Nature: More than 10 years later, genes that help prevent brain disease have been discovered.
May 18, 2018 Source: Biological Exploration of: Tierna
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)];More than 10 years ago, Professor Susan L. Ackerman of the University of California, San Diego, and his colleagues first highlighted the causes of brain disease. After years of in-depth research into this cause, she and her colleagues have now made new breakthroughs: they found that a gene called Ankrd16 prevents the accumulation of defective proteins they initially observed, or for the prevention of brain disease. Come hope.
DOI: 10.1038/s41586-018-0137-8
On May 16th, Nature reported this research with the title "ANKRD16prevents neuron loss caused by an editing-defective tRNA synthetase".
Scientists have previously found that defective proteins cause harmful deposition or "aggregates" in neurological diseases such as Alzheimer's and Parkinson's. Although the cause of these protein deposits remains a mystery, it is well known that when cells fail to deliver the appropriate genetic information to proteins, abnormal aggregation occurs.
Imagereveals Purkinje cells(gray)and their dendrites,as well as an accumulation of protein deposits(red dots). Credit:AckermanLab/UC San Diego
Often, the transfer of information from genes to proteins is tightly controlled—biologically proofreading and correcting—a process that avoids the production of inappropriate proteins. In the latest study, lead authors Ackerman and My- Nuong Vo found that the Ankrd16 gene rescued specific neurons known as Purkinje cells, which die when proofreading fails. (In the absence of normal levels of Ankrd16, these cerebellar nerve cells erroneously activate the amino acid serine, and then the serine incorrectly binds to the protein and causes protein aggregation).
“In short, you can think of Ankrd16 as a sponge or “failsafe†that captures the falsely activated serine and prevents it from binding incorrectly to the protein. When nerve cells are proofread and corrected This is especially useful when the ability to fail is degraded," Ackerman said.
Proofreadingdefect bypassed. Credit: Ackerman Lab/UC San Diego
In Purkinje cells, the level of Ankrd16 is usually low, making these neurons susceptible to proofreading defects. Increasing the level of Ankrd16 protects these cells from death, and removal of Ankrd16 from other neurons that correct defective mice results in extensive accumulation of abnormal proteins that ultimately lead to neuronal death.
Finally, the researchers pointed out that the identification of a few disease mutations (such as Ankrd16) can help understand the underlying pathology of neurodegenerative diseases, which may be a promising way to understand the development of the disease.
References: 1) Researchersidentify gene that helps prevent brain disease
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