Biologists and biomedical engineers are proposing to define the term “yank” for changes in force over time, something that our muscles cause and nerves can sense and respond to. Their ideas were published on September 12 in Journal of Experimental Biology.
Expressed mathematically, acceleration is the derivative of speed or velocity with respect to time. The term for the time derivative of acceleration is “jerk,” and additional time derivatives after jerk are called “snap,” “crackle” and “pop.”
The corresponding term for force – in physics, force is measured in units of mass times acceleration – has never been defined, the researchers say.
Scientists that study sports often use the term “rate of force development”, a measure of explosive strength. Scientists who study gait and balance — in animals and humans — also often analyze how quickly forces on the body change. It could be useful in understanding spasticity, a common neuromuscular reflex impairment in multiple sclerosis, spinal cord injury, stroke and cerebral palsy.
“Understanding how reflexes and sensory signals from the muscles are affected by neurological disorders is how we ended up needing to define the rate change in force,” says Lena Ting, PhD, professor of rehabilitation medicine at Emory University School of Medicine and the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory. Read more
Interest in bacteria and other creatures living on and inside us keeps climbing. On August 15 and 16, scientists from a wide array of disciplines will gather for the Emory Microbiome Research Center inaugural symposium.
On the first day, Lab Land is looking forward to hearing from several of the speakers, touching on topics stretching from insects/agricultural pathogens to neurodegenerative disease. The second day is a hands on workshop organized by instructor Anna Knight on sorting through microbiome data. The symposium will be at WHSCAB (Woodruff Health Sciences Center Auditorium). Registration before August 2 is encouraged!
Many of the projects that we highlighted four years ago, when Emory held its first microbiome symposium, have continued and gathered momentum. Guest keynotes are from Rodney Newberry from WUSTL and Gary Wu from Penn.
At the sleep research meeting in San Antonio this year, there were signs of an impending pharmaceutical arms race in the realm of narcolepsy.
The big fish in a small pond, Jazz Pharmaceuticals, was preparing to market its recently FDA-approved medication: Sunosi/solriamfetol. Startup Harmony Biosciences was close behind with pitolisant, already approved in Europe. On the horizon are experimental drugs designed to more precisely target the neuropeptide deficiency in people with classic narcolepsy type 1 (for narcolepsy with cataplexy: hypocretin/orexin agonists).
Amidst this commercial maneuvering, a new clinical trial is underway at Emory Sleep Center. The study compares modafinil versus amphetamines for narcolepsy type 2 (NT2) and idiopathic hypersomnia (IH).
These are not new drugs; they are old standards, when used to treat other sleep disorders. What’s remarkable here is that they are being tested “head-to-head.” In addition, the study explicitly tracks outcomes that people with NT2 and IH often talk about: sleep inertia, or difficulty waking up and getting out of bed in the morning, and brain fog, which is difficulty thinking/concentrating/paying attention. The main outcome measure is the Epworth Sleepiness Scale, which asks how likely someone is to fall asleep during daytime situations such as reading or while stopped in traffic. Read more
Emory is full of fledgling biomedical proto-companies. Some of them are actual corporations with employees, while others are ideas that need a push to get them to that point. Along with the companies highlighted by the Emory Biotech Consulting Club, Dean Sukhatme’s recent announcement of five I3 Venture research awards gives more examples of early stage research projects with commercial potential.
This is the third round of the I3 awards; the first two were Wow! (basic discovery) and Synergy II/Nexus (promoting interdisciplinary collaboration). For the five Venture awards, the Dean’s office is providing a total of $100,000. The companies will then use the momentum to seek larger amounts of funding from various sources. Lab Land is still collecting information on the projects:
If you’re wondering where Alzheimer’s research might be headed after the latest large-scale failure of a clinical trial based on the “amyloid hypothesis,” check this out.
Plaques. Tangles. Clumps. These are all pathological signs of neurodegenerative diseases that scientists can see under the microscope. But they don’t explain most of the broader trends of cognitive resilience or decline in aging individuals. What’s missing?
A recent proteomics analysis in Nature Communications from Emory researchers identifies key proteins connected with cognitive trajectory – meaning the rate at which someone starts to decline and develop mild cognitive impairment or dementia.
This paper fits in with the multi-year push for “unbiased” Alzheimer’s/aging research at Emory. The lead and senior authors are Aliza and Thomas Wingo, with proteomics from biochemist Nick Seyfried and company.
The proteins the Emory team spotlights are not the usual suspects that scientists have been grinding on for years in the Alzheimer’s field, such as beta-amyloid and tau. They’re proteins connected with cellular energy factories (mitochondria) or with synapses, the connections between brain cells.
