Using sugar, silicone, and a 3D printer, bioengineers at Rice University and surgeons at the University of Pennsylvania have created an implant with an intricate network of blood vessels that points toward a future of growing replacement tissues and organs for transplantation.

The research may provide a method to overcome one of the biggest challenges in regenerative medicine, i.e., how to deliver oxygen and nutrients to all cells in an artificial organ or tissue implant that takes days or weeks to grow in the lab prior to surgery.

The new study was performed by a research team led by Jordan Miller, Ph.D., assistant professor of bioengineering at Rice, and Pavan Atluri, M.D., assistant professor of surgery at Penn. The study showed that blood flowed normally through test constructs that were surgically connected to native blood vessels. The study (?In vivo anastomosis and perfusion of a 3D printed construct containing microchannel networks?) was published in Tissue Engineering Part C: Methods.

Dr. Miller said one of the hurdles of engineering large artificial tissues, such as livers or kidneys, is keeping the cells inside them alive. Tissue engineers have typically relied on the body’s own ability to grow blood vessels, for example, by implanting engineered tissue scaffolds inside the body and waiting for blood vessels from nearby tissues to spread to the engineered constructs. Dr. Miller noted that that process can take weeks, and cells deep inside the constructs often starve or die from lack of oxygen before they’re reached by the slow-approaching blood vessels.

“We had a theory that maybe we shouldn’t be waiting,” he explained. “We wondered if there were a way to implant a 3D printed construct where we could connect host arteries directly to the construct and get perfusion immediately. In this study, we are taking the first step toward applying an analogy from transplant surgery to 3D printed constructs we make in the lab.”

Dr. Miller and his team thought long-term about what the needs would be for transplantation of large tissues made in the laboratory. “What a surgeon needs in order to do transplant surgery isn’t just a mass of cells; the surgeon needs a vessel inlet and an outlet that can be directly connected to arteries and veins,” he added.

The research team worked together to develop a proof-of-concept construct, a small silicone gel about the size of a small candy gummy bear, using 3D printing. But rather than printing a whole construct directly, the scientists fabricated sacrificial templates for the vessels that would be inside the construct.

It’s a technique pioneered by Dr. Miller in 2012 and inspired by the intricate sugar glass cages crafted by pastry chefs to garnish desserts.

Using an open-source 3D printer that lays down individual filaments of sugar glass one layer at a time, the researchers printed a lattice of would-be blood vessels. Once the sugar hardened, the investigators placed it in a mold and poured in silicone gel. After the gel cured, Dr. Miller’s team dissolved the sugar, leaving behind a network of small channels in the silicone.

“They don’t yet look like the blood vessels found in organs, but they have some of the key features relevant for a transplant surgeon,” said Dr. Miller. “We created a construct that has one inlet and one outlet, which are about 1 millimeter in diameter, and these main vessels branch into multiple smaller vessels, which are about 600 to 800 microns.”

Collaborating surgeons at Penn in Dr. Atluri’s group connected the inlet and outlet of the engineered gel to a major artery in a small animal model. Using Doppler imaging technology, the team observed and measured blood flow through the construct and found that it withstood physiologic pressures and remained open and unobstructed for up to three hours.

“This study provides a first step toward developing a transplant model for tissue engineering where the surgeon can directly connect arteries to an engineered tissue,” said Dr. Miller. “In the future we aim to utilize a biodegradable material that also contains live cells next to these perfusable vessels for direct transplantation and monitoring long term.”

Back in the 1950s in a weird, vampiric experiment, scientists first showed that connecting the circulatory systems of old and young mice seems to rejuvenate the more elderly animals. A handful of labs have recently been racing to find factors in young blood that may explain this effect. Now, a Harvard University group that claims to have found one such antiaging protein has published a study countering critics who dismissed the work on the molecule as flawed.

Harvard stem cell biologist Amy Wagers, cardiologist Richard Lee of the Harvard-affiliated Brigham and Women?s Hospital in Boston, and their colleagues claim that a specific protein, GDF11, may explain young blood?s beneficial effects. They have reported that blood levels of GDF11 drop in mice as the animals get older and that injecting old mice with GDF11 can partially reverse age-related thickening of the heart. In two papers last year in Science, Wagers and collaborators also reported that GDF11 can rejuvenate the rodents? muscles and brains.

