Tag: blood-brain barrier

Nutrient’s Pathway into the Brain could be Used to Treat Neurological Disorders

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A University of Queensland researcher has found molecular doorways that could be used to help deliver drugs into the brain to treat neurological disorders. Dr Rosemary Cater from UQ’s Institute for Molecular Bioscience led a team which discovered that an essential nutrient called choline is transported into the brain by a protein called FLVCR2.

“Choline is a vitamin-like nutrient that is essential for many important functions in the body, particularly for brain development,” Dr Cater said.

“We need to consume 400-500mg of choline per day to support cell regeneration, gene expression regulation, and for sending signals between neurons.”

Dr Cater said that until now, little was known about how dietary choline travels past the layer of specialised cells that separates the blood from the brain.

“This blood-brain barrier prevents molecules in the blood that are toxic to the brain from entering,” she explained. “The brain still needs to absorb nutrients from the blood, so the barrier contains specialised cellular machines – called transporters – that allow specific nutrients such as glucose, omega-3 fatty acids and choline to enter. While this barrier is an important line of defence, it presents a challenge for designing drugs to treat neurological disorders.”

Dr Cater was able to show that choline sits in a cavity of FLVCR2 as it travels across the blood-brain barrier and is kept in place by a cage of protein residues.

“We used high-powered cryo-electron microscopes to see exactly how choline binds to FLVCR2,” she said. “This is critical information for understanding how to design drugs that mimic choline so that they can be transported by FLVCR2 to reach their site of action within the brain. These findings will inform the future design of drugs for diseases such as Alzheimer’s and stroke.”

The research also highlights the importance of eating choline-rich foods – such as eggs, vegetables, meat, nuts and beans.

The research is published in Nature and funded by the National Institutes of Health.

Source: University of Queensland

Crafting a ‘Key’ to Cross the Blood-brain Boundary

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Researchers led by Michael Mitchell of the University of Pennsylvania are close to gaining access through the blood-brain barrier, a long-standing boundary in biology, by granting molecules a special ‘key’ to gain access.

Their findings, published in the journal Nano Letters, present a model that uses lipid nanoparticles (LNPs) to deliver mRNA, offering new hope for treating conditions like Alzheimer’s disease and seizures.

“Our model performed better at crossing the blood-brain barrier than others and helped us identify organ-specific particles that we later validated in future models,” says Mitchell, associate professor of bioengineering at Penn’s School of Engineering and Applied Science, and senior author on the study.

“It’s an exciting proof of concept that will no doubt inform novel approaches to treating conditions like traumatic brain injury, stroke, and Alzheimer’s.”

Search for the key

To develop the model, Emily Han, a PhD candidate and NSF Graduate Research Fellow in the Mitchell Lab and first author of the paper, explains that it started with a search for the right in vitro screening platform, saying, “I was combing through the literature, most of the platforms I found were limited to a regular 96-well plate, a two-dimensional array that can’t represent both the upper and lower parts of the blood-brain barrier, which correspond to the blood and brain, respectively.”

Han then explored high-throughput transwell systems with both compartments but found they didn’t account for mRNA transfection of the cells, revealing a gap in the development process.

This led her to create a platform capable of measuring mRNA transport from the blood compartment to the brain, as well as transfection of various brain cell types including endothelial cells and neurons.

“I spent months figuring out the optimal conditions for this new in vitro system, including which cell growth conditions and fluorescent reporters to use,” Han explains.

“Once robust, we screened our library of LNPs and tested them on animal models. Seeing the brains express protein as a result of the mRNA we delivered was thrilling and confirmed we were on the right track.”

The team’s platform is poised to significantly advance treatments for neurological disorders.

It’s currently tailored for testing a range of LNPs with brain-targeted peptides, antibodies, and various lipid compositions.

However, it could also deliver other therapeutic agents like siRNA, DNA, proteins, or small molecule drugs directly to the brain after intravenous administration.

What’s more, this approach isn’t limited to the blood-brain barrier as it shows promise for exploring treatments for pregnancy-related diseases by targeting the blood-placental barrier, and for retinal diseases focusing on the blood-retinal barrier.

Next Steps

The team is eager to use this platform to screen new designs and test their effectiveness in different animal models.

They are particularly interested in working with collaborators with advanced animal models of neurological disorders.

