Two consecutive Neurons! Brain immune cells, the key to treating dementia?
March 13, 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)];Microglia are phagocytic cells in the brain that are responsible for the removal of harmful nerve cells, toxic proteins and other harmful substances. The surface of the TREM2 receptor has been a hot target in the research of Alzheimer's disease. Recently, scientists published two articles in the journal Neuron to reveal the "entanglement" between TREM2 and β-amyloid and provide new therapeutic strategies.
Huaxi Xu, Ph.D., professor and director of SBP's Neuroscience Initiative. Credit: Sanford Burnham Prebys Medical Discovery Institute
Alzheimer's disease (AD) threatens the health of more than 47 million people worldwide, and this number is still rising as the population ages. Typical conditions of this common disease include excessive accumulation of β-amyloid in the brain and tangling of Tau protein. Scientists have been trying to slow down and prevent Alzheimer's disease by eliminating the accumulation of disease-causing proteins, but with little success.
On March 7, two articles published in the journal Neuron revealed that the brain's "scavenger", the receptor for microglia surface TREM2, is expected to play a potential role in the treatment of AD.
1. Paper 1: TREM2 receptor is responsible for binding amyloid
TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function
DOI: https://doi.org/10.1016/j.neuron.2018.01.031
Dr. Huaxi Xu, a professor of neurology at the Sanford Burnham Prebys Institute of Medicine (SBP), and the team found that TREM2 inhibits damage to nerve cells by binding to β-amyloid, which stimulates microglia to surround and clear protein lesions.
Moreover, the interaction of TREM2 with amyloid is quite specific - TREM2 binds to amyloid oligomers (the most toxic structures of proteins). In the absence of TREM2, microglia do not efficiently bind to amyloid and ultimately fail to clear pathogenic proteins. Moreover, removal of TREM2 further inhibits potassium channels in downstream nerve cells, thereby affecting the current activities associated with immune cells in the brain.
This latest study reveals the details of the association between TREM2 and amyloid and provides a potential therapeutic strategy.
2, paper 2: upregulate TREM2, slow down the symptoms of dementia
Elevated TREM2 Gene Dosage Reprograms Microglia Responsivity and Ameliorates Pathological Phenotypes in Alzheimer's Disease Models
DOI: https://doi.org/10.1016/j.neuron.2018.02.002
Professor X. William Yang of the University of California, Los Angeles, and the team of Huaxi Xu found that up-regulating the level of TREM2 in the brain of AD mice can prevent or slow the occurrence and development of neurodegenerative diseases.
Specifically, upregulation of TREM2 levels can increase the sensitivity of microglia, thereby preventing the deterioration of AD mice and even recovering their cognitive ability. This means that in addition to addressing the pathology associated with AD, targeting TREM2 can also reduce behavioral deficits.
3. Research significance
"Enhancing microglia activity in the early stages of illness, using it to clear amyloid, this is an effective treatment. But we need to treat side effects, such as excessive activation of immune cells, easy release of excessive cytokines, thereby destroying healthy nerves Connection.†Professor Huaxi Xu stressed.
He believes that studying microglia, rather than amyloid, may be a new way to treat Alzheimer's disease. In other words, we can use the brain immune cells to solve the health crisis!
References: 1) The brain's immune system may be key to new Alzheimer's treatments
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