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Undark

Ashley Smart, associate director of the Knight Science Journalism Program, writes for Undark about the impact of commercialized genetic tests on research involving new genetic links. “Even among some researchers who are optimistic about using polygenic scores to screen for physical health conditions, there is one emerging application of polygenic scores that makes them uneasy: the prediction of risks for depression and other psychiatric conditions,” writes Smart.

Nature

Researchers at MIT and elsewhere have identified key cell types that may protect the brain against Alzheimer’s symptoms, reports Sara Reardon for Nature. “Most Alzheimer’s research has focused on excitatory neurons, which relay electrical signals to activate other neurons,” explains Reardon. “But the authors found that the cells with reelin or somatostatin were inhibitory neurons, which halt neuronal communication. These inhibitory cells might therefore have a previously unknown role in the types of cognitive function that are lost during Alzheimer’s.”

The Washington Post

Writing for The Washington Post, research affiliate Bina Venkataraman emphasizes that “if biomedical breakthroughs are to benefit the millions of children afflicted with rare diseases, genetic testing of babies needs to expand.” Venkataraman adds: “By screening newborn genomes for currently known genetic diseases, patients and scientists could gain insights that lead to the treatment and prevention of thousands of illnesses that currently lack cures.”

Science

MIT researchers have discovered an RNA-guided DNA-cutting enzyme in eukaryotes, reports Science. “The researchers speculate that eukaryotic cells may have gained the newly identified editing genes from transposable elements—so-called jumping genes—they received from bacteria,” writes Science.

Popular Science

MIT researchers have identified a new biological editing system that could “potentially be even more precise than CRISPR gene editing,” reports Laura Baisas for Popular Science. The new system, based on a protein called Fanzor, is “the first programmable RNA-guided system discovered in eukaryotes,” Baisas notes.

New York Post

In a new study, researchers at MIT showed that they “were able to interfere with an enzyme typically found to be overactive in the brains of Alzheimer’s patients,” reports Alex Mitchell for The New York Post. After using a peptide to treat the overactive enzyme, they found that “the peptide shows protective effects against loss of neurons and also appears to be able to rescue some of the behavior deficits,” says Prof. Li-Huei Tsai.

The Boston Globe

Boston Globe reporter Ryan Cross spotlights Chroma Medicine, a biotech startup co-founded by MIT researchers that is “developing a new class of gene editing technologies that could control how our genetic code is read without changing the code itself.” Cross explains that Chroma Medicine’s technology could “have broad applications for treating both rare and common diseases.”

Forbes

Researchers at MIT have found that those with an E4 variant display abnormalities in cholesterol metabolism, reports William A. Haseltine for Forbes. “The MIT team suggest that the disruption of cholesterol metabolism could be a fundamental reason why those with the E4 variant are more likely to develop Alzheimer’s disease symptoms,” writes Haseltine.

NPR

Lydia Villa Komaroff PhD ’75 speaks with NPR reporter Emily Kwong about her work in gene editing. Biotechnology and genetic engineering were “enormously impactful,” says Komaroff. “So impactful that molecular biology pretty much disappeared as a field, it has become a tool that is of use in every field of biology and medicine today.”

Forbes

An MIT research study suggests that those with the E4 variant of the APOE gene are more likely to develop Alzheimer’s symptoms, reports William A. Haseltine for Forbes. The variant “disrupts how fat molecules are processed in the brain,” writes Haseltine. “It appears that the disruption of these fat molecules could be the fundamental reason why those that contain the E4 variant are more likely to develop Alzheimer’s symptoms.”

The Boston Globe

Researchers at MIT have developed new gene-editing technology that can move large sequences of DNA into the human genome, reports Ryan Cross for The Boston Globe. “The molecular tool gives scientists a new way to completely replace broken genes, paving the way to potential cures for diseases such as cystic fibrosis,” writes Cross.

Nature

Nature reporter Elie Dolgin writes that a new study by MIT researchers explores the role of the gene variant APOE4 in Alzheimer’s, and finds that the gene is linked with faulty cholesterol processing in the brain, impacting the insulation around nerve cells and potentially causing memory and learning deficits. “The work suggests that drugs that restore the brain’s cholesterol processing could treat the disease,” writes Dolgin. 

Wired

Research from Synlogic, a biotech company founded by Profs James Collins and Timothy Lu, has found that it’s the company’s engineered bacteria could provide some benefit to patients with a rare genetic disease, reports Emily Mullin for Wired. “Similar to how you might program a computer, we can tinker with the DNA of bacteria and have them do things like produce a drug at the right time and the right place, or in this case, break down a toxic metabolite,” says Lu.

The Boston Globe

Scientists from MIT, Duke and Stanford have developed a new technique to make gene therapies safer and more effective, reports Ryan Cross for The Boston Globe. “It’s about making these therapies much smarter and programmable,” says Jonathan S. Gootenberg, a research scientist at the McGovern Institute.

Nature

Nature reporter Neil Savage spotlights Prof. Michael Strano’s work developing a new technique to use nanoparticles to alter the biology of living plants. Savage writes that the new technique can allow for "the design of nanoparticles that carry gene-editing machinery to targeted areas to rewrite the plant’s genome and imbue it with properties such as pest and disease resistance,” writes Savage.