a federal funding agency for a more ambitious, longer-range project. This continuum can support researchers at both earlier and later stages of their scientific thinking.
Second, and more importantly, it shows the potential for catalysis when researchers, looking at a problem from different points of view, collaborate. In this case, high-performance computing (HPC), communications and imaging capabilities were brought to bear on an interesting scientific question that, arguably, couldn’t have been addressed as efficiently otherwise. This is an important example of the value of advanced technology resources set up by NIH, such as NCMIR and other research resources, and how they apply their open-access, state-of-the-art technologies and staff expertise to answer hard questions, materially advance scientific understanding, and benefit society as a result.
This project, transcontinental in nature, was made possible by continuing large federal investments (primarily by NIH and the National Science Foundation) in cyberinfrastructure: HPC, high-bandwidth telecommunications networks, infrastructure to support large data (acquisition, storage, analysis, and curation), high-resolution imaging systems, access gateways, and related digital technology and development.
Today researchers, regardless of location, can choose their collaborators more selectively than ever, which leads to creation of large teams working across disciplinary boundaries, which, common wisdom holds, is where the most innovative work takes place.

Getting Rid of Old Mitochondria
Some neurons turn to neighbors to help take out the trash

It’s broadly assumed that cells degrade and recycle their own old or damaged organelles, but researchers at University of California, San Diego School of Medicine, The Johns Hopkins University School of Medicine and Kennedy Krieger Institute have discovered that some neurons transfer unwanted mitochondria – the tiny power plants inside cells – to supporting glial cells called astrocytes for disposal. 

The findings, published in the June 17 online Early Edition of PNAS, suggest some basic biology may need revising, but they also have potential implications for improving the understanding and treatment of many neurodegenerative and metabolic disorders.

“It does call into question the conventional assumption that cells necessarily degrade their own organelles. We don’t yet know how generalized this process is throughout the brain, but our work suggests it’s probably widespread,” said Mark H. Ellisman, PhD, Distinguished Professor of Neurosciences, director of the National Center for Microscopy and Imaging Research (NCMIR) at UC San Diego and co-senior author of the study with Nicholas Marsh-Armstrong, PhD, in the Department of Neuroscience at Johns Hopkins University and the Hugo W. Moser Research Institute at Kennedy Krieger Institute in Baltimore.

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Brain cells of a laboratory mouse glowing with multicolor fluorescent proteins. Image courtesy of Harvard University, Livett-Weissman-Sanes-Lichtman
Early growth factor treatment may help prevent cell loss in Alzheimer’s disease
Brain-derived neurotrophic factor or BDNF has long been a target of interest among Alzheimer’s disease (AD) researchers and the Alzheimer’s community at large.
Four years ago, Mark Tuszynski, MD, PhD, professor of neurosciences at UC San Diego School of Medicine and director of the Center for Neural Repair and colleagues showed that a BDNF-based treatment measurably improved neural dysfunction in animal models of Alzheimer’s disease. The findings garnered international headlines.
Now there is new evidence that BDNF may be effective as a preventive measure for AD. 
In a paper, published yesterday in The Journal of Neuroscience, Tuszynski and colleagues follow up with evidence that early life BDNF treatment prevents neuronal loss in mutant mice genetically predisposed to early-onset familial Alzheimer’s disease.
Specifically, mice engineered to express APP, a protein strongly linked to AD development, received injections of the BDNF gene at two months of age and were examined five months later. The researchers found that BDNF-treated mice exhibited better behavior and brain function than untreated APP mutant mice and suffered significantly less neuron loss in the entorhinal cortex, a region of the brain that helps mediate learning and memory.
In addition, they noted that BDNF did not affect amyloid plaque accumulation, another major indicator of AD, suggesting that direct amyloid reduction is not necessary to achieving significant neuroprotective benefits in mutant amyloid models of AD.
“These findings strengthen the rationale for planning human clinical trials of BDNF therapy in AD,” said Tuszynski. “This is an effort that we are actively engaged in.” 
Tuszynski also noted that there is a possibility that BDNF therapy and anti-amyloid therapies for AD could be combined to yield better treatments than either treatment alone.

