Friday Stem Cell Roundup: Making Nerves from Blood; New Clues to Treating Parkinson’s

Stanford lab develops method to make nerve cells from blood.

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Induced neuronal (iN) cells derived from adult human blood cells. Credit: Marius Wernig, Stanford University.

Back in 2010, Stanford Professor Marius Wernig and his team devised a method to directly convert skin cells into neurons, a nerve cell. This so-called transdifferentiation technique leapfrogs over the need to first reprogram the skin cells into induced pluripotent stem cells. This breakthrough provided a more efficient path to studying how genetics plays a role in various mental disorders, like autism or schizophrenia, using patient-derived cells. But these types of genetic analyses require data from many patients and obtaining patient skin samples hampered progress because it’s not only an invasive, somewhat painful procedure but it also takes time and money to prepare the tissue sample for the transdifferentiation method.

This week, the Wernig lab reported on a solution to this bottleneck in the journal, PNAS. The study, funded in part by CIRM, describes a variation on their transdifferentiation method which converts T cells from the immune system, instead of skin cells, into neurons. The huge advantage with T cells is that they can be isolated from readily available blood samples, both fresh or frozen. In a press release, Wernig explains this unexpected but very welcomed result:

“It’s kind of shocking how simple it is to convert T cells into functional neurons in just a few days. T cells are very specialized immune cells with a simple round shape, so the rapid transformation is somewhat mind-boggling. We now have a way to directly study the neuronal function of, in principle, hundreds of people with schizophrenia and autism. For decades we’ve had very few clues about the origins of these disorders or how to treat them. Now we can start to answer so many questions.”

Two studies targeting Parkinson’s offer new clues to treating the disease (Kevin McCormack)
Despite decades of study, Parkinson’s disease remains something of a mystery. We know many of the symptoms – trembling hands and legs, stiff muscles – are triggered by the loss of dopamine producing cells in the brain, but we are not sure what causes those cells to die. Despite that lack of certainty researchers in Germany may have found a way to treat the disease.

Mitochondria

Simple diagram of a mitochondria.

They took skin cells from people with Parkinson’s and turned them into the kinds of nerve cell destroyed by the disease. They found the cells had defective mitochondria, which help produce energy for the cells. Then they added a form of vitamin B3, called nicotinamide, which helped create new, healthy mitochondria.

In an article in Science & Technology Research News Dr. Michela Deleidi, the lead researcher on the team, said this could offer new pathways to treat Parkinson’s:

“This substance stimulates the faulty energy metabolism in the affected nerve cells and protects them from dying off. Our results suggest that the loss of mitochondria does indeed play a significant role in the genesis of Parkinson’s disease. Administering nicotinamide riboside may be a new starting-point for treatment.”

The study is published in the journal Cell Reports.

While movement disorders are a well-recognized feature of Parkinson’s another problem people with the condition suffer is sleep disturbances. Many people with Parkinson’s have trouble falling asleep or remaining asleep resulting in insomnia and daytime sleepiness. Now researchers in Belgium may have uncovered the cause.

Working with fruit flies that had been genetically modified to have Parkinson’s symptoms, the researchers discovered problems with neuropeptidergic neurons, the type of brain cell that helps regulate sleep patterns. Those cells seemed to lack a lipid, a fat-like substance, called phosphatidylserine.

In a news release Jorge Valadas, one of the lead researchers, said replacing the missing lipid produced promising results:

“When we model Parkinson’s disease in fruit flies, we find that they have fragmented sleep patterns and difficulties in knowing when to go to sleep or when to wake up. But when we feed them phosphatidylserine–the lipid that is depleted in the neuropeptidergic neurons–we see an improvement in a matter of days.”

Next, the team wants to see if the same lipids are low in people with Parkinson’s and if they are, look into phosphatidylserine – which is already approved in supplement form – as a means to help ease sleep problems.

Stem Cell Roundup: better model of schizophrenia, fasting boosts stem cells, and why does our hair gray.

Stem cell photo of the week:
Recreating brain cell interactions for studying schizophrenia

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Salk researchers used stem cells to derive CA3 pyramidal neurons (green), including a rare subtype of the cells (red). Image: Salk Institute

Our pick for the stem cell image of the week is from the laboratory of Rusty Gage at the Salk Institute. The team generated multiple types of nerve cells from stem cells to more closely represent the interactions that occur in the brain. They’re using this system to show how the communication between these nerve cells becomes faulty in people with schizophrenia. A Salk Institute press release provides more details about their study which was published in Cell Stem Cell.