“We’re collaborating with researchers at Penn to establish brain disease models,” Han says.

“We’re examining how these LNPs impact mice with various brain conditions, ranging from glioblastoma to traumatic brain injuries. We hope to make inroads towards repairing the blood-brain barrier or target neurons damaged post-injury.”

Source: University of Pennsylvania

Microplastics Rapidly Bioaccumulate Everywhere in the Body

Photo by FLY:D on Unsplash

The prevalence of microplastics in the environment is well known, along with their harm to marine organisms, but few studies have examined the potential health impacts on mammals. Now, a new study published in the International Journal of Molecular Sciences has found that in mice, the infiltration of microplastics was as widespread in the body as it is in the environment, leading to behavioural changes, especially in older test subjects.

Study leader University of Rhode Island Professor Jaime Ross and her team focused on neurobehavioural effects and inflammatory response to exposure to microplastics, as well as the accumulation of microplastics in tissues, including the brain.

“Current research suggests that these microplastics are transported throughout the environment and can accumulate in human tissues; however, research on the health effects of microplastics, especially in mammals, is still very limited,” said Ross, an assistant professor of biomedical and pharmaceutical sciences at the Ryan Institute for Neuroscience and the College of Pharmacy. “This has led our group to explore the biological and cognitive consequences of exposure to microplastics.”

Behavioural changes detected

Ross’ team exposed young and old mice to varying levels of microplastics in drinking water over the course of three weeks. They found that microplastic exposure induces both behavioural changes and alterations in immune markers in liver and brain tissues. The study mice began to exhibit behaviours akin to dementia in humans. The results were even more profound in older animals.

“To us, this was striking. These were not high doses of microplastics, but in only a short period of time, we saw these changes,” Ross said. “Nobody really understands the life cycle of these microplastics in the body, so part of what we want to address is the question of what happens as you get older. Are you more susceptible to systemic inflammation from these microplastics as you age? Can your body get rid of them as easily? Do your cells respond differently to these toxins?”

To understand the physiological systems that may be contributing to these changes in behaviour, Ross’ team investigated how widespread the microplastic exposure was in the body, dissecting several major tissues including the brain, liver, kidney, gastrointestinal tract, heart, spleen and lungs. The researchers found that the particles had begun to bioaccumulate in every organ, including the brain, as well as in bodily waste.

“Given that in this study the microplastics were delivered orally via drinking water, detection in tissues such as the gastrointestinal tract, which is a major part of the digestive system, or in the liver and kidneys was always probable,” Ross said. “The detection of microplastics in tissues such as the heart and lungs, however, suggests that the microplastics are going beyond the digestive system and likely undergoing systemic circulation. The brain blood barrier is supposed to be very difficult to permeate. It is a protective mechanism against viruses and bacteria, yet these particles were able to get in there. It was actually deep in the brain tissue.”

Possible mechanism

That brain infiltration also may cause a decrease in glial fibrillary acidic protein (called “GFAP”), a protein that supports many cell processes in the brain, results have shown. “A decrease in GFAP has been associated with early stages of some neurodegenerative diseases, including mouse models of Alzheimer’s disease, as well as depression,” Ross said. “We were very surprised to see that the microplastics could induce altered GFAP signalling.”

She intends to investigate this finding further in future work. “We want to understand how plastics may change the ability for the brain to maintain its homeostasis or how exposure may lead to neurological disorders and diseases, such as Alzheimer’s disease,” she said.

Source: University of Rhode Island

Restoring the Integrity of the Blood–Brain Barrier

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A new paper published in Nature Communications describes a treatment that restores intercellular signalling and which could be instrumental in restoring the barrier’s normal function. Key to the process is ‘frizzled’, a key protein receptor implicated in blood-brain abnormalities.

When the blood-brain barrier isn’t working properly, a variety of conditions can crop up. Barrier-invading cancer cells can develop into tumours, and multiple sclerosis can occur when too many white blood cells slip pass the barrier, leading to an autoimmune attack on the protective layer of brain nerves, hindering their communication with the rest of the body.

“A leaky blood-brain barrier is a common pathway for a lot of brain diseases, so to be able to seal off the barrier has been a long sought-after goal in medicine,” said senior author Calvin Kuo, MD, PhD, professor of hematology.

Methods of repairing the blood-brain barrier remain understudied, according to Kuo. But the recent paper he and colleagues led describes a possible treatment.