Last May, however, a group led by muscle disease researcher David Glass of the Novartis Institutes for Biomedical Research in Cambridge, Massachusetts, reported that the antibody the Harvard team used to measure levels of GDF11 also detected myostatin (also known as GDF8), a similar protein that hinders muscle growth. The Novartis group concluded from a different assay that GDF11 levels in blood actually rise with age in rats and people. And in their lab, GDF11 injections inhibited muscle regeneration in young mice.

Now, the Wagers and Lee group says the assay Novartis used to detect GDF11 and GDF8 was itself flawed. They found that the main protein detected by the antibody test is immunoglobulin, another protein that rises in blood level with age. Mice lacking the gene for immunoglobulin tested negative for the active form of GDF11/8 that the Novartis assay was thought to reveal, they report today online in Circulation Research.

?They actually had very consistent findings to ours with respect to the blood levels of GDF11/8 with the antibody we all used,? Wagers says. But ?their interpretation was confused by this case of mistaken identity.? A recently published study by University of California, San Francisco, researchers finding that GDF11/8 blood levels decline with age in people and are low in those with heart disease supports the contention that GDF11 has an antiaging role, her paper notes.

The Harvard team?s paper also disputes a recent study in which cardiac physiologist Steven Houser?s group at Temple University in Philadelphia, Pennsylvania, found that GDF11 injections have no effect on heart thickness in older mice. The problem, according to Wagers, is that commercially purchased GDF11 can vary in the actual level and activity of protein. ?It wasn?t something that affected us early on, but we figured out it was an issue,? she says. That lot-to-lot variability likely explains why the Houser group didn?t see any effects from GDF11 at the same apparent dose the Harvard group reported using, she adds. (Lee says his group now suspects that the dose was higher than they realized.)

To back up their earlier results, Wagers and collaborators again show in the new paper that daily GDF11 injections can shrink heart muscle in both old and new mice. But this time they note another observation: The mice also lost weight. ?We don?t have much insight into that right now, but we?re looking into it,? Wagers says. She says the findings suggest that as with other hormones, GDF11 may have ?a therapeutic window? for beneficial effects?too much may cause harm.

Houser says he agrees that one of the Novartis team?s assays for GDF11 was probably detecting immunoglobulin. But Houser notes that the group also used a different assay to detect GDF11 and that isn?t challenged by the new paper. (David Glass makes the same point.) Sorting out what role GDF11 may play in aging is important, Houser adds. ?I’m going to be 65 in a couple months. I’d love to have something that improves my heart, brain, and muscle function,? Houser says. ?I think the field is going to figure this out and this is another piece of the puzzle.?

Aging insidiously leaves its mark on our brains.

With age, our well-oiled neuronal machinery slowly breaks down: gene expression patterns turn wacky, the nuclear membrane disintegrates, and neatly organized molecules inside the cells break out of their segregated compartments, turning the intracellular environment into a maladaptive, muddled molecular soup.

Yet the aging phenomenon has been very tough to study. Historically, scientists relied on fast-aging animal models ? from fruit flies to primitive worms to mice ? to tease out the biological mechanisms of aging, especially for tissues that are hard to biopsy from patients, including the brain.

Despite the value of these reductionist models, many life-lengthening treatments fail in clinical trials, and the leap from flies to mice to men remains insurmountable.

With the rise of induced pluripotent stem cell (iPSC) technology, scientists have been able to transform patients? skin cells into iPSCs, which can then be coaxed into neurons for further study.

It?s a powerful technique: iPSCs derived from patients with Parkinson?s disease, for example, contain the same genetic underpinnings of the disease, which let scientists cheaply and efficiently test out theories and potential drug treatments?on human cells within the tightly controlled environment of a culture dish.

But the conversion process essentially turns back the clock: because iPSCs resemble early stage embryonic development, even when taken from an elder donor, they ? and the neurons generated from them ? lose their ?aged? signature. Previous research found that their epigenetic landscapes, which dictate what genes are expressed where via small chemical attachments to the DNA, are reset to match that of a younger cell?s profile during the reprogramming process.

For example, genes that promote cell division are jacked up, whereas genes involved in inflammation ? a strong correlate of aging ? are tuned down. This discrepancy hardly makes them a good model of their aged donors.

It?s a thorny problem that?s plagued the field for decades. But now, published last week in Cell Stem Cell, a team led by Salk Institute professor Dr. Fred ?Rusty? Gage has offered a clever solution.