Regenerative power of intestinal stem cells maintained via fasting
For many decades, researchers have known that restricting food intake in mice can extend life span. Why it happens hasn’t been well understood. This week, a team at MIT uncovered a possible explanation: fasting increases the regenerative power of stem cells.

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Intestinal stem cells from mice that fasted for 24 hours, at right, produced much more substantial intestinal organoids than stem cells from mice that did not fast, at left.
Image: Maria Mihaylova and Chia-Wei Cheng, MIT

The report, published in Cell Stem Cell, focused on the well-studied intestinal stem cell, which renews the intestinal lining every five days. As we age, the intestinal stem cell’s regenerative abilities wane and damage to the intestinal lining takes longer to repair.

Mice were fasted for 24 hours and then their intestinal stem cells were retrieved and grown into mini-intestine organoids in petri dishes. According to Maria Mihaylova, PhD, one of the lead authors, the results of the experiment were very clear:

“It was very obvious that fasting had this really immense effect on the ability of intestinal crypts to form more organoids, which is stem-cell-driven,” Mihaylova said in a press release. “This was something that we saw in both the young mice and the aged mice, and we really wanted to understand the molecular mechanisms driving this.”

Mihaylova and the team went on to show that fasting caused the stem cells to burn fat instead of carbohydrates for their energy needs. Inhibiting the gene pathways that flip this metabolic switch also blocks the regenerative capacity of fasting. On the other hand, molecules that boost the gene pathways mimic the effects of fasting without changing food intake. This intriguing finding could potentially have clinical applications for cancer patients who suffer intestinal injury from the toxic effects of chemotherapy drugs but who certainly aren’t in a condition to fast.

Premature graying, our immune system and stem cells: a surprising link. (Kevin McCormack)
As someone whose hair went gray at a relatively young age – well, it seemed young to me! – this next story naturally caught my eye. It highlights how our immune systems may play a key role in determining our hair color and, in particular, when that hair turns gray.

Our bodies are constantly shedding hairs and replacing them with new ones. Normally stem cells called melanocytes help ensure the new hairs have your original color, be it black, blonde, brunette or red.

Researchers at the National Institutes of Health and the University of Alabama, Birmingham, found that when the body is attacked by a virus, our immune system kicks in and respond by producing interferon to fight off the infection. However, when a protein called MITF, that is involved in regulating how cells use interferon, fails to work properly it can also affect melanocytes causing them to lose their pigmentation. Without that pigmentation the new hairs are gray.

The study, which appears in the journal PLOS Biology, is too late to help me and my gray hair – particularly as it was done in mice – but it could pave the way for further research that identifies how genes that control pigment in our hair and skin also control our immune system.

Stem Cell Roundup: The brain & obesity; iPSCs & sex chromosomes; modeling mental illness

Stem Cell Image of the Week:
Obesity-in-a-dish reveals mutations and abnormal function in nerve cells

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Image shows two types of hypothalamic neurons (in magenta and cyan) that were derived from human induced pluripotent stem cells.
Credit: Cedars-Sinai Board of Governors Regenerative Medicine Institute

Our stem cell image of the week looks like the work of a pre-historic cave dweller who got their hands on some DayGlo paint. But, in fact, it’s a fluorescence microscopy image of stem cell-derived brain cells from the lab of Dhruv Sareen, PhD, at Cedars-Sinai Medical Center. Sareen’s team is investigating the role of the brain in obesity. Since the brain is a not readily accessible organ, the team reprogrammed skin and blood cell samples from severely obese and normal weight individuals into induced pluripotent stem cells (iPSCs). These iPSCs were then matured into nerve cells found in the hypothalamus, an area of the brain that regulates hunger and other functions.

A comparative analysis showed that the nerve cells derived from the obese individuals had several genetic mutations and had an abnormal response to hormones that play a role in telling our brains that we are hungry or full. The Cedars-Sinai team is excited to use this obesity-in-a-dish system to further explore the underlying cellular changes that lead to excessive weight gain. Ultimately, these studies may reveal ways to combat the ever-growing obesity epidemic, as Dr. Sareen states in a press release:

“We are paving the way for personalized medicine, in which drugs could be customized for obese patients with different genetic backgrounds and disease statuses.”