“We have evaluated a new therapeutic class of molecules that can be used to treat a leaky blood-brain barrier; previously, there were no treatments directed at the blood-brain barrier specifically,” Kuo said.

The researchers started their quest by looking at WNT signalling, a communication pathway used by cells to promote tissue regeneration and wound healing. WNT signalling helps maintain the blood-brain barrier by promoting cell-to-cell communication that lines brain blood vessels.

“There’s a lot of historical data that indicated that the WNT signalling pathway would be important for maintaining the blood-brain barrier,” Kuo said. “The opportunity arose to test a novel WNT signalling pathway that would turn on signalling in the blood-brain barrier by binding very selectively to a receptor called frizzled.”

Scientists have been focusing on ‘frizzled’, a protein receptor that initiates the WNT pathway, for blood-brain barrier therapies since mouse mutations in the frizzled gene cause blood-brain barrier abnormalities.

How it’s made

Many different molecules bind to frizzled protein receptors, so to narrow their search for a potential therapeutic molecule, the researchers selected only those that specifically target cells that line the brain’s blood vessels.

Chris Garcia, PhD, a professor of molecular and cellular physiology as well as the Younger Family Professor, developed prototype therapeutic WNT pathway molecules in the lab, including a molecule that activates the frizzled receptor FZD4. Building off of the work of Garcia and Kuo, collaborators at a research company created L6-F4-2, a FZD4 binding molecule that activates WNT signalling 100 times more efficiently than other FZD4 binders.

When the team, including Jie Ding, a research scientist and the lead author of the paper, activated WNT signaling at a higher rate, they saw an increase in blood-brain barrier strength.

Keeping the barrier up

The researchers wanted to study what happens when the natural molecular key for frizzled is missing, and whether it can be replaced successfully with L6-F4-2. So they turned to Norrie disease, a genetic abnormality that results in a leaky blood-retinal barrier.

The blood-retinal barrier performs the same function for the eye as the blood-brain barrier does for the brain. In Norrie disease, the development of blood vessels of the retina is hindered, resulting in leaky blood vessel connections, improper development and blindness.

Norrie disease results from mutations in the NDP gene, which provides instructions for making a protein called Norrin, which is the key that fits the lock of the FZDreceptor and turns it on. In the study’s mice, the gene is inactivated, and the key is missing causing a leaky barrier and blindness. The scientists replaced the missing Norrin protein with L6-F4-2, which they call a surrogate.

When L6-F4-2 replaced the missing Norrin protein, the blood-retinal layer was restored in the mice. Researchers knew this because they imaged the blood vessels and found them to be denser, and less leaky, than before treatment. Scientists also showed that, for the blood-brain barrier surrounding the mice cerebellum L6-F4-2 replaced Norrin and activated WNT signalling.

Next, the researchers wanted to study a more common human condition — ischemic stroke (in which blood vessels and the blood-brain barrier are damaged, and fluid, blood and inflammatory proteins involved in cellular communication can leak into the brain. They found that L6-F4-2 reduced the severity of stroke and improved survival of mice compared with mice that had untreated strokes. Importantly, L6-F4-2 reversed the leakiness of brain blood vessels after stroke. Mice treated with L6-F4-2 had increased stroke survival, compared to those that were not treated.

The finding shows that, in mice, the blood-brain barrier could be restored by drugs that activate FZD receptors and the WNT signalling pathway.

Because a variety of disorders have their origin in blood-brain barrier dysfunction, Kuo is excited about the treatment potential for a variety of other neurological diseases, such as Alzheimer’s, multiple sclerosis and brain tumours.

“We hope this will be a first step toward developing a new generation of drugs that can repair the blood-brain barrier, using a very different strategy and molecular target than current medications,” Kuo said.

Source: Stanford Medicine

Antibiotic Regimen may be Ineffective in TB Meningitis

Tuberculosis bacteria
Tuberculosis bacteria. Credit: CDC

Research in animal models published in Nature Communications shows that an approved antibiotic regimen for multidrug-resistant (MDR) tuberculosis (TB) may not work for TB meningitis. Limited human studies also provide evidence that a new combination of drugs is needed to develop effective treatments for TB meningitis due to MDR strains.

