Release date: 2016-03-31 A paper pointed out that the herpes virus and the bacteria that cause Lyme disease are the main culprit in the deprivation of human brain disease, but the academic community is still skeptical. Alzheimer's disease is a devastating disease, and more than 5 million Americans have lost cognitive and memory functions, and scientists have been confused about the root causes of their disease. But in a controversial editorial about to be published in the Journal of Alzheimer's Disease, a group of scientists suggest that the cause of this complex disease may be simple: some can cause brain Infected microorganisms. This controversial view is not new. It has long been considered by the academic community to be too absurd to ignore it, but more and more work points out that this may be a direction worth considering and studying in depth. If researchers can prove this theory and explain some of the details of the previous controversy (both of which are difficult because of the difficulty of research on brain infections), then people can fundamentally stop the disease. happened. The editorial, co-published by 31 scientists around the world, believes that in certain susceptible populations, such as those carrying the APOE ε4 gene mutation (a known risk factor for Alzheimer's disease) - Common microbial infections can invade the aging brain and cause damage to its function. These microorganisms may include herpes simplex virus 1 (HSV-1), a common virus that causes cold sores, and Chlamydophila pneumoniae and Borrelia burgdorferi, which can cause Pneumonia and Lyme disease. This controversial idea runs counter to mainstream theory, and it has been thought that the accumulation of amyloid-beta proteins and tau tangles in the brain of Alzheimer's disease patients, It is the main cause of cell death caused by this disease. Proponents of the so-called "pathogen hypothesis" believe that either pathogenic microorganisms induce brain cells to produce amyloid and neurofibrillary tangles, or that nerve cells infected with infection produce them during the immune response to pathogens. Brian Balin, co-author of the editorial, is director of the Center for Chronic Disorders of Aging (Philadelphia College of Osteopathic Medicine). He said, "We acknowledge that the phenomenon described by the theory of amyloid does exist, but this is a follow-up reaction secondary to the initial infection." Critics of the "pathogen hypothesis" point out that many human studies supporting the theory do not establish a causal relationship between pathogens and Alzheimer's disease. Ruth Itzhaki is a molecular neuroscientist at the University of Manchester in the United Kingdom, and his team reported a phenomenon in a 1997 study published in The Lancet. - For those who are infected with the HSV-1 virus in the presence of the APOE ε4 gene mutation, they are more likely to develop Alzheimer's disease than those with HSV-1 alone or HSV-1 alone. 12 times as much. There is a hypothesis that APOE ε4 mutations make HSV-1 more susceptible to brain infection – but critics believe that it is also possible that such genetic mutations and infections are associated with Alzheimer's disease, but there is no cause and effect between them. relationship. Scientists have also tried to use animal experiments to confirm this hypothesis. For example, researchers in Spain have found that when the rat brain is infected with HSV-1, the virus containing the APOE ε4 mutation produces 14 times more viral DNA than normal rats. When HSV-1 infects the brain of rats, Itzhaki's team found that their brains accumulated amyloid. But these studies have also been blamed—after all, what happens in the brain of a mouse does not necessarily happen in the human brain. Demonstrating this hypothesis is a very difficult task, in part because it is almost impossible to detect viral infections like HSV-1 in the brains of living people - they can only be found during autopsy. “Proving that causality is a major, critical, and complex issue,†said David Relman, an infectious disease expert at Stanford University. Itzhaki also agrees with this view, stating that people can't simply inject the virus into living people and see if they develop Alzheimer's disease. (Australian microbiologist Barry Marshall, who inoculated the pathogen into his body, finally confirmed that Helicobacter pylori is indeed the chief culprit in causing stomach ulcers, calming people's doubts.) Itzhaki said a potential solution is to conduct clinical trials. Antiviral drugs were used to treat patients with mild Alzheimer's disease who were infected with HSV-1 and carry the APOE ε4 mutation, and to assess whether their condition improved. They have experimentally demonstrated that these antiviral drugs can inhibit the formation of amyloid plaques in HSV-1 infected cells. She has also submitted funding applications for human research on several occasions, but has not been successful so far. Rudolph Ranzi is a neuroscientist at Harvard University and a leader in the Genetics and Aging Research Unit at Massachusetts General Hospital. He also believes that microbes may play a role in the development of Alzheimer's disease, but his research shows that the brain's response to infection may be more dangerous than the infection itself. Ranzi reminds people, “We really need to seriously consider the role of microbes in brain diseases, but this is a complicated matter, not just saying that 'infection leads to Alzheimer's disease.'