The study was published in Cell Stem Cell

Differences found in stem cells derived from male vs female.

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Microscope picture of a colony of iPS cells. Credit: Vincent Pasque

Scientists at UCLA and KU Leuven University in Belgium carried out a study to better understand the molecular mechanisms that control the process of reprogramming adult cells back into the embryonic stem cell-like state of induced pluripotent stem cells (iPSCs). Previous studies have shown that female vs male embryonic stem cells have different patterns of gene regulation. So, in the current study, male and female cells were analyzed side-by-side during the reprogramming process.  First author Victor Pasquale explained in a press release that the underlying differences stemmed from the sex chromosomes:

In a normal situation, one of the two X chromosomes in female cells is inactive. But when these cells are reprogrammed into iPS cells, the inactive X becomes active. So, the female iPS cells now have two active X chromosomes, while males have only one. Our results show that studying male and female cells separately is key to a better understanding of how iPS cells are made. And we really need to understand the process if we want to create better disease models and to help the millions of patients waiting for more effective treatments.”

The CIRM-funded study was published in Stem Cell Reports.

Using mini-brains and CRISPR to study genetic linkage of schizophrenia, depression and bipolar disorder.

If you haven’t already picked up on a common thread in this week’s stories, this last entry should make it apparent: iPSC cells are the go-to method to gain insight in the underlying mechanisms of a wide range of biology topics. In this case, researchers at Brigham and Women’s Hospital at Harvard Medical School were interested in understanding how mutations in a gene called DISC1 were linked to several mental illnesses including schizophrenia, bipolar disorder and severe depression. While much has been gleaned from animal models, there’s limited knowledge of how DISC1 affects the development of the human brain.

The team used human iPSCs to grow cerebral organoids, also called mini-brains, which are three-dimensional balls of cells that mimic particular parts of the brain’s anatomy. Using CRISPR-Cas9 gene-editing technology – another very popular research tool – the team introduced DISC1 mutations found in families suffering from these mental disorders.

Compared to cells with normal copies of the DISC1 gene, the mutant organoids showed abnormal structure and excessive cell signaling. When an inhibitor of that cell signaling was added to the growing mutant organoids, the irregular structures did not develop.

These studies using human cells provide an important system for gaining a better understanding of, and potentially treating, mental illnesses that victimize generations of families.

The study was published in Translation Psychiatry and picked up by Eureka Alert.

CIRM-funded team uncovers novel function for protein linked to autism and schizophrenia

Imagine you’ve just stopped your car at the top of the steepest street in San Francisco. Now, if want to stay at the top of the hill you’re going to need to keep your foot on the brakes. Let go and you’ll start rolling down. Fast.

Don’t step off the brake pedal! Photo: Wikipedia

Conceptually, similar decision points happen in human development. A brain cell, for instance, has the DNA instructions to become any cell in the body but must “keep the brakes on”, or repress, genes responsible for other cell types. Release the silencing of those genes and the brain cell’s properties will get pulled toward other fates.

That’s the subject of a CIRM-funded research study published today in Nature which reports on the identification of a new type of repressor protein which opens up a new understanding of how brain cells establish and keep their identity. That may not sound so exciting to our non-scientist readers but this discovery could lead to new therapy approaches for neurological disorders like autism, schizophrenia, major depression and low I.Q.

Skin cells to brain cells with just three genes
In previous experiments, this Stanford University research team led by Marius Wernig, showed it’s possible to convert a skin cell to a brain cell, or neuron, by adding just three genes to the cells, including one called Myt1l. The other two genes were known to act as master “on switches” that activate a cascade of genes responsible for making neuron-specific proteins. Myt1l also helped increase the efficiency of this direct reprogramming but it’s exact role in the process wasn’t clear.

Direct conversion of skin cell into a neuron.
Image: Wernig Lab, Stanford

A closer examination of Myt1l protein function revealed that instead of being an on switch for neuron-specific genes, it was actually an off switch for skin-specific genes. Now, there’s nothing unusual about the existence of a protein that represses gene activity to help determine cell identity. But up until now, these repressors were thought to be “lineage specific” meaning they specifically switched off genes of a specific cell type. For example, a well-studied repressor called REST affects cell fate by putting the brakes on only nerve-specific genes. The case of Myt1l was different.