The answer is to eschew iPSCs altogether, and take the road less traveled.

Using a method first discovered a few years ago at Stanford University, the team realized that with a series of careful biochemical tweaks, they could directly coax skin cells into fully functional neurons. Since these ?induced neurons? skipped the embryonic stage, they reasoned, maybe their age counters were not reset.

No one knew if and how cells created in this way differed from neurons that naturally aged in the human brain, says lead author Dr. Jermone Mertens.

To find out, the team took skin biopsies from 19 volunteers aged from infancy to 89 years old, and transformed those skin cells into neurons using both the iPSC method and the direct conversion approach.

They then compared these ?test tube neurons? to neurons obtained from autopsies of age-matched controls by looking at their transcriptomics ? that is, a bird?s eye view of gene expression patterns that change with age.

As expected, iPSC-generated neurons lost their life history, reverting back to a baby-like state.

In stark contrast, neurons generated by direct conversion significantly differed in their transcriptomes based on the donor?s age. ?They actually show changes in gene expression that have been previously implicated in brain aging,? said Mertens.

It?s a first, and it could be a game changer.

He pointed to a protein called RanBP17, which shuttles proteins in-and-out of the nucleus. The decline of RanBP17 was previously hypothesized to play a role in brain aging, but the theory was difficult to model in animals. However, to the team?s excitement, this abnormal decrease was recapitulated in neurons directly converted from older patients.

Other cellular assays also showed that the lab-grown neurons retained their telltale signs of aging. With age, the fragile membrane that separates the nucleus from other cellular component begins to fail, and proteins ? no longer confined to their physiological working space ? run amok.

This process could lead to aging or increase our susceptibility to age-related neurodegenerative disorders, but we don?t know, said Martens. He?s eager to put the new system to use. With this new culture system, we can now directly test these ideas, Martens said.

?The results are obviously going to have an impact,? agrees Dr. John Gearhart, an expert in regenerative medicine at the University of Pennsylvania, who wasn?t involved in the study.

Although the team only tried their cell-transforming method in neurons, Gage expects it to work for other organs as well, allowing scientists to create aged heart or liver cells. The technique could also be expanded to highly-structured 3D cultures such as organoids, and used to model aging human organs.

“We expect that the paradigm of direct conversion into age-equivalent cells can be very important for future studies of age-related diseases,” said Gage.

An unexpected factor may be influencing stem cell transplants, suggests a new study by researchers at the Stanford University School of Medicine. They found that a sleep deprived donor has a huge effect on the ability of blood and immune system stem cells to migrate to their proper spots in the bone marrow of a recipient.

The research was conducted on laboratory mice, but may have implications for human stem cell transplants. Thousands of procedures often referred to as bone marrow transplants (but more accurately called hematopoietic stem cell transplants) are performed every year.

In the experiment, a sleep deficit of only four hours could affect by as much as 50 percent the ability of stem cells to migrate successfully.

?Considering how little attention we typically pay to sleep in the hospital setting, this finding is troubling,? said Dr. Asya Rolls, an assistant professor at the Israel Institute of Technology, in a statement. ?We go to all this trouble to find a matching donor, but this research suggests that if the donor is not well-rested it can impact the outcome of the transplantation. However, it?s heartening to think that this is not an insurmountable obstacle; a short period of recovery sleep before transplant can restore the donor?s cells? ability to function normally.?

Rolls is co-lead author of the study along with Dr. Wendy Pang, a postdoctoral scholar at Stanford, and Dr. Ingrid Ibarra, the assistant director of the Stanford Cardiovascular Institute.

The team conducted research comparing mice who had been gently handled for four hours to prevent sleep with mice who were well-rested. They collected stem cells from the bone marrow of both groups of mice and injected them into 12 mice who had received what would normally be a deadly dose of radiation. The recipient mice also got a dose of their own bone marrow cells, so it would be possible to track the abilities of the donated cells in relation.

The researchers assessed the prevalence of myeloid cells, a type of immune cell, at both eight and 16 weeks after the transplant. They found that stem cells from the well-rested mice made up about 26 percent of myeloid cells over time, but stem cells from sleep deprived donors made up only about 12 percent of the recipient?s myeloid cells.

The team also looked at the ability of the stem cells to migrate properly from the blood into the bone marrow. After 12 hours, 3.3 percent of the stem cells from rested mice had found their way to the bone marrow, compared to only 1.7 percent of stem cells from sleepy mice.

