New evidence! Alzheimer's disease-causing protein can spread
New evidence! Alzheimer's disease-causing protein can spread
January 9, 2018 Source: Biological Exploration of: Flora
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];The pathogenic protein of Alzheimer's disease, the Tau protein, spreads in the patient's brain and spreads from one neuron to another, causing an increase in dementia symptoms. Scientists hope that the "new evidence" found in this latest study is expected to provide support for slowing disease progression by blocking protein transmission.
This breakthrough is due to the development of brain imaging technology—the development of positron emission tomography (PET) technology that allows scientists to observe the patient's brain (no longer relying on dissecting the brains of deceased patients).
Scientists at the University of Cambridge used PET technology to analyze the brains of 17 patients with Alzheimer's disease and found evidence that the Tau protein was transmitted in different parts of the brain. The relevant research results are published in the latest issue of "Brain" magazine.
1. Hypothesis about Tau protein
Studies have shown that this neurodegenerative disease is associated with two proteins that accumulate abnormally in the brain: Tau protein and β-amyloid (Aβ). The most mainstream reasoning is that β-amyloid is the first to accumulate, triggering neuronal synaptic dysfunction, Tau protein hyperphosphorylation and secondary inflammatory reaction, leading to neuronal degeneration and death, thereby phagocytizing memory and cognition.
Scientists have been speculating about the details of Tau protein in the brain. There are three assumptions:
1) "transneuronal spread" hypothesis: Tau protein accumulates at one location and then spreads to other brain regions, triggering a chain reaction. The most favorable illustration of this speculation is a mouse-based study that when mice are injected with abnormal human Tau protein, the protein spreads rapidly in its brain.
2) "metabolic vulnerability" hypothesis: Tau protein is produced (not transmitted) in nerve cells, but different cells have different sensitivities to the protein (different metabolic requirements), resulting in different effects.
3) "trophic support" hypothesis: Tau protein does not spread, but some brain regions are more susceptible to damage than other regions, which is mainly related to nutritional deficiencies or gene expression patterns.
Some scientists questioned the first speculation because the amount of Tau protein injected in the mouse study far exceeded the amount of pathogenic protein in the brain of normal dementia patients. Moreover, scientists believe that proteins spread rapidly in the mouse brain but spread slowly in the human brain. However, there has been no conclusion.
2 , the new discovery testimony hypothesis
Professor James Rowe from the University of Cambridge clinical neuroscience expert and the team found the answer - after studying the functional connections within the brain of Alzheimer's patients and comparing it with the level of Tau protein, it proves that "trans-neuronal transmission "Assume that the Tau protein will spread between neurons.
According to Thomas Cope, the first author of the article, this finding means that the Tau protein spreads out with functionally connected neurons and accumulates layer by layer. This mode of transmission is similar to the flu virus. The virus first infects people around the patient and then passes it on to other people who have contact.
Tau protein is first present in the entorhinal cortex of the brain of AD patients, located next to the hippocampus (supervised memory function). This may be the first reason for dementia patients to experience memory loss. Moreover, Tau protein is transmitted in the brain, infecting and destroying nerve cells, causing the symptoms of patients to become more and more serious.
In the brains of Alzheimer's patients, the spread of Tau protein is relatively random, which may explain why patients have symptoms of memory and cognitive confusion. This study reminds everyone that it may slow the progression of dementia by blocking the spread of Tau protein.
References: 1) Advances in brain imaging settle debate over spread of key protein in Alzheimer's
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