Many but one
The researchers found that, in brain cells, Myt1l not only blocked the activation of skin-specific genes, it also shut down genes related to lung, cartilage, heart and other cells fates. The one set of genes that Mytl1 repressor did not appear to act on was neuron-specific genes. From these results a “many but one” pattern emerged. That is; it seems Myt1l helps drive and maintain a neuron cell fate by shutting off gene networks for many different cell identities except for neurons. It’s a novel way to regulate cell fate, as Wernig explained in a press release:

Marius Wernig
Photo: Steve Fisch

“The concept of an inverse master regulator, one that represses many different developmental programs rather than activating a single program, is a unique way to control neuronal cell identity, and a completely new paradigm as to how cells maintain their cell fate throughout an organism’s lifetime.”

To build a stronger case for Myt1l function, the team looked at the effect of blocking the protein in the developing mouse brain. Sure enough, lifting Myt1l repression lead to a decrease in the number of neurons in the brain. Wernig described the impact of also inhibiting Myt1l in mature neurons:

“When this protein is missing, neural cells get a little confused. They become less efficient at transmitting nerve signals and begin to express genes associated with other cell fates.”

Potential cures can be uncovered withfundamental lab research
It turns out that Myt1l mutations have been recently found in people with autism, schizophrenia, major depression and low I.Q. Based on their new insights, the author suggest that in adults, these disorders may be caused by a neuron’s inability to maintain its identity rather than by a more permanent abnormality that occurred during fetal brain development. This hypothesis presents the exciting possibility of developing therapies that could improve symptoms.

Stem cell stories that caught our eye: Amy Schumer’s MS fundraising; healing traumatic brain injury; schizophrenia iPS insights

Amy Schumer and Paul Shaffer raise money for MS. (Karen Ring)
Two famous individuals, one a comedian/movie star, the other a well-known musician, have combined forces to raise money for an important cause. Amy Schumer and Paul Shaffer have pledged to raise $2.5 million dollars to help support research into multiple sclerosis (MS). This disease affects the nerve cells in both the brain and spinal cord. It eats away at the protective myelin sheaths that coat and protect nerve cells and allow them to relay signals between the brain and the rest of the body. As a result, patients experience a wide range of symptoms including physical, mental and psychiatric problems.

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Comedian Amy Schumer and her Dad who has MS.
(National MS Society)

The jury is still out on the exact cause of MS and there is no cure available. But the Tisch MS Research Center of New York is trying to change that. It is “dedicated to finding the cause and cure for MS” and recently announced, at its annual Future Without MS Gala, that it has pledged to raise $10 million to fund the stem cell research efforts ongoing at the Center. Currently, Tisch is “the only center with an FDA approved stem cell clinical trial for MS in the United States.” You can read more about this clinical trial, which is transplanting mesenchymal stem cell-derived brain progenitor cells into the spinal cord, on the Tisch website.

At the gala, both Amy Schumer and Paul Shaffer were present to show their support for MS research. In an interview with People magazine, Amy revealed that her father struggles with MS. She explained, “Some days he’s really good and he’s with it and we’re joking around. And some days I go to visit my dad and it’s so painful. I can’t believe it.” Her experience watching her dad battle with MS inspired her to write and star in the movie TRAINWRECK, and also to get involved in supporting MS research. “If I can help at all I’m gonna try, even if that means I’ll get hurt,” she said.

Stem cells may help traumatic brain injuries (Kevin McCormack
Traumatic brain injury (TBI) is a huge problem in the US. According to the Centers for Disease Control and Prevention around 1.7 million Americans suffer a TBI every year; 250,000 of those are serious enough to result in a hospitalization; 52,000 are fatal. Even those who survive a TBI are often left with permanent disabilities, caused by swelling in the brain that destroys brain cells.

Now researchers at the University of Texas Health Science Center at Houston say using a person’s own stem cells could help reduce the severity of a TBI.

The study, published in the journal Stem Cells, found that taking stem cells from a person’s own bone marrow and then re-infusing them into the bloodstream, within 48 hours of the injury, can help reduce the swelling and inflammation that damages the brain.