In the study from Johns Hopkins Children’s Center, the investigators showed that the Food and Drug Administration (FDA)-approved regimen of three antibiotics – bedaquiline, pretomanid and linezolid (BPaL) – used for treating TB of the lungs due to MDR strains, is not effective in treating TB meningitis because bedaquiline and linezolid struggle to cross the blood-brain barrier.

Tuberculosis, caused by the bacteria Mycobacterium tuberculosis, is a global public health threat. About 1%–2% of TB cases progress into TB meningitis, the worst form of TB, which leads to an infection in the brain that causes increased fluid and inflammation.

“Most treatments for TB meningitis are based on studies of treatments for pulmonary TB, so we don’t have good treatment options for TB meningitis,” explains Sanjay Jain, M.D., senior author of the study and director of the Johns Hopkins Medicine Center for Infection and Inflammation Imaging Research.

In 2019, the FDA approved the BPaL regimen to treat MDR strains of TB, specifically those that lead to pulmonary TB. However, there are limited data on how well these antibiotics cross the blood-brain barrier.

In an effort to learn more, the research team synthesised a chemically identical and imageable version of the antibiotic pretomanid. They conducted experiments in mouse and rabbit models of TB meningitis using positron emission tomography (PET) imaging to noninvasively measure pretomanid penetration into the central nervous system as well as using direct drug measurements in mouse brains. In both models, researchers say PET imaging demonstrated excellent penetration of pretomanid into the brain or the central nervous system. However, the pretomanid levels in the cerebrospinal fluid (CSF) that bathes the brain were many times lower than in the brains of mice.

“When we have measured drug concentrations in the spinal fluid, we have found that many times they have no relation to what’s happening in the brain,” says Elizabeth Tucker, MD, a study first author and an assistant professor of anaesthesiology and critical care medicine. “This finding will change how we interpret data from clinical trials and, ultimately, treat infections in the brain.”

Next, researchers measured the efficacy of the BPaL regimen compared with the standard TB treatment for drug-susceptible strains, a combination of the antibiotics rifampin, isoniazid and pyrazinamide. Results showed that the antibacterial effect in the brain using the BPaL regimen in the mouse model was about 50 times lower than the standard TB regimen after six weeks of treatment, likely due to restricted penetration of bedaquiline and linezolid into the brain. The bottom line, says Jain, is that the “regimen that we think works really well for MDR-TB in the lung does not work in the brain.”

In another experiment involving healthy participants, three male and three female aged 20–53 years, first-in-human PET imaging was used to show pretomanid distribution to major organs, according to researchers.

Similar to the work with mice, this study revealed high penetration of pretomanid into the brain or central nervous system with CSF levels lower than those seen in the brain. “Our findings suggest pretomanid-based regimens, in combination with other antibiotics active against MDR strains with high brain penetration, should be tested for treating MDR-TB meningitis,” says study author Xueyi Chen, MD, a paediatric infectious diseases fellow, who is now studying combinations of such therapies.

Limitations included the small quantities of the imageable version of pretomanid per subject (micrograms) used. However, current evidence suggests that studies with small quantities of a drug are a reliable predictor of the drug biodistribution.

Source: Johns Hopkins Medicine

Early Sensing of Malaria in the Brain Leads to Cerebral Malaria

Colourised scanning electron micrograph of red blood cell infected with malaria parasites, which are colourised in blue. The infected cell is in the centre of the image area. To the left are uninfected cells with a smooth red surface. Credit: National Institute of Allergy and Infectious Diseases, NIH

A recent study published in PNAS revealed that endothelial cells in the brain are able to sense the infection by the malaria parasite at an early phase, triggering the inflammation underlying cerebral malaria. This discovery identified new targets for adjuvant therapies that could restrain brain damage in initial phases of the disease and avoid neurological sequelae.

Cerebral malaria is a severe complication of infection with Plasmodium falciparum, the most lethal of the parasites causing malaria. This form of the disease manifests through impaired consciousness and coma and affects mainly children under 5, being one of the main causes of death in this age group in countries of Sub-Saharan Africa. Survivors are frequently affected by debilitating neurological sequelae, such as motor deficits, paralysis, and speech, hearing, and visual impairment.

To prevent certain molecules and cells from reaching the brain, which would disturb its normal functioning, endothelial cells forming a tight barrier between the blood and this organ. Cerebral malaria results from an unrestrained inflammatory response to infection which leads to significant alterations in this barrier and, consequently, neurological complications.

