Metabolism Program

New image-based cellular profiling tool peers deeply into metabolic biology

makenziekohler — Fri, 30 Jun 2023 14:30:09 +0000

New image-based cellular profiling tool peers deeply into metabolic biology

By Makenzie Kohler June 30, 2023

New image-based cellular profiling tool peers deeply into metabolic biology

LipocyteProfiler captures disease-relevant phenotypes in an inexpensive microscopy assay

By Makenzie Kohler

June 30, 2023

Credit: Phil Kubitz, Claussnitzer lab

Fat cells, or adipocytes, with stains highlighting nuclei (blue); mitochondria (red); lipid droplets (green); and the actin cytoskeleton, plasma membrane, and Golgi apparatus (yellow).

The field of microscopy has advanced immensely over the last fifty years in its ability to extract both quantitative and qualitative data from microscopy images. In a paper published in Cell Genomics, researchers at the ӳ��ý, Harvard Medical School, Massachusetts General Hospital, Technical School of Munich (TUM), and the University of Oxford have presented LipocyteProfiler, a new, high-throughput quantitative bioimaging tool to help bridge the gap between morphological observation and functional profiling.

LipocyteProfiler is a powerful imaging technique that generates comprehensive microscopy-based profiles of cells using multiple fluorescent dyes chosen specifically for studies of cardiometabolic biology. Image analysis software captures information about more than 3,000 cellular features, providing a deep view into the impacts of genetic variants, small molecule or genetic perturbations, and more on cellular shape, structure, and function.

“It moves the community from a very targeted, hypothesis-driven, unidimensional cell-based assay framework to one that allows us to survey biological processes in a cell and assign function to genes and genetic variations in an unbiased manner,” said Melina Claussnitzer, who is a ӳ��ý institute member, associate director of the institute's Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, faculty of the Center for Genomic Medicine at Mass General, and the senior researcher of the study.

Common genetic variants associated with cardiometabolic disease can produce phenotype changes of such small effect that they can be difficult to characterize. The current proof-of-concept study showcases how the use of a set of dyes chosen with a disease or trait in mind can illuminate cellular and subcellular behaviors at unprecedented depth and scale.

LipocyteProfiler builds on the concept of image-based profiling that was first introduced in the context of morphology mapping by Cell Painting, a high-content imaging assay developed by ӳ��ý institute scientist and Imaging Platform senior director Anne Carpenter. Whereas Cell Painting labels eight general organelles or components of the cell, LipocyteProfiler uses six fluorescent dyes that together illuminate the morphology and activity of nine cellular compartments: the nucleus, nucleoli, mitochondria, endoplasmic reticulum (ER), Golgi apparatus, cytoplasmic RNA, f-actin cytoskeleton, and plasma membrane, and lipid droplets (fat-storing organelles that regulate lipids within every type of cell and which are particularly common in adipocytes). It then extracts features from images of stained cells and creates cellular profiles, categorizing cells based on patterns (often imperceptible to the human eye) that they share with other cells, which directly inform disease biology.

Fat cells stained yellow to show the actin cytoskeleton, plasma membrane, and Golgi apparatus. Credit: Phil Kubitz, Claussnitzer lab

Fat cells stained blue to show nuclei. Credit: Phil Kubitz, Claussnitzer lab

Fat cells stained red to show mitochondria. Credit: Phil Kubitz, Claussnitzer lab

Fat cells stained green to show lipid droplets. Credit: Phil Kubitz, Claussnitzer lab

A merged image showing all of the stained cellular components together. Credit: Phil Kubitz, Claussnitzer lab.

To assess LipocyteProfiler, the researchers analyzed white and brown fat cells and liver cells, focusing on traits such as the size, the number, and the location of lipid droplets in a cell. When comparing cells with a particular genetic variant to those without, the team found that the LipocyteProfiler protocol detects morphological and mechanistic differences between the cells, allowing for linkage of genetic variation to phenotypic traits. LipocyteProfiler also highlighted discrete cellular mechanisms and pathways when used to analyze metabolic traits associated with high polygenic risk scores.

“We could identify and examine more than 700 features just related to lipid accumulation,” said Sophie Strobel, a lead author on the paper who is now at TUM. “That teaches us far more than looking for just a single informative data point.”

The researchers also looked at the tool’s ability to detect changes in cellular phenotypes after exposure to drugs and small molecule compounds. Typically, studying drug therapies is an expensive and time-consuming undertaking. With high-resolution, cell-based profiling techniques, extracting a large amount of data can be done cheaply and efficiently.

“I think drug screens are an obvious next step for using the platform because image-based screens tend to be pretty inexpensive, and they can be scaled up so that you can assess and evaluate hundreds of thousands of compounds and see which ones impact the phenotypes that are associated with disease,” said Cell Painting creator Carpenter, who collaborated on the LipocyteProfiler project.

LipocyteProfiler is already being used experimentally to look at relationships between genetic variants and their functions. Claussnitzer and the University of Chicago's Marcelo Nobrega recently used LipocyteProfiler to reveal a mechanism connecting the gene COBLL1 and a diabetes-related metabolic phenotype called metabolically obese normal weight. By using the tool, Clausnnitzer and others saw how a variant that reduces COBLL1 expression interferes with lipid droplets' growth within a cell.

