News Releases

Working with lab-grown human brain cells, Johns Hopkins researchers report they have uncovered a much sought-after connection between one of the most common genetic mutations in Parkinson’s disease and the formation of fatty plaques in the brain thought to contribute to the destruction of motor neurons that characterize the disease.

A new institute for stroke research and clinical care was announced today by the United Arab Emirates (UAE) Embassy in Washington, D.C., and Johns Hopkins. The Sheikh Khalifa Stroke Institute, funded by a $50 million gift from the United Arab Emirates, will focus Johns Hopkins’ efforts to leverage advances in engineering, artificial intelligence and precision medicine to better diagnose, treat and restore function to stroke patients. The gift is believed to be the largest ever for a stroke-specific initiative.  

In an effort to reduce patient misdiagnoses and associated poor patient outcomes from lack of prompt treatment, a Johns Hopkins Armstrong Institute for Patient Safety and Quality researcher is helping to lead the way in providing hospitals a new approach to quantify and monitor diagnostic errors in their quality improvement efforts. The approach, called Symptom-Disease Pair Analysis of Diagnostic Error, or SPADE, is featured in a paper published today in BMJ Quality & Safety.

Researchers at Johns Hopkins Medicine report they have identified rare genetic variations in a protein called Thorase, which is responsible for breaking down receptors at the connections between neurons in the brain.

A new study led by Johns Hopkins researchers found that measures of connectivity within specific cerebral networks were strongly linked to long-term functional outcomes in patients who had suffered severe brain injury following a cardiac arrest.

Congress of Neurological Surgeons (CNS) Meeting
Boston Convention and Exhibition Center, Boston, Massachusetts
Oct. 7-11, 2017

Surgeons at The Johns Hopkins Hospital have for the first time used a real-time, image-guided robot to insert screws into a patient’s spine. With last week’s surgery, Johns Hopkins joins the growing number of hospitals in the United States that offer robotic-assisted spine surgery.

Below are brief descriptions of research results scheduled for presentation by Johns Hopkins Kimmel Cancer Center scientists at the 2017 Annual Meeting of the American Society for Radiation Oncology (ASTRO), Sept. 24–27, in San Diego.

Ellen Mowry, M.D., M.C.R., an associate professor of neurology and epidemiology, and Scott Newsome, D.O., an associate professor of neurology, both of the Johns Hopkins University Department of Neurology, have been approved for a $13.4 million funding award by the Patient-Centered Outcomes Research Institute (PCORI) to conduct a study comparing two treatment options for people newly diagnosed with the relapsing-remitting form of multiple sclerosis (MS).

Sleep apnea, left untreated for even a few days, can increase blood sugar and fat levels, stress hormones and blood pressure, according to a new study of sleeping subjects. A report of the study’s findings, published in the August issue of The Journal of Clinical Endocrinology & Metabolism, adds further support for the consistent use of continuous positive airway pressure (CPAP), a machine that increases air pressure in the throat to keep the airway open during sleep. 

In a study looking at brain scans of people with mild loss of thought and memory ability, Johns Hopkins researchers report evidence of lower levels of the serotonin transporter — a natural brain chemical that regulates mood, sleep and appetite.

Johns Hopkins physicians report success in a small study of a modified skin biopsy that hastens the earlier diagnosis of an inherited and progressively fatal nerve disease and seems to offer a clearer view of the disorder’s severity and progression. With a quicker and less invasive way to visualize the hallmark protein clumps of the rare but lethal disease — familial transthyretin amyloidosis — the researchers say they hope to more rapidly advance clinical trials of treatments that may slow the disease and extend patients’ lives.

Johns Hopkins researchers say they have identified a new way that cells in the brain alert the rest of the body to recruit immune cells when the brain is injured. The work was completed in mouse models that mimic infection, stroke or trauma in humans.

Working with mouse, fly and human cells and tissue, Johns Hopkins researchers report new evidence that disruptions in the movement of cellular materials in and out of a cell’s control center — the nucleus — appear to be a direct cause of brain cell death in Huntington’s disease, an inherited adult neurodegenerative disorder.

Working with human brain tissue samples and genetically engineered mice, Johns Hopkins Medicine researchers together with colleagues at the National Institutes of Health, the University of California San Diego Shiley-Marcos Alzheimer's Disease Research Center, Columbia University, and the Institute for Basic Research in Staten Island say that consequences of low levels of the protein NPTX2 in the brains of people with Alzheimer’s disease (AD) may change the pattern of neural activity in ways that lead to the learning and memory loss that are hallmarks of the disease.

In a clinical trial conducted among adults in 11 hospitals, researchers have shown that a hand-held EEG device approved in 2016 by the U.S. Food and Drug Administration that is commercially available can quickly and with 97 percent accuracy rule out whether a person with a head injury likely has brain bleeding and needs further evaluation and treatment.

The human brain’s cerebellum controls the body’s ability to tightly and accurately coordinate and time movements as fine as picking up a pin and as muscular as running a foot race. Now, Johns Hopkins researchers have added to evidence that this structure also helps transfer so-called motor learning from one part of the body to another.

In experiments with a protein called Ephexin5 that appears to be elevated in the brain cells of Alzheimer’s disease patients and mouse models of the disease, Johns Hopkins researchers say removing it prevents animals from developing Alzheimer’s characteristic memory losses. In a report on the studies, published online March 27 in The Journal of Clinical Investigation, the researchers say the findings could eventually advance development of drugs that target Ephexin5 to prevent or treat symptoms of the disorder.

In a first-of-its-kind study published in the March 1, 2017 edition of Molecular Therapy, researchers from the National Institute on Deafness and Other Communication Disorders (NIDCD) and Johns Hopkins University School of Medicine showed that gene therapy was able to restore balance and hearing in genetically modified mice that mimic Usher Syndrome, a genetic condition in humans characterized by partial or total hearing loss, dizziness, and vision loss that worsens over time. The hearing loss and dizziness is caused by abnormalities of the inner ear.

Results of a small study of adults with autism at Johns Hopkins has added to evidence that their brains can learn to compensate for some language comprehension challenges that are a hallmark of the disorder in children.