Brain cells of a laboratory mouse glowing with multicolor fluorescent proteins. Image courtesy of Harvard University, Livett-Weissman-Sanes-Lichtman

Early growth factor treatment may help prevent cell loss in Alzheimer’s disease

Brain-derived neurotrophic factor or BDNF has long been a target of interest among Alzheimer’s disease (AD) researchers and the Alzheimer’s community at large.

Four years ago, Mark Tuszynski, MD, PhD, professor of neurosciences at UC San Diego School of Medicine and director of the Center for Neural Repair and colleagues showed that a BDNF-based treatment measurably improved neural dysfunction in animal models of Alzheimer’s disease. The findings garnered international headlines.

Now there is new evidence that BDNF may be effective as a preventive measure for AD. 

In a paper, published yesterday in The Journal of Neuroscience, Tuszynski and colleagues follow up with evidence that early life BDNF treatment prevents neuronal loss in mutant mice genetically predisposed to early-onset familial Alzheimer’s disease.

Specifically, mice engineered to express APP, a protein strongly linked to AD development, received injections of the BDNF gene at two months of age and were examined five months later. The researchers found that BDNF-treated mice exhibited better behavior and brain function than untreated APP mutant mice and suffered significantly less neuron loss in the entorhinal cortex, a region of the brain that helps mediate learning and memory.

In addition, they noted that BDNF did not affect amyloid plaque accumulation, another major indicator of AD, suggesting that direct amyloid reduction is not necessary to achieving significant neuroprotective benefits in mutant amyloid models of AD.

“These findings strengthen the rationale for planning human clinical trials of BDNF therapy in AD,” said Tuszynski. “This is an effort that we are actively engaged in.” 

Tuszynski also noted that there is a possibility that BDNF therapy and anti-amyloid therapies for AD could be combined to yield better treatments than either treatment alone.

In this schematic, reduced activation in discrete medial prefrontal brain regions is depicted (in blue) in schizophrenia patients, occurring 0.2 seconds after sound changes (top panel), cascading forward to widespread brain regions associated with the automatic activation of attentional networks 0.1 second later (bottom panel).
In Schizophrenia Patients, Auditory Cues Sound Bigger Problems
Researchers at the University of California, San Diego School of Medicine and the VA San Diego Healthcare System have found that deficiencies in the neural processing of simple auditory tones can evolve into a cascade of dysfunctional information processing across wide swaths of the brain in patients with schizophrenia.
The findings are published in the current online edition of the journal Neuroimage.
Schizophrenia is a mental disorder characterized by disturbed thought processes and difficulty in discerning real from unreal perceptions. Common symptoms include auditory hallucinations and unfounded suspicious ideas. The disorder affects about 1 percent of the U.S. population, or roughly 3 million people.
“Impairments in the early stages of sensory information processing are associated with a constellation of abnormalities in schizophrenia patients,” said Gregory Light, PhD, associate professor of psychiatry at UC San Diego and senior author of the study.
These impairments, according to Light, may explain how schizophrenia patients develop clinical symptoms such as hearing voices that others cannot hear and difficulty with cognitive tasks involving attention, learning and recalling information. “If someone’s brain is unable to efficiently detect subtle changes in sounds despite normal hearing, they may not be able to automatically direct their attention and rapidly encode new information as it is being presented.”
Light and colleagues used electroencephalography – a technique that records patterns of electrical brain activity using electrodes positioned on the scalp – on 410 schizophrenia patients and 247 nonpsychiatric comparison subjects. The researchers employed novel computational imaging approaches to deconstruct the brain dynamics that underlie two leading neurobiological markers used in schizophrenia research: mismatch negativity (MMN) and P3a event-related potentials.
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In healthy volunteers, a specific pattern of EEG responses across a complex network of brain structures is elicited within a fraction of a second in response to changes in auditory tones. In patients with schizophrenia, the researchers found that this normal process is disrupted. Reduced activity in specific areas of the medial frontal lobe quickly propagated to other regions of the brain that support activation of attentional networks.
“Changes in the tone of speech convey complex information including nuances of emotional meaning and content,” said Light, who is also associate director of the VISN-22 Mental Illness, Research, Education and Clinical Center (MIRECC) at the San Diego VA Medical Center. “If a patient’s brain is not processing auditory information optimally, he or she may miss out on important-but-subtle social cues and other critical information. They may not properly recognize sarcasm or humor that is carried by pitch changes in speech. This can be a major barrier to achieving better functioning in social relationships, school or job performance, and ultimately limit their overall quality of life.”
In research published earlier this year, Light and colleagues established that MMN and P3a showed promise for unlocking the elusive brain and molecular dysfunctions of schizophrenia patients. “These brain-based biomarkers may eventually prove to be useful for assisting clinicians with diagnosis, guiding treatment decisions, and tracking therapeutic response over time. These measures may also predict which individuals are at risk for developing a serious mental illness and are most likely to benefit from course-altering early interventions.”
According to Stephen R. Marder, MD, VISN-22 MIRECC director and a professor at UCLA’s Semel Institute for Neuroscience and Human Behavior, “this study makes a valuable contribution to our understanding of how impairments in the very early processing of sensory information in schizophrenia can explain the complex symptoms of the illness. This new knowledge may also be useful in developing better pharmacological and non-pharmacological treatments for schizophrenia.”