Claussnitzer's lab is now working to expand the machine-learning aspect of LipocyteProfiler, with an eye towards tracking information flow within single cells from transcription to phenotypes. Experimentally, the lab continues to use LipocyteProfiler to assess the relationships between genetic variants and cellular programs, to understand highly granular processes of disease biology.

Claussnitzer notes that LipocyteProfiler is a powerful addition to the -omics tool box, one that looks beyond epigenomics, transcriptomics, and proteomics to allow systematic, unbiased, image-based profiling of cellular phenotypes. And while the technology is the first to adapt the Cell Painting protocol, researchers at the ӳ��ý and beyond are already working to create assays like LipocyteProfiler for their own respective fields.

“Just as we applied stains related to lipid biology and metabolism,” Strobel said, “one could instead swap in stains for something related to, say, lymphocyte biology, depending on the question you want to answer and what disease you are looking at.”

Carpenter notes that she is satisfied seeing people expand on her work on Cell Painting, saying “in the end, none of the work matters if biologists aren't adapting it in their labs for the myriad of disease areas that people work on.”

Funding

Support for this work was provided by Novo Nordisk Foundation, the Foundation for the National Institutes of Health, the National Institute of Diabetes and Digestive and Kidney Diseases, the National Human Genome Research Institute, the American Diabetes Association, the Gates Foundation, the Doris Duke Charitable Foundation, the ӳ��ý, and other sources.

Papers cited

Laber S, Strobel SM, et al. Discovering cellular programs of intrinsic and extrinsic drivers of metabolic traits using LipocyteProfiler. Cell Genomics. Online June 20, 2023. DOI: 10.1016/j.xgen.2023.100346

Tags:

Imaging Platform

Metabolism Program

Connecting variants to functions

Cardiovascular disease

Diabetes

Obesity

Heart Disease

Image-Based Profiling

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

adicorat — Wed, 21 Jun 2023 16:58:24 +0000

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Now, researchers at the ӳ��ý of MIT and Harvard have found that treatment with continuous hypoxia — low-oxygen conditions comparable to levels at a Mount Everest base camp — restores balance and coordination in a mouse model of Friedreich’s ataxia. With further development, the findings could inform a potential treatment that lowers oxygen levels in certain tissues in humans to reverse advanced disease. The study appeared recently in Human Molecular Genetics.

“If we accept that disease stems from the interaction of genes and environment, then why not manipulate the environment?” said Vamsi Mootha, senior author of the study, an institute member at the ӳ��ý, professor of systems biology and medicine at Harvard Medical School, and professor of molecular biology at Massachusetts General Hospital. “Through a series of papers we have reported a strong interaction between genetic pathways related to energy metabolism and environmental oxygen. By attacking disease from the environment side of things, we think our quest for a hypoxia-in-a-pill approach could impact a number of genetically diverse diseases.”

Mootha’s lab has been studying hypoxia as a potential treatment for rare neurological diseases since 2016. Previous work from his lab suggested that hypoxia could prevent ataxia — impaired balance and coordination — in Friedreich’s ataxia mice, and the new findings now show that the approach can even reverse it in animals with more advanced disease.

The latest study also adds to a growing body of evidence that hypoxia could treat a broad range of conditions. Last month, for instance, Mootha’s team showed that a mouse model of an accelerated aging disease lived 50 percent longer and showed slower neurological decline in low-oxygen conditions. The work appeared in PLOS Biology.

“Oxygen restriction is an exciting experimental modality, and it's now been shown to have pretty potent beneficial effects across multiple models of aging and disease,” said Robert Rogers, first author on the PLOS study, postdoctoral fellow in Mootha’s lab, and an instructor in the Division of Pulmonary and Critical Care Medicine at Massachusetts General Hospital. “It deserves a lot of further exploration to understand its mechanism so that we can recapitulate it in a form that’s easier to deliver, like a pill.”

Treatment comparison

Friedreich’s ataxia is caused by loss of a mitochondrial protein called frataxin, which helps make molecular complexes called iron-sulfur clusters required for a number of cellular pathways, including those involved in energy metabolism. Patients with Friedreich’s ataxia have fewer of these clusters than people without the disease, resulting in impaired energy production in the affected cells.

In 2019, Mootha’s team found that continuously exposing young mice with Friedreich’s ataxia to 11 percent oxygen, as opposed to 21 percent at sea level, early in the disease prevented ataxia. They also found that hypoxia restored iron-sulfur cluster levels in cells. However, most patients are diagnosed later in the disease, after symptoms develop, so the researchers wanted to test whether hypoxia could reverse — rather than simply prevent — advanced disease. And because extreme hypoxia can be harmful, the scientists knew they’d have to keep optimizing the treatment.

To look for other possible regimens, Mootha’s team, in their latest study, tested seven different hypoxia treatments in the same mouse model of Friedreich’s ataxia and included animals in later stages of the disease. A few treatments stood out.