Rolls and her colleagues found that the effects of sleep deprivation could be reversed by catching only a couple hours of sleep.

?Everyone has these stem cells, and they continuously replenish our blood and immune system,? Rolls said. ?We still don?t know how sleep deprivation affects us all, not just bone marrow transplant donors. The fact that recovery sleep is so helpful only emphasizes how important it is to pay attention to sleep.?

A Johns Hopkins University biologist has led a research team reporting progress in understanding the shape-shifting ways of stem cells, which have vast potential for medical research and disease treatment.

In a research paper published in Cell Reports on Oct. 13, Xin Chen, an associate professor of biology in the university’s Krieger School of Arts and Sciences, and her six co-authors report on how stem cells are affected by their immediate surroundings. The scientists found that an enzyme present in the spot where stem cells are found can help nurture a greater abundance of these cells by sustaining them in their original state, and by promoting other cells to lose their specialized traits and transform into stem cells.

The results show that the enzyme aminopeptidase in the stem cell niche?in this case, the area where stem cells are found in the testicular tissue in fruit flies?plays a role in both of these functions. How the niche itself plays this role, however, remains unclear.

That the enzyme in that spot promotes more specialized cells to become like stem cells “suggests that this change of cell fate needs cues from where stem cells normally reside, but not randomly,” said Chen, the principal investigator. “These results have medical implications because if this cell fate change could happen randomly, it may lead to diseases such as cancers.”

That’s because there’s a delicate balance to be struck in managing the proliferation of undifferentiated stem cells in tissue, Chen said. Too few can cause tissue deterioration, too many can promote tumors.

The study focused on fruit flies in part because they share with humans about three-quarters of the genes that cause disease, making them a fine research model. The work on this paper focused on the testis because stem cells are found there in both fruit flies and humans.

Stem cells are found in humans in an array of tissues, including skin, blood vessels, teeth, heart, brain, and liver.

Because they can develop from their original state into specialized or differentiated cells, stem cells have long held out the promise of being used to replace damaged organs and muscle. Stem cells have been used to treat illness in limited ways for decades, including transplantation from bone marrow.

However, their application could be much wider with reliable techniques to control how they take on specialized functions, how they can revert to their stem state, and in some instances, how they proliferate in their original state to form potentially dangerous tumors.

One question now is whether the activity of the niche and of the enzyme reported in this research can be harnessed to manipulate stem cells to differentiate in useful ways. There’s a lot of work yet to be done, Chen said.

“How cells become different, it’s very important to understand that,” Chen said.

Chen’s six collaborators on this paper were Cindy Lim, who earned her doctorate at Johns Hopkins and now works for the U.S. Food and Drug Administration; Lijuan Feng of the Johns Hopkins University Department of Biology; Shiv Gandhi and Sinisa Urban of the Howard Hughes Medical Institute, Department of Molecular Biology and Genetics at the Johns Hopkins University School of Medicine; and Martin L. Biniossek and Oliver Schilling of the Institute of Molecular Medicine and Cell Research at the University of Freiburg.

Researchers in Melbourne and Brisbane have successfully grown a human ‘mini-kidney’ from stem cells.

Published in the journal Nature, the results have significant implications for medical research, as the mini-organ mimics normal kidney development.

It means laboratory-grown kidneys can be used for drug testing and potentially the bioengineering of replacement kidneys for patients with renal failure as they can be grown from any person using cells such as skin or blood.

It also opens the door for cell therapy and other new treatments for kidney disease – not to mention giving researchers a chance to grow ‘kidney models’ to learn more about how the human kidney forms normally.

“For us it’s a pretty exciting advance,” said stem cell biologist Melissa Little, of the Murdoch Childrens Research Institute.

“This organ is making its own blood vessels, it’s making it’s own tubules for filtering and cleaning the blood, so it’s really a very complex structure,” she said of the kidney, which was observed three weeks after creation.

An author on the paper, Professor Little said it was equally important to learn how healthy and diseased kidneys functioned but that ethical reasons often limited research on human kidneys. Instead mice were used. However, she said while the mouse kidney was similar to humans, it was structurally different.

“Now for the first time we have a chance to ask what is different between a human and a mouse kidney because we don’t study human kidneys for obvious reasons,” she said. “From a research point of view it is going to tell us a great deal more than we knew before.”