In an interview with the Houston Chronicle Charles Cox, the lead researcher – and a member of CIRM’s Grants Working Group panel of experts – says the results are not a cure but they are encouraging:

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Charles Cox
(Drew Donovan / UTHealth)

“I’m talking about the difference between someone who recovers to the point that they can take care of themselves, and someone who is totally dependent on someone else for even simple tasks, like using the bathroom and bathing. That’s a dramatic difference.”

Schizophrenia: an imbalance of brain cell types?

Schizophrenia is a chronic mental disorder with a wide range of disabling symptoms such as delusional thoughts, hearing voices, anxiety and an inability to experience pleasure. It’s estimated that half of those with schizophrenia abuse drugs and alcohol, which likely contributes to increased incidence of unemployment, homelessness and suicide. No cure exists for the disorder because scientists don’t fully understand what causes it, and available treatments only mask the symptoms.

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A patient’s artistic representation of living with schizophrenia
(Wikipedia)

This week, researchers at the RIKEN Brain Science Institute in Japan reported new clues about what goes wrong at a cellular and molecular level in the brains of people with schizophrenia. The scientists created induced pluripotent stem cells (iPSCs) from healthy donors, as well as patients with schizophrenia, and then changed or specialized them into nerve cells, or neurons. They found that fewer iPSCs developed into neurons when comparing the cells from people with schizophrenia to the healthy donor cells. Instead, more iPSCs specialized into astrocytes, another type of brain cell. This fewer neurons/more astrocytes shift was also seen in brains of deceased donors who had schizophrenia.

Looking inside the cells, the researchers found higher levels of a protein called p38 in the neurons derived from the people with schizophrenia. Inhibiting the activity of p38 led to increased number of neurons and fewer astrocytes, which resembles the healthy state. These results, published in Translational Psychiatry and picked up by Health Canal, point to inhibitors of p38 activity as a potential path for developing new treatments.

Stem cell stories that caught our eye: functioning liver tissue, making new bone, stem cells and mental health

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Functioning liver tissue. Scientists are looking to stem cells as a potential alternative treatment to liver transplantation for patients with end-stage liver disease. Efforts are still in their early stages but a study published this week in Stem Cells Translational Medicine, shows how a CIRM-funded team at the Children’s Hospital Los Angeles (CHLA) successfully generated partially functional liver tissue from mouse and human stem cells.

Biodegradable scaffold (left) and human tissue-engineered liver (right) (Photo courtesy of The Saban Research Institute at Children’s Hospital Los Angeles)

Biodegradable scaffold (left) and human tissue-engineered liver (right) (Photo courtesy of The Saban Research Institute at Children’s Hospital Los Angeles)

The lab had previously developed a protocol to make intestinal organoids from mouse and human stem cells. They were able to tweak the protocol to generate what they called liver organoid units and transplanted the tissue-engineered livers into mice. The transplants developed cells and structures found in normal healthy livers, but their organization was different – something that the authors said they would address in future experiments.

Impressively, when the tissue-engineered liver was transplanted into mice with liver failure, the transplants had some liver function and the liver cells in these transplants were able to grow and regenerate like in normal livers.

In a USC press release, Dr. Kasper Wang from CHLA and the Keck school of medicine at USC commented:

“A cellular therapy for liver disease would be a game-changer for many patients, particularly children with metabolic disorders. By demonstrating the ability to generate hepatocytes comparable to those in native liver, and to show that these cells are functional and proliferative, we’ve moved one step closer to that goal.”

 

Making new bone. Next up is a story about making new bone from stem cells. A group at UC San Diego published a study this week in the journal Science Advances detailing a new way to make bone forming cells called osteoblasts from human pluripotent stem cells.

Stem cell-derived osteoblasts (bone cells). Image credit Varghese lab/UCSD.

Stem cell-derived osteoblasts (bone cells). Image credit Varghese lab/UCSD.

One way that scientists can turn pluripotent stem cells into mature cells like bone is to culture the stem cells in a growth medium supplemented with small molecules that can influence the fate of the stem cells. The group discovered that by adding a single molecule called adenosine to the growth medium, the stem cells turned into osteoblasts that developed vascularized bone tissue.

When they transplanted the stem cell-derived osteoblasts into mice with bone defects, the transplanted cells developed new bone tissue and importantly didn’t develop tumors.