Intermittent hypoxia — 16 hours of 11 percent oxygen and 8 hours of 21 percent oxygen — was harmful, and mice developed cardiac stress and died more quickly than those without treatment. The group hypothesized that the animals’ red blood cell levels increased due to hypoxia, and then when exposed to normal oxygen levels, created a temporary but toxic flood of oxygen. They supported this hypothesis by using a drug that pharmacologically blocks this response.

The team reported that treatment with mild hypoxia — 17 percent oxygen, equivalent to the levels in Denver — was moderately beneficial, and mice developed ataxia later than those without treatment.

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

“We've shown how amenable the nervous system is to recovering from damage,” said Tslil Ast, a co-first author on the study along with Hong Wang, a research scientist in Mootha’s lab. Ast was a postdoctoral fellow in Mootha’s lab when the study began and is currently a team leader at the Weizmann Institute of Science in Israel. “Even with profound ataxia, these mice can still, under the correct therapeutic regimen, reverse course.”

The treatment did not improve the disease’s cardiovascular symptoms, suggesting that more work, potentially towards a combination therapy, is needed to transform these insights into a curative treatment.

In the PLOS study from last month, Mootha’s group demonstrated that the same treatment — continuous exposure to 11 percent oxygen — increased lifespan by 50 percent in mice with mutations in the Ercc1 gene that lead to accelerated aging and early death in the animals.

In the future, the researchers aim to continue to uncover the full mechanism by which hypoxia alleviates ataxia, which could inform hypoxia-inspired therapies such as a pill that could decrease oxygen or blunt the body’s ability to deliver oxygen to tissues.

In the meantime, Ast and Mootha say that hypoxia can be deadly if not done in a controlled clinical setting. For example, in the current work they noted that not only were intermittent regimens not helpful, but even harmful, underscoring the need for and value of continued pre-clinical testing before moving into humans.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Ast T et al. Continuous, but not intermittent, regimens of hypoxia prevent and reverse ataxia in a murine model of Friedreich’s ataxia. Human Molecular Genetics. Online June 1, 2023. DOI:10.1093/hmg/ddad091.

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

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tulrich@broadinstitute.org — Thu, 25 May 2023 15:01:46 +0000

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Treatment comparison

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

Cells can use uridine, a component of RNA, as a source of energy

adicorat — Wed, 17 May 2023 15:00:00 +0000

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Treatment comparison

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

Targeting a unique metabolic pathway might starve pancreatic cancer

tulrich@broadinstitute.org — Thu, 06 Apr 2023 13:41:25 +0000

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Treatment comparison

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

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Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Treatment comparison

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

HHMI honors five ӳ��ý researchers

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Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Treatment comparison

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

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Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Treatment comparison

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

ӳ��ý launches new effort to study rare neuromuscular disorder

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Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Treatment comparison

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

A single-cell atlas of nerve cells in the gut reveals web of connections

kzusi@broadinstitute.org — Thu, 03 Sep 2020 15:49:58 +0000

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

By Allessandra DiCorato June 21, 2023

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

New study suggests that treatments that mimic the effects of a low-oxygen environment could one day help reverse Friedreich’s ataxia.

By Allessandra DiCorato

June 21, 2023

Credit: Susanna Hamilton, ӳ��ý Communications

Friedreich’s ataxia is a rare, inherited disease that causes progressive nervous system damage, impairing balance and coordination and leaving patients unable to walk by early adulthood.

Treatment comparison

But the researchers were excited when they found that continuous hypoxia at 11 percent oxygen reversed neurological symptoms and ataxia, even at advanced disease.

Funding

This work was supported in part by the Friedreich’s Ataxia Research Alliance, Marriott Family Foundation, and the National Institutes of Health.

Papers cited

Rogers RS et al. Hypoxia extends lifespan and neurological function in a mouse model of aging. PLOS Biology. Online May 23, 2023. DOI:10.1371/journal.pbio.3002117.

Tags:

Metabolism Program

Rare Disease

Metabolism Program

New image-based cellular profiling tool peers deeply into metabolic biology

New image-based cellular profiling tool peers deeply into metabolic biology

New image-based cellular profiling tool peers deeply into metabolic biology

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

Study finds how a genetic variant raises diabetes risk through an unexpected mechanism

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

Cells can use uridine, a component of RNA, as a source of energy

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

Targeting a unique metabolic pathway might starve pancreatic cancer

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

ӳ����ý Discovery Center in Cambridge opens to the public this October

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

HHMI honors five ӳ����ý researchers

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

SARS-CoV-2 hijacks two key metabolic pathways to rapidly replicate in host cells

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

ӳ����ý launches new effort to study rare neuromuscular disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

A single-cell atlas of nerve cells in the gut reveals web of connections

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Low oxygen levels restore balance and coordination in a mouse model of a movement disorder

Treatment comparison

ӳ��ý Discovery Center in Cambridge opens to the public this October

HHMI honors five ӳ��ý researchers

ӳ��ý launches new effort to study rare neuromuscular disorder