About half the children with kidney disease had inherited the condition via a genetic mutation. Being able to grow a kidney using a patient’s stem cells meant a diseased kidney could be grown to test a patient’s response to treatment before drugs were administered.

The breakthrough follows Professor Little’s team’s first creation of a mini-kidney in 2013, which was able to form two cell-types.

This kidney, grown in collaboration with colleagues from Melbourne University and the University of Queensland, is different. No longer than a centimetre, it features up to 12 types of cell normally found in the human body making it equivalent to a foetal kidney. An adult kidney has around 20 cell types and is the size of a large softball.

It was also created using stem cells made from adult skin, rather than embryonic stem cells which were used in the 2013 kidney.

Following an exhaustive, ten-year effort, scientists at the Buck Institute for Research on Aging and the University of Washington have identified 238 genes that, when removed, increase the replicative lifespan of S. cerevisiae yeast cells. This is the first time 189 of these genes have been linked to aging. These results provide new genomic targets that could eventually be used to improve human health. The research was published online on October 8th in the journal Cell Metabolism.

“This study looks at aging in the context of the whole genome and gives us a more complete picture of what aging is,” said Brian Kennedy, PhD, lead author and the Buck Institute’s president and CEO. “It also sets up a framework to define the entire network that influences aging in this organism.”

The Kennedy lab collaborated closely with Matt Kaeberlein, PhD, a professor in the Department of Pathology at the University of Washington, and his team. The two groups began the painstaking process of examining 4,698 yeast strains, each with a single gene deletion. To determine which strains yielded increased lifespan, the researchers counted yeast cells, logging how many daughter cells a mother produced before it stopped dividing.

“We had a small needle attached to a microscope, and we used that needle to tease out the daughter cells away from the mother every time it divided and then count how many times the mother cells divides,” said Dr. Kennedy. “We had several microscopes running all the time.”

These efforts produced a wealth of information about how different genes, and their associated pathways, modulate aging in yeast. Deleting a gene called LOS1 produced particularly stunning results. LOS1 helps relocate transfer RNA (tRNA), which bring amino acids to ribosomes to build proteins. LOS1 is influenced by mTOR, a genetic master switch long associated with caloric restriction and increased lifespan. In turn, LOS1 influences Gcn4, a gene that helps govern DNA damage control.

“Calorie restriction has been known to extend lifespan for a long time.” said Dr. Kennedy. “The DNA damage response is linked to aging as well. LOS1 may be connecting these different processes.”

A number of the age-extending genes the team identified are also found in C. elegans roundworms, indicating these mechanisms are conserved in higher organisms. In fact, many of the anti-aging pathways associated with yeast genes are maintained all the way to humans.

The research produced another positive result: exposing emerging scientists to advanced lab techniques, many for the first time.

“This project has been a great way to get new researchers into the field,” said Dr. Kennedy. “We did a lot of the work by recruiting undergraduates, teaching them how to do experiments and how dedicated you have to be to get results. After a year of dissecting yeast cells, we move them into other projects.”

Though quite extensive, this research is only part of a larger process to map the relationships between all the gene pathways that govern aging, illuminating this critical process in yeast, worms and mammals. The researchers hope that, ultimately, these efforts will produce new therapies.

“Almost half of the genes we found that affect aging are conserved in mammals,” said Dr. Kennedy. “In theory, any of these factors could be therapeutic targets to extend healthspan. What we have to do now is figure out which ones are amenable to targeting.”

The human cerebral cortex contains 16 billion neurons, wired together into arcane, layered circuits responsible for everything from our ability to walk and talk to our sense of nostalgia and drive to dream of the future. In the course of human evolution, the cortex has expanded as much as 1,000-fold, but how this occurred is still a mystery to scientists.

Now, researchers at UC San Francisco have succeeded in mapping the genetic signature of a unique group of stem cells in the human brain that seem to generate most of the neurons in our massive cerebral cortex.

The new findings, published Sept. 24 in the journal Cell, support the notion that these unusual stem cells may have played an important role in the remarkable evolutionary expansion of the primate brain.

?We want to know what it is about our genetic heritage that makes us unique,? said Arnold Kriegstein, MD, PhD, professor of developmental and stem cell biology and director of the Eli and Edyth Broad Center of Regeneration Medicine and Stem Cell Research at UCSF. ?Looking at these early stages in development is the best opportunity to understand our brain?s evolution.?