In this schematic, reduced activation in discrete medial prefrontal brain regions is depicted (in blue) in schizophrenia patients, occurring 0.2 seconds after sound changes (top panel), cascading forward to widespread brain regions associated with the automatic activation of attentional networks 0.1 second later (bottom panel).

In Schizophrenia Patients, Auditory Cues Sound Bigger Problems

Researchers at the University of California, San Diego School of Medicine and the VA San Diego Healthcare System have found that deficiencies in the neural processing of simple auditory tones can evolve into a cascade of dysfunctional information processing across wide swaths of the brain in patients with schizophrenia.

The findings are published in the current online edition of the journal Neuroimage.

Schizophrenia is a mental disorder characterized by disturbed thought processes and difficulty in discerning real from unreal perceptions. Common symptoms include auditory hallucinations and unfounded suspicious ideas. The disorder affects about 1 percent of the U.S. population, or roughly 3 million people.

“Impairments in the early stages of sensory information processing are associated with a constellation of abnormalities in schizophrenia patients,” said Gregory Light, PhD, associate professor of psychiatry at UC San Diego and senior author of the study.

These impairments, according to Light, may explain how schizophrenia patients develop clinical symptoms such as hearing voices that others cannot hear and difficulty with cognitive tasks involving attention, learning and recalling information. “If someone’s brain is unable to efficiently detect subtle changes in sounds despite normal hearing, they may not be able to automatically direct their attention and rapidly encode new information as it is being presented.”

Light and colleagues used electroencephalography – a technique that records patterns of electrical brain activity using electrodes positioned on the scalp – on 410 schizophrenia patients and 247 nonpsychiatric comparison subjects. The researchers employed novel computational imaging approaches to deconstruct the brain dynamics that underlie two leading neurobiological markers used in schizophrenia research: mismatch negativity (MMN) and P3a event-related potentials.