 In a UC newsroom release, senior author on the study and UC San Diego Bioengineering Professor Shyni Varghese concluded:

“It’s amazing that a single molecule can direct stem cell fate. We don’t need to use a cocktail of small molecules, growth factors or other supplements to create a population of bone cells from human pluripotent stem cells like induced pluripotent stem cells.”

 

Stem cells and mental health. Brad Fikes from the San Diego Union Tribune wrote a great article on a new academic-industry partnership whose goal is to use human stem cells to find new drugs for mental disorders. The project is funded by a $15.4 million grant from the National Institute of Mental Health.

Academic scientists, including Rusty Gage from the Salk Institute and Hongjun Song from Johns Hopkins University, are collaborating with pharmaceutical company Janssen and Cellular Dynamics International to develop induced pluripotent stem cells (iPSCs) from patients with mental disorders like bipolar disorder and schizophrenia. The scientists will generate brain cells from the iPSCs and then work with the companies to test for potential drugs that could be used to treat these disorders.

In the article, Fred Gage explained that the goal of this project will be used to help patients rather than generate data points:

Rusty Gage, Salk Institute.

Rusty Gage, Salk Institute.

“Gage said the stem cell project is focused on getting results that make a difference to patients, not simply piling up research information. Being able to replicate results is critical; Gage said. Recent studies have found that many research findings of potential therapies don’t hold up in clinical testing. This is not only frustrating to patients, but failed clinical trials are expensive, and must be paid for with successful drugs.”

“The future of this will require more patients, replication between labs, and standardization of the procedures used.”

Stem cell techniques yield new clues to the origins of schizophrenia

Although the word “schizophrenia” was coined over 100 years ago, scientists are still stumped by what causes this severe brain disorder, which afflicts an estimated three million Americans and presents a financial burden of $63 billion each year. People with schizophrenia suffer debilitating delusional and hallucinatory symptoms, such as hearing voices or believing that tragedy is imminent. Life-long drug treatment and psychotherapy can help keep symptoms in check—but ten percent still surrender to the disease by taking their own lives.

Studying the brains of schizophrenic patients after death reveals abnormalities in brain cells. But these defects seen at the end of life tell very little about what initiates the disease or predisposes someone to it. Clearly new approaches are needed to tackle schizophrenia.

Sounds like a job for stem cells.

In fact, results published this week reveal just that. In a study published by CIRM grantees at the Salk Institute and their collaborators in Molecular Psychiatry report on using stem cell techniques to glimpse early hallmarks of schizophrenia in stem-cell derived brain cells that resemble those of the developing brain.

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As an initial pilot study, the researchers collected skin samples from four people with schizophrenia and six individuals without the disease and then reprogrammed those skin cells into embryonic-like stem cells. From there, they transformed the stem cells into immature brain cells called neural precursor cells, or NPCs.

With the NPCs in hand, the researchers ran two analyses that can look for differences in a vast array of genes and proteins in the schizophrenia (SZ)-derived cells compared to non-SZ cells. Both tests indicated abnormal gene activity and protein levels related to cell movement and cell stress in the SZ cells. And as predicted by these molecular tests, examination of cell function showed that the SZ-derived NPCs indeed had poor cell migration, which could lead to abnormal communication among brain cells and increased cell stress which could stimulate brain cell death.

These results are in line with previous studies that suggest schizophrenia begins during early fetal brain development—possibly due to extreme stress or infection during pregnancy. In a Salk Institute press release picked up by Health Canal first author Kristen Brennand, assistant professor at Icahn School of Medicine at Mount Sinai in New York, spoke about the advantage of using these NPCs:

We realized they weren’t mature neurons but only as old as neurons in the first trimester. So we weren’t studying schizophrenia but the things that go wrong a long time before patients actually get sick.

And since the gene and protein tests used in this pilot study are highly scalable, the logical next step is to perform the analysis on hundreds or thousands of patient samples to better reflect the complexity and variation in the disease. As senior author Fred Gage, a CIRM grantee and professor at the Salk Institute, points out in the press release:

The study hints that there may be opportunities to create diagnostic tests for schizophrenia at an early stage.

For more from Dr. Gage about modeling disease with stem cells, check out this video from our stem cell basics series.

CIRM Funding: New Cell Lines Award: RL1-00649

Todd Dubnicoff