†(He is not here The author of the editorial.) In a 2010 study, Tanzi and his colleagues reported a phenomenon: amyloid strongly inhibits the growth of microorganisms in the brain, which may mean that the accumulation is brain-to-infection a response. He explained: "In the five years after the publication of the article in 2010, in each of the Alzheimer models we tested (from cells, flies, dirty worms to rats), beta-starch Proteins play an important role in the fight against infection," he said, even if only a few microbes invade the brain, triggering the accumulation of the protein. Infection can also induce a strong immune response, and this seems to make this problem even more difficult. Usually, an immune cell called microglia in the brain is able to clear amyloid. But when the body responds to an infection, these cells are "activated" and their "daily clearance" is no longer carried out, causing amyloid to increase at a faster rate. As Tanzi's team showed in a 2014 nature article, brain-filled amyloid stimulates the formation of neurofibrillary tangles, which leads to more brain cell death. “At this point, the disease has entered its heyday,†Tanzi said. Tanzi believes that HSV-1 is an alternative answer to the question of which pathogen may trigger Alzheimer's disease, but it is still too early to conclude. "I think we should look back a few steps, such as 'Which bacteria, viruses or fungi will accumulate in the brain as we get older?' and we should systematically and skeptically Study this issue," he said. Tanzi is now leading a group funded by the Cure Alzheimer's Fund, a non-profit organization that aims to match microbial groups in the human brain; he believes that once By discovering potentially important micro-organisms, it is possible to develop neuroimaging techniques in the living human brain to track them. Even so, other scientists in the field of Alzheimer's disease are still not fully convinced. David Holtzman is president of the Department of Neurology at Washington University School of Medicine, St. Louis, and is the Knight Alzheimer's Disease Research Center. Deputy director. He told Scientific American that although we need more research on this idea, "but there is no clear or conclusive evidence to show whether or not different types of infections can affect people. The risk of Alzheimer's disease.†Tanzi said that when he presented his thoughts or findings in a scientific conference, the participants' reactions were indeed mixed. One of the opinions that Itzhaki often hears is that if HSV-1 is also found in the brains of healthy elderly people, and in fact it is, then the virus cannot be considered to cause Alzheimer's disease. However, she pointed out that other pathogens, including Mycobacterium tuberculosis, can only cause infection symptoms in some susceptible people. If we finally discover that microbes are indeed a potential trigger for Alzheimer's disease – and for most researchers, this is really just “if†– then the effect of this discovery will be enormous. : We may only need to vaccinate to prevent annoying infections and stop this terrible disease. At the very least, doctors can control them with antimicrobials before they cause damage to the brain. However, it may take decades to accumulate enough proof for this hypothesis. As for the other challenges that exist, the most problematic for the researchers is the financial problem. Itzhaki said, “I have been working on this task for almost 50 years and the team has been facing extremely difficult financial problems – our funds are too little.†However, considering the clinical trials of numerous Alzheimer's disease drugs based on mainstream theory have failed, those who are committed to various "pathogen hypotheses" believe that it is meaningful to continue this theory. Most importantly, they hope that this editorial will at least enable skeptics to consider the possibility that microbes will play a role in Alzheimer's disease and support them for further research. Balin said: "We just want to say 'Wait, man - we have a lot of evidence accumulated from decades of work that people need to examine carefully.'" Source: Global Science Reagent Bottle,Clear Reagent Bottle,Clear Glass Reagent Bottle,Pp Cap Reagent Bottle Yancheng Rongtai Labware Co.,Ltd , https://www.shtestlab.com