Read More

Neural Stem Cells Regenerate Axons in Severe Spinal Cord InjuryNew relay circuits, formed across sites of complete spinal transaction, result in functional recovery in ratsIn a study at the University of California, San Diego and VA San Diego Healthcare, researchers were able to regenerate “an astonishing degree” of axonal growth at the site of severe spinal cord injury in rats.  Their research revealed that early stage neurons have the ability to survive and extend axons to form new, functional neuronal relays across an injury site in the adult central nervous system (CNS).   The study also proved that at least some types of adult CNS axons can overcome a normally inhibitory growth environment to grow over long distances.  Importantly, stem cells across species exhibit these properties. The work will be published in the journal Cell on September 14. (For a history of spinal cord repair science and the significance of this latest work, read Ohio State University neuroscientist Phillip Popovich’s review here.) The UC San Diego-led team embedded neural stem cells in a matrix of fibrin (a protein key to blood-clotting that is already used in human neuron procedures), mixed with growth factors to form a gel.  The gel was then applied to the injury site in rats with completely severed spinal cords.“Using this method, after six weeks, the number of axons emerging from the injury site exceeded by 200-fold what had ever been seen before,” said Mark Tuszynski, MD, PhD, professor in the UC San Diego Department of Neurosciences and director of the UCSD Center for Neural Repair, who headed the study. “The axons also grew 10 times the length of axons in any previous study and, importantly, the regeneration of these axons resulted in significant functional improvement.”In addition, adult cells above the injury site regenerated into the neural stem cells, establishing a new relay circuit that could be measured electrically. “By stimulating the spinal cord four segments above the injury and recording this electrical stimulation three segments below, we detected new relays across the transaction site,” said Tuszynski. To confirm that the mechanism underlying recovery was due to formation of new relays, when rats recovered, their spinal cords were re-transected above the implant.  The rats lost motor function – confirming formation of new relays across the injury.  The grafting procedure resulted in significant functional improvement: On a 21-point walking scale, without treatment, the rats score was only 1.5; following the stem cell therapy, it rose to 7 – a score reflecting the animals’ ability to move all joints of affected legs.Results were then replicated using two human stem cell lines, one already in human trials for ALS.  “We obtained the exact results using human cells as we had in the rat cells,” said Tuszynski.The study made use of green fluorescent proteins (GFP), a technique that had never before been used to track neural stem cell growth. “By tagging the cells with GFP, we were able to observe the stem cells grow, become neurons and grow axons, showing us the full ability of these cells to grow and make connections with the host neurons,” said first author Paul Lu, PhD, assistant research scientist at UCSD’s Center for Neural Repair. “This is very exciting, because the technology didn’t exist before.”Pictured: Artist’s rendering of neurons

Neural Stem Cells Regenerate Axons in Severe Spinal Cord Injury
New relay circuits, formed across sites of complete spinal transaction, result in functional recovery in rats

In a study at the University of California, San Diego and VA San Diego Healthcare, researchers were able to regenerate “an astonishing degree” of axonal growth at the site of severe spinal cord injury in rats.  Their research revealed that early stage neurons have the ability to survive and extend axons to form new, functional neuronal relays across an injury site in the adult central nervous system (CNS).  

The study also proved that at least some types of adult CNS axons can overcome a normally inhibitory growth environment to grow over long distances.  Importantly, stem cells across species exhibit these properties. The work will be published in the journal Cell on September 14.

(For a history of spinal cord repair science and the significance of this latest work, read Ohio State University neuroscientist Phillip Popovich’s review here.)

The UC San Diego-led team embedded neural stem cells in a matrix of fibrin (a protein key to blood-clotting that is already used in human neuron procedures), mixed with growth factors to form a gel.  The gel was then applied to the injury site in rats with completely severed spinal cords.

“Using this method, after six weeks, the number of axons emerging from the injury site exceeded by 200-fold what had ever been seen before,” said Mark Tuszynski, MD, PhD, professor in the UC San Diego Department of Neurosciences and director of the UCSD Center for Neural Repair, who headed the study. “The axons also grew 10 times the length of axons in any previous study and, importantly, the regeneration of these axons resulted in significant functional improvement.”

In addition, adult cells above the injury site regenerated into the neural stem cells, establishing a new relay circuit that could be measured electrically. “By stimulating the spinal cord four segments above the injury and recording this electrical stimulation three segments below, we detected new relays across the transaction site,” said Tuszynski.

To confirm that the mechanism underlying recovery was due to formation of new relays, when rats recovered, their spinal cords were re-transected above the implant.  The rats lost motor function – confirming formation of new relays across the injury. 

The grafting procedure resulted in significant functional improvement: On a 21-point walking scale, without treatment, the rats score was only 1.5; following the stem cell therapy, it rose to 7 – a score reflecting the animals’ ability to move all joints of affected legs.

Results were then replicated using two human stem cell lines, one already in human trials for ALS.  “We obtained the exact results using human cells as we had in the rat cells,” said Tuszynski.

