According to previous research, by 2030, it is expected that the number of patients suffering from Alzheimer’s disease will exceed 70 million, and the treatment cost will be as high as 2 trillion US dollars. However, we still do not know how all the factors interact to make it happen. It attacks.
For a long time, Alzheimer had plagued the body and mind of all humans, and scientists have not been able to break the real cause of Alzheimer’s disease. In fact, as to why Alzheimer’s disease will occur, the scientific community has always had an unpopular theory: This mysterious disease is caused by a potential virus. Just this Thursday, an article published in Neuron, an authoritative journal in the field of neuroscience, provided support for this theory and is expected to become a new breakthrough in Alzheimer’s therapeutic drug development, which is already very difficult. Not only that, according to this discovery, some viruses are not only more likely to appear in the brains of people with Alzheimer’s disease, but also cause a series of fatal neurodegenerative disorders. The process plays an important role.
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Unexpected discovery of unpopular theories
In the beginning, researchers were not interested in demonstrating that the so-called “viral theory” of Alzheimer’s disease was right or wrong. However, this study seems to have no intention of touching this theory. According to Joel Dudley, an assistant professor of genetics at Mount Sinai’s Icahn School of Medicine and author of the study, all the findings were unexpected. He even felt that the existence of this theory made the results of this study more convincing. “When I read this article, I was very happy because this is another article that supports the relationship between the onset of Alzheimer’s disease and microorganisms, and there are more and more such articles.” University of Manchester, UK Ruth Itzhaki, professor of molecular neurobiology for honorary retirement, commented.
Since 1991, he has always insisted on the virus theory. He believes that most scientists in the past have always viewed themselves in decades of theory with sarcasm or hostility. Dudley said: “Originally the research team focused on finding new drug targets. There was no intention to pay attention to the theory of viruses and Alzheimer’s disease. However, because the test needs to be based on a large amount of data, the During the process, we gradually discovered the special relationship between viruses and neurological diseases, and we revised the research topics.”
In this study, the team compared brain samples of patients who died of Alzheimer’s disease with normal brain samples. As the research team is a member of the Accelerating Medicines Partnership (Alzheimer’s Disease) consortium, all sample data come from the National Institute of Health. The database stores brain information, which allows them to directly obtain information on the original brain genome sequence. In general experiments, scientists can only see genes that humans have studied, but this time it was because of a lot of raw data that Dudley’s team was able to reinvent the genes that have lived in the brain for a while. Sorting, analysis.
According to the information provided by the gene, the team identified several different types of herpesviruses in the brain samples that are more common in the brains of patients with Alzheimer’s disease. Not only that, they found that the more severe the dementia before death, the more the number of herpes virus in the brain. This clearly implies that the virus is closely related to the occurrence of brain diseases. Of all the viruses studied, there are two viral species that are most closely related to Alzheimer’s disease: human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7).
However, Dudley initially thought that these findings were just a beginning. The number of viruses found only in the brains of people with Alzheimer’s disease is very large. This result does not rule out the possibility that these viruses are just passers-by. So Dudley began further exploration. They used a sample of the brain to create a computer model to observe how the genes that are carried by the human brain interact with viral DNA/RNA found in the human brain. According to a computer model, the HHV-6A and HHV-7 genes regularly turn on and off the genes that come from the human brain, and the latter regularly turns on and off the former. In those areas of the brain affected by the disease (such as the hippocampus), such activities are more common. Dudley commented: “We can see that it is very likely that these viruses started genes related to Alzheimer’s disease and deliberately suppressed other genes. So we infer that these viruses may be particularly vulnerable to someone The environmental factors of Alzheimer’s disease.”
Why are these two viruses?
Most people are infected with the HHV-6A and HHV-7 viruses at a young age, and the common symptoms in children are mild roseola skin disease. However, in recent years, it has been suggested that these viruses may cause other diseases of the nervous system. For example, HHV-6 always seems to be associated with a neurodegenerative disease called multiple sclerosis. Some scientists believe that the virus hibernates somewhere in the body and only slowly migrates and then quietly infects the brain or nervous system at specific times. But there must be something that starts the virus, such as stress or diseases that weaken the immune system.
Next, there must be something else that makes the human brain interact with these viruses and move toward accelerating Alzheimer’s disease. For example, in the study of Itzhaki, the first proponent of virus theory, he discovered that people only suffer from HSV when they carry the E-4 variant of the APOE gene (which was originally associated with Alzheimer’s disease). The chance of Alzheimer’s disease is even greater with the infection of the -1 virus (herpes simplex virus 1, the culprit of cold sores, also written as HHV-1). However, because the HHV is widely distributed (about 90% of Americans have this virus), the distribution of HSV-1 is generally (about 54% of Americans, but about 67% of the world), and Not everyone has Alzheimer’s disease, so viral infection is also considered to be a very small factor that causes the onset of Alzheimer’s disease.
Dudley’s study found that both HHV-6A and HHV-7 viruses interact with genes responsible for β-amyloid production in the human brain, while β-amyloids misfold and form abnormalities after deposition. Plaques eventually cause severe damage to the brain of people with Alzheimer’s disease. This discovery also reinforces the previous theory that our innate immune system would inadvertently cause the onset of certain diseases. Itzhaki is also one of the supporters of this theory, he explained that the brain will use beta-amyloid to protect itself from infection. Those who eventually suffer from Alzheimer’s disease actually have problems with this “security system.” However, most of the scientists who studied Alzheimer’s disease caused by the virus, including Itzhaki, mainly focused on HSV-1 mentioned above. Itzhaki noted that of the 130 articles that investigated the virus that may indirectly cause Alzheimer’s disease, only a few focused on other HHVs. Dudley’s team did find some connections between HSV-1 and Alzheimer’s disease, but the link was not as close as the link between HHV-6A and HH7 and the disease.
However, Dudley believes that this does not mean that HSV-1 has nothing to do with the onset of Alzheimer’s disease. While explaining why other HHVs are less of a concern, he said that HSV-1 is usually easier to identify in blood tests, so scientists who rely on traditional methods to study the disease may not have thought of other HHVs. Related to Alzheimer’s disease. Dudley believes that there may be more viruses or even bacterial species in the brain. These microorganisms may become inducing factors for other neurological diseases such as Alzheimer’s disease.
According to previous research, by 2030, it is expected that the number of patients suffering from Alzheimer’s disease will exceed 70 million, and the treatment cost will be as high as 2 trillion US dollars. However, we still do not know how all the factors interact to make it happen. It attacks. However, this study and several recent articles supporting the virus hypothesis have provided ideas for how to study the disease. For example, we can design experiments based on the newly proposed hypothesis and even try antiviral treatment in the future.