Over the last years, specialists in this field have turned their attention to a molecule, named interferon-β, which seems to be associated with this pathological process. So called for interfering with viral replication, this highly inflammatory molecule has two sides: it can either be protecting or cause tissue destruction. It is known, for example, that despite its antiviral role in COVID-19, at a given concentration and phase of infection, it can cause lung damage. A similar dynamic is thought to occur in cerebral malaria. However, we still don’t know what leads to the secretion of interferon-β, nor the main cells involved.

The present study revealed that endothelial cells in the brain play a crucial role, being able to sense the infection by the malaria parasite at an early phase. These detect the infection through an internal sensor which triggers a cascade of events, starting with the production of interferon-β. Next, they release a signalling molecule that attracts cells of the immune system to the brain, initiating the inflammatory process.

To reach these conclusions, researchers used mice that mimic several symptoms described in human malaria and a genetic manipulation system that allowed them to delete this sensor in several types of cells. When they deleted this sensor in brain endothelial cells, the animals’ symptoms were not as severe with lower mortality. They then realised these brain cells contributed greatly to the pathology of cerebral malaria. “We thought brain endothelial cells acted in a later phase, but we ended up realising that they are participants from the very beginning”, explained Teresa Pais, a post-doctoral researcher at the IGC and first author of the study. “Normally we associate this initial phase of the response to infection with cells of the immune system. These are already known to respond, but cells of the brain, and maybe other organs, also have this ability to sense the infection because they have the same sensors.”

But what really surprised the researchers was the factor activating the sensor and triggering this cell response. This factor is nothing more nothing less than a by-product of the activity of the parasite. Once in the blood, the parasite invades the host’s red blood cells, where it multiplies. Here, it digests haemoglobin, a protein that transports oxygen, to get nutrients. During this process, a molecule named haeme is formed and it can be transported in tiny particles in the blood that are internalised by endothelial cells. When this happens, haeme acts as an alarm for the immune system. “We weren’t expecting that haeme could enter cells this way and activate this response involving interferon-β in endothelial cells”, the researcher confessed.

This six-year project allowed the researchers to identify a molecular mechanism that is critical for the destruction of brain tissue during infection with the malaria parasite and, with that, new therapeutic targets. “The next step will be to try to inhibit the activity of this sensor inside the endothelial cells and understand if we can act on the host’s response and stop brain pathology in an initial phase,” explained principal investigator Carlos Penha Gonçalves. “If we could use inhibitors of the sensor in parallel with antiparasitic drugs maybe we could stop the loss of neuronal function and avoid sequelae which are a major problem for children surviving cerebral malaria.”

Source: Instituto Gulbenkian de Ciência (IGC)

MRI and Ultrasound Combo Opens Blood-brain Barrier

In a mouse model study of MRI-guided focused ultrasound-induced blood-brain barrier (BBB) opening at MRI field strengths ranging from ­approximately 0 T (outside the magnetic field) to 4.7 T, the static magnetic field dampened the detected microbubble cavitation signal and decreased the BBB opening volume. Credit: Washington University School of Medicine in St. Louis

Using a combination of ultrasound, MRI field strength and microbubbles can open the blood-brain barrier (BBB) and allow therapeutic drugs to reach the diseased brain location with MRI guidance. 

Using the physical phenomenon of cavitation, it is a promising technique that has been shown safe in patients with various brain diseases, such as Alzheimer’s diseases, Parkinson’s disease, ALS, and glioblastoma.
While MRI has been commonly used for treatment guidance and assessment in preclinical research and clinical studies, until now, researchers did not know the impact that MRI scanner’s magnetic field had on the BBB opening size and drug delivery efficiency.

Hong Chen, associate professor of biomedical engineering at Washington University in St. Louis, and her lab have found for the first time that the magnetic field of the MRI scanner decreased the BBB opening volume by 3.3-fold to 11.7-fold, depending on the strength of the magnetic field, in a mouse model. The findings were in Radiology.

Prof Chen conducted the study on four groups of mice. After they were injected microbubbles, three groups received focused-ultrasound sonication at different strengths of the magnetic field: 1.5 T (teslas), 3 T and 4.7 T, and one group was never exposed to the field. 