Building a Brain from the Inside Out

The grand architecture of the human cortex, with its hundreds of distinct cell types, begins as a uniform layer of neural stem cells and builds itself from the inside out during several months of embryonic development.

Until recently, most of what scientists knew about this process came from studies of model organisms such as mice, where nearly all neurons are produced by stem cells called ventricular radial glia (vRGs) that inhabit a fertile layer of tissue deep in the brain called the ventricular zone (VZ). But recent insights suggested that the development of the human cortex might have some additional wrinkles.

In 2010, Kriegstein?s lab discovered a new type of neural stem cell in the human brain, which they dubbed outer radial glia (oRGs) because these cells reside farther away from the nurturing ventricles, in an outer layer of the subventricular zone (oSVZ). To the researchers? surprise, further investigations revealed that during the peak of cortical development in humans, most of the neuron production was happening in the oSVZ rather than the familiar VZ.

oRG stem cells are extremely rare in mice, but common in primates, and look and behave quite differently from familiar ventricular radial glia. Their discovery immediately made Kriegstein and colleagues wonder whether this unusual group of stem cells could be a key to understanding what allowed primate brains to grow to their immense size and complexity.

?We wanted to know more about the differences between these two different stem cell populations,? said Alex Pollen, PhD, a postdoctoral researcher in Kriegstein?s lab and co-lead author of the new study. ?We predicted oRGs could be a major contributor to the development of the human cortex, but at first we only had circumstantial evidence that these cells even made neurons.?

Outsider Stem Cells Make Their Own Niche

In the new research, Pollen and co-first author Tomasz Nowakowski, PhD, also a postdoctoral researcher in the Kriegstein lab, partnered with Fluidigm Corp. to develop a microfluidic approach to map out the transcriptional profile ? the set of genes that are actively producing RNA ? of cells collected from the VZ and SVZ during embryonic development.

They identified gene expression profiles typical of different types of neurons, newborn neural progenitors and radial glia, as well as molecular markers differentiating oRGs and vRGs, which allowed the researchers to isolate these cells for further study.

The gene activity profiles also provided several novel insights into the biology of outer radial glia. For example, researchers had previously been puzzled as to how oRG cells could maintain their generative vitality so far away from the nurturing VZ. ?In the mouse, as cells move away from the ventricles, they lose their ability to differentiate into neurons,? Kriegstein explained.

But the new data reveals that oRGs bring a support group with them: The cells express genes for surface markers and molecular signals that enhance their own ability to proliferate, the researchers found.

?This is a surprising new feature of their biology,? Pollen said. ?They generate their own stem cell niche.?

The researchers used their new molecular insights to isolate oRGs in culture for the first time, and showed that these cells are prolific neuron factories. In contrast to mouse vRGs, which produce 10 to 100 daughter cells during brain development, a single human oRG can produce thousands of daughter neurons, as well as glial cells?non-neuronal brain cells increasingly recognized as being responsible for a broad array of maintenance functions in the brain.

New Insights into Brain Evolution, Development and Disease

The discovery of human oRGs? self-renewing niche and remarkable generative capacity reinforces the idea that these cells may have been responsible for the expansion of the cerebral cortex in our primate ancestors, the researchers said.

The research also presents an opportunity to greatly improve techniques for growing brain circuits in a dish that reflect the true diversity of the human brain, they said. Such techniques have the potential to enhance research into the origins of neurodevelopmental and neuropsychiatric disorders such as microcephaly, lissencephaly, autism and schizophrenia, which are thought to affect cell types not found in the mouse models that are often used to study such diseases.

The findings may even have implications for studying glioblastoma, a common brain cancer whose ability to grow, migrate and hack into the brain?s blood supply appears to rely on a pattern of gene activity similar to that now identified in these neural stem cells.

?The cerebral cortex is so different in humans than in mice,? Kriegstein said. ?If you?re interested in how our brains evolved or in diseases of the cerebral cortex, this is a really exciting discovery.?

The study represents the first salvo of a larger BRAIN Initiative-funded project in Kriegstein?s lab to understand the thousands of different cell types that occupy the developing human brain

?At the moment, we simply don?t have a good understanding of the brain?s ?parts list,?? Kriegstein said, ?but studies like this are beginning to give us a real blueprint of how our brains are built.?