Without this barrier in the brain, people might die, and now scientists have decided to open it.
Global science
Neurons in the human brain are very fragile and need to be protected by a stable blood-brain barrier. Usually, it is a variety of diseases that open the barrier, and in order to treat these and more diseases, scientists decide to open it themselves.
In April 2016, 29-year-old Brooke Bergfeld became a novice mother. She gave birth to her son smoothly, but a week after her son was born, she felt something wrong with her body. Her left arm hurt and her head hurt badly. She didn't think much about it, thinking that the pain in her arm was that she had been holding the baby for too long, and that the headache might be the recurrence of her previous migraine. Her mother noticed that something was wrong-she spoke vaguely and her face drooped, so she was taken to the hospital at once.
Bergfeld shows some of the most typical symptoms of stroke (stroke). After arriving at the hospital, the doctor found a thrombus in her artery and quickly underwent thrombectomy. They found that Bergfeld had fibromuscular dysplasia, which narrowed her blood vessels and reduced the amount of blood flowing into her brain from the neck, which in turn affected the function of parts of the brain and caused a stroke. After treatment, she recovered, but still needed medication to control her blood pressure and inhibit thrombosis.
Diseases related to the brain
Compared with many patients with similar diseases, Bergfeld is lucky. We may be familiar with the word "stroke", but we may not know it that well. Stroke, also known as stroke, is an acute cerebrovascular disease. If the blood vessels are blocked and the blood cannot enter the brain, it can cause an ischemic stroke. If a blood vessel ruptures in the brain, it can cause a hemorrhagic stroke, which has a higher mortality rate. According to the statistics of 2020, this disease is the leading cause of death and disability of adults in China, currently endangering about 13 million people, and this number is still on the rise.
This is a disease that is difficult to treat and continues to worsen. Because when an ischemic stroke occurs, the key blood-brain barrier (blood-brain barrier) in the brain is destroyed. This barrier lies between the brain and the blood, protecting tens of billions of fragile neurons from toxic substances and pathogens in the blood, as well as immune cells, inflammatory factors and antibodies.
However, once the blood-brain barrier is damaged, these "dangerous molecules" can enter the brain, which in turn damage the brain, and may lead to other types of diseases. For example, multiple sclerosis (multiple sclerosis), a rare disease caused by T cells crossing the blood-brain barrier, attacks the axons of neurons and the myelin sheath on their surface, causing neurons to slowly and permanently lose function. Patients generally have general weakness, vision problems, and even blindness in one eye, and may not be able to control voiding function. And if the disease becomes serious, they may be paralyzed. Like the sequelae of a stroke, the disease is incurable.
But while protecting the brain, the blood-brain barrier can sometimes cause trouble: because of the blood-brain barrier, many drugs that treat diseases inside the brain do not work well. The most common drugs are drugs to treat Alzheimer's disease, Parkinson's disease and tumors in the brain. It can be seen that the blood-brain barrier plays a key role in these diseases, but scientists do not know much about the blood-brain barrier, so there is nothing they can do about many brain-related diseases.
Maintain the stability of blood-brain barrier
Simply put, the blood-brain barrier is a barrier that protects the brain. It consists of vascular endothelial cells, basement membrane and glial boundary membrane (composed of processes of glial cells) between brain cells and blood. These membranes are lipophilic, meaning that some fat-soluble organic molecules, such as hormones, amino acids, anesthetics and alcohol, can cross the blood-brain barrier and enter the brain.
Oxygen and water have molecular weights small enough to cross the blood-brain barrier. However, many hydrophilic molecules, such as glucose, are stopped. Of course, without energy, brain cells will be cool, so there are special channels on the blood-brain barrier for these substances-proteins that can be transported actively across the membrane-to transport these basic nutrients into the brain.
From the above diseases, we can see that the permeability of the blood-brain barrier can be changed. So, can we first increase its permeability, allow drugs to enter, and then restore it to its original properties, making it more protective of the brain? recently, an article published in Nature Communications gives an accurate answer to this question: yes.
Human and mouse vascular endothelial cells express a receptor Unc5B, which binds to many ligands, plays a key role in vascular development, and participates in material exchange between blood vessels and surrounding tissues. Previous studies have found that if the gene that expresses the receptor is knocked out, the mice will die of vascular defects during the embryonic period.
To study the role of this receptor in the brains of adult mice, the scientists also knocked out their genes that express Unc5B, and seven days later they were injected intraperitoneally with cadaverine (molecular weight 950Da Daqing 1g / mol). The molecule is a toxic diamine that normally cannot enter the brain. After half an hour, they found that cadaverine had entered several areas of the brain of the mice, including piriform cortex, hippocampus, hypothalamus, thalamus and striatum, but there were some differences in cadaverine concentrations between brain regions.
This phenomenon also shows that knocking out Unc5B receptors can destroy the stability of the blood-brain barrier. In fact, due to the loss of Unc5B receptors, the concentration of a protein called Claudin-5 in vascular endothelial cells decreases, leading to abnormalities in the blood-brain barrier in the capillaries that are in close contact with brain tissue.
After more in-depth study of these defective mice, they also found that Unc5B receptor fitness is associated with a common signaling pathway, the wnt/ β-catenin pathway. Lack of Unc5B protein will lead to a decrease in the expression of β-catenin and a significant increase in blood-brain barrier permeability. But this process will not last forever, and if β-catenin is overexpressed, the permeability of the blood-brain barrier will return to normal again.
The above processes are actually regulated by glial cells, vascular endothelial cells and pericytes in the basement membrane that make up the blood-brain barrier. These cells can express a molecule, Netrin-1, which binds to Unc5B receptors to maintain the stability of the blood-brain barrier.
Open the blood-brain barrier
After discovering how to change the permeability of the blood-brain barrier, scientists came up with an external way to control the blood-brain barrier. They quickly abandoned the idea of regulating the wnt/-β-catenin pathway, which is so common in cells that trying to change it could have incalculable effects.
And changing Unc5B may be a good choice. They found that in normal mice, blocking Unc5B receptors with antibodies would inhibit the wnt/ β-catenin pathway, which would increase the permeability of the blood-brain barrier for about 1 to 8 hours and allow up to 40 kDa of molecules to enter the brain, which means that many drugs will be able to enter the brain.
Similar attempts have been made in some studies before. In a study published in the journal Neuron in 2017, scientists at Harvard University made their first attempt to increase the permeability of the blood-brain barrier. They suppressed the expression of Mfsd2a, a protein responsible for lipid transport-a protein that inhibits endocytosis at the blood-brain barrier (a pathway that cells use to transport substances such
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