The researchers found that the microbubble cavitation activity, or the growing, shrinking and collapse of the microbubbles, decreased by 2.1 decibels at 1.5 T; 2.9 decibels at 3 T; and 3 decibels at 4.7 T, compared with those that had received the dose outside of the magnetic field. Additionally, the magnetic field decreased the BBB opening volume by 3.3-fold at 1.5 T; 4.4-fold at 3 T; and 11.7-fold at 4.7 T. No tissue damage from the procedure was seen.

Following focused-ultrasound sonication, the team injected a model drug, Evans blue dye, to investigate whether the magnetic field affected drug delivery across the BBB. The images showed that the fluorescence intensity of the Evans blue was lower in mice that received the treatment in one of the three strengths of magnetic fields compared with mice treated outside the magnetic field. The Evans blue trans-BBB delivery was decreased by 1.4-fold at1.5 T, 1.6-fold at 3.0 T and 1.9-fold at 4.7 T when compared with those treated outside of the magnetic field.

“The dampening effect of the magnetic field on the microbubble is likely caused by the loss of bubble kinetic energy due to the Lorentz force acting on the moving charged lipid molecules on the microbubble shell and dipolar water molecules surrounding the microbubbles,” said Yaoheng (Mack) Yang, a doctoral student in Prof Chen’s lab and the lead author of the study.

“Findings from this study suggest that the impact of the magnetic field needs to be considered in the clinical applications of focused ultrasound in brain drug delivery,” Prof Chen said.

In addition to brain drug delivery, cavitation is also used in several other therapeutic techniques, such as histotripsy, the use of cavitation to mechanically destroy regions of tissue, and sonothrombolysis, a therapy used after acute ischaemic stroke. The magnetic field’s damping effect on cavitation is expected to affect the treatment outcomes of other cavitation-mediated techniques when MRI-guided focused-ultrasound systems are used.

Source: Washington University in St. Louis

Journal information: Yang, Y., et al. (2021) Static Magnetic Fields Dampen Focused Ultrasound–mediated Blood-Brain Barrier Opening. Radiology. doi.org/10.1148/radiol.2021204441

New Study Finds Critical Flaw in Blood-brain Model

The wrong kind of cells have been used to make in vitro models of the blood-brain barrier, which now throws a decade’s worth of research into question.

The present in vitro human blood-brain barrier model was developed in 2012. By inducing differentiated adult cells, such as skin cells, into developing into stem cells, the pluripotent stem cells obtained from the process are then transformed into nearly any type of mature cell. This includes the type of endothelial cell that lines brain and spinal cord blood vessels, and making a unique barrier that acts as a gatekeeper, restricting potentially dangerous substances, antibodies, and immune cells from entering the brain from the bloodstream.

“The blood-brain barrier is difficult to study in humans and there are many differences between the human and animal blood-brain barrier. So it’s very helpful to have a model of the human blood-brain barrier in a dish,” said co-study leader Dritan Agalliu, PhD, associate professor at Columbia University Vagelos College of Physicians and Surgeons.

Agalliu had noticed that these endothelial cells produced in this manner, did not behave like normal endothelial cells in the human brain. “This raised my suspicion that the protocol for making the barrier’s endothelial cells may have generated cells of the wrong identity,” said Agalliu.
“At the same time the Weill Cornell Medicine team had similar suspicions, so we teamed up to reproduce the protocol and perform bulk and single-cell RNA sequencing of these cells.”

Upon analysis, the researchers discovered that the supposed human brain endothelial cells were missing several key proteins found in natural endothelial cells and had more in common with epithelial cells, which is not usually found in the brain.

The team also identified three genes that, when activated within induced pluripotent cells, lead to the creation of cells that behave more like actual endothelial cells. More work is still needed, Agalliu says, to create endothelial cells that produce a reliable model of the human blood-brain barrier. His team is working to address this problem.

“The misidentification of human brain endothelial cells may be an issue for other types of cells made from induced pluripotent cells such as astrocytes or pericytes that form the neurovascular unit,” said Agalliu. The protocols to produce these cells were drawn up prior to the advent of single-cell technologies that are better at identifying cells.

“Cell misidentification remains a major problem that needs to be addressed in the scientific community in order to develop cells that mirror those found in the human brain. This will allow us to use these cells to study the role of genetic risk factors for neurological disorders and develop drug therapies that target the correct cells that contribute to the blood-brain barrier.”

Source: Medical Xpress