The study made use of green fluorescent proteins (GFP), a technique that had never before been used to track neural stem cell growth. “By tagging the cells with GFP, we were able to observe the stem cells grow, become neurons and grow axons, showing us the full ability of these cells to grow and make connections with the host neurons,” said first author Paul Lu, PhD, assistant research scientist at UCSD’s Center for Neural Repair. “This is very exciting, because the technology didn’t exist before.”

Pictured: Artist’s rendering of neurons

Color-coded representations of human and mouse brains show similarities in cortical functional organization, with some variance according to species-specific needs. F/M indicates the frontal/motor cortex; S1, primary somatosensory cortex; A1, auditory cortex and V1, visual cortex.
Of Mice and Men, a Common Cortical ConnectionMRI study finds genetic basis of brain development largely similar in mice and humans
A new study using magnetic resonance imaging data of 406 adult human twins affirms the long-standing idea that the genetic basis of human cortical regionalization – the organization of the outer brain into specific functional areas – is similar to and consistent with patterns found in other mammals, indicating a common conservation mechanism in evolution.
The findings by researchers at the University of California, San Diego School of Medicine and colleagues are published in the November 17 issue of the journal Neuron.
Past animal studies, primarily in rodents, have shown that development of distinct areas of the cortex – the outer layer of the brain – is influenced by genes exhibiting highly regionalized expression patterns. The new study is among the first to confirm these findings using data from human subjects.  As in other mammals, the researchers found that that genetic influences in human brain development progress along a graduating scale anterior-to-posterior (front-to-back) in a bilateral, symmetric pattern.
There were, of course, differences based upon the particular needs and functions of each species.
More here

Color-coded representations of human and mouse brains show similarities in cortical functional organization, with some variance according to species-specific needs. F/M indicates the frontal/motor cortex; S1, primary somatosensory cortex; A1, auditory cortex and V1, visual cortex.

Of Mice and Men, a Common Cortical Connection
MRI study finds genetic basis of brain development largely similar in mice and humans

A new study using magnetic resonance imaging data of 406 adult human twins affirms the long-standing idea that the genetic basis of human cortical regionalization – the organization of the outer brain into specific functional areas – is similar to and consistent with patterns found in other mammals, indicating a common conservation mechanism in evolution.

The findings by researchers at the University of California, San Diego School of Medicine and colleagues are published in the November 17 issue of the journal Neuron.

Past animal studies, primarily in rodents, have shown that development of distinct areas of the cortex – the outer layer of the brain – is influenced by genes exhibiting highly regionalized expression patterns. The new study is among the first to confirm these findings using data from human subjects.  As in other mammals, the researchers found that that genetic influences in human brain development progress along a graduating scale anterior-to-posterior (front-to-back) in a bilateral, symmetric pattern.

There were, of course, differences based upon the particular needs and functions of each species.

More here


Ferguson’s ability to remember the cities she’s lived in, jobs she’s worked and, yes, all the men she’s married, makes her very valuable to Jacopo Annese, a neuroanatomist at the University of California, San Diego. Annese is director of The Brain Observatory, a research center at UCSD where brains are sliced up, laid out on slides and then scanned into digital images, which researchers can use to visualize what a variety of brains look like. Scientists can use Annese’s images to see how diseases like Alzheimer’s physically change the brain.
Annese became well-known for his work with Henry Molaison, a famous amnesiac whose brain images will be studied by scientists across the world for insights into memory impairment.

"The Few, the Proud, the Brain Donors" (Voice of San Diego)

Ferguson’s ability to remember the cities she’s lived in, jobs she’s worked and, yes, all the men she’s married, makes her very valuable to Jacopo Annese, a neuroanatomist at the University of California, San Diego. Annese is director of The Brain Observatory, a research center at UCSD where brains are sliced up, laid out on slides and then scanned into digital images, which researchers can use to visualize what a variety of brains look like. Scientists can use Annese’s images to see how diseases like Alzheimer’s physically change the brain.

Annese became well-known for his work with Henry Molaison, a famous amnesiac whose brain images will be studied by scientists across the world for insights into memory impairment.

"The Few, the Proud, the Brain Donors" (Voice of San Diego)

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