“Our most notable finding is that proteins involving mitochondrial activities or synaptic functions had increased abundance among individuals with cognitive stability regardless of the burden of β-amyloid plaques or neurofibrillary tangles,” the authors write. “Taken together, our findings and others highlight that mitochondrial activities would be a fruitful research target for early prevention of cognitive decline and enhancement of cognitive stability.” Read more
Despite advances in genomics in recent years, schizophrenia remains one of the most complex challenges of both genetics and neuroscience. The chromosomal abnormality 22q11 deletion syndrome, also known as DiGeorge syndrome, offers a way in, since it is one of the strongest genetic risk factors for schizophrenia.
Out of dozens of genes within the 22q11 deletion, several encode proteins found in mitochondria. A team of Emory scientists, led by cell biologist Victor Faundez, recently analyzed the network of proteins found in human cells, both from individuals affected by 22q11 deletion syndrome and their healthy relatives.
The results are published in Journal of Neuroscience. Note: this is a sprawling paper, involving both proteomics (courtesy of Nick Seyfried, whose Emory epithet is “wizard”) and mutant Drosophila fruit flies. There are four co-first authors: , ,
Victor Faundez, PhD
Mitochondrial proteins are important for keeping cells fueled up and in metabolic balance, but how does altering them affect the brain in a way that leads to schizophrenia? That’s the overall question: how do changes in the miniature power plants within the cell affect synapses, the junctions between cells?
The scientists were focusing on one particular mitochondrial protein, SLC25A1, whose corresponding gene is in the 22q11 deletion. Faundez says that SCL25A1 has been largely ignored by other scientists studying 22q11.
“We think SLC25A1 exerts a powerful influence on the neurodevelopmental phenotypes in 22q11,” he says. “Our main focus forward is going to be the function that mitochondria play in synapse biology.” Read more
Nothing he tried had worked. For Sigurjon Jakobsson, the trip to Atlanta with his family was a last-ditch effort to wake up. He had struggled with sleeping excessively for several years before coming from Iceland to see a visionary neurologist, who might have answers.
In high school, Sigurjon was a decathlete competing as part of Iceland’s national sports team. But at the age of 16, an increasing need for sleep began to encroach upon his life. Sigurjon needed several alarm clocks to get out of bed and was frequently late to school or his job at a construction company. He often slept more than 16 hours in a day.
Sigurjon feeling awake (Atlanta, summer 2018)
When Sigurjon describes his experiences, they sound like depression, although his mood and lack of motivation appear more a consequence of his insatiable desire to sleep. He quit sports. He dropped out of college and became isolated and lost touch with close friends.
“Your will to do things just kinda dies,” he says. “And then you’re always trying and trying again. It just gets worse. You kinda die inside from being tired all the time.”
At the recommendation of a neurologist in Iceland, Sigurjon’s family sought out David Rye, who is known internationally for his research on idiopathic hypersomnia, a poorly understood sleep disorder. Read more
Neuroscientists at Emory University School of Medicine have discovered a focal pathway in the brain that when electrically stimulated causes immediate laughter, followed by a sense of calm and happiness, even during awake brain surgery. The effects of stimulation were observed in an epilepsy patient undergoing diagnostic monitoring for seizure diagnosis. These effects were then harnessed to help her complete a separate awake brain surgery two days later.
The behavioral effects of direct electrical stimulation of the cingulum bundle, a white matter tract in the brain, were confirmed in two other epilepsy patients undergoing diagnostic monitoring. The findings are scheduled for publication in the Journal of Clinical Investigation.
Emory neurosurgeons see the technique as a “potentially transformative” way to calm some patients during awake brain surgery, even those who are not especially anxious. For optimal protection of critical brain functions during surgery, patients may need to be awake and not sedated, so that doctors can talk with them, assess their language skills, and detect impairments that may arise from resection. Read more
Researchers at Emory University School of Medicine have gained insight into a feature of fragile X syndrome, which is also seen in other neurological and neurodevelopmental disorders.
In a mouse model of fragile X syndrome, homeostatic mechanisms that would normally help brain cells adjust to developmental changes don’t work properly. This helps explain why cortical hyperexcitability, which is linked to sensory sensitivity and seizure susceptibility, gradually appears during brain development.
Studying a model of fragile X syndrome, Emory researchers were looking at neurons displaying single spiking and multi-spiking behavior.
These physiological insights could help guide clinical research and efforts at early intervention, the scientists say. The results were published Feb. 5 by Cell Reports (open access).
Fragile X syndrome is the most common inherited form of intellectual disability and a leading single-gene cause of autism. Individuals with fragile X syndrome often display sensory sensitivity and some — about 15 percent— have seizures.
Scientists’ explanation for these phenomena is cortical hyperexcitability, meaning that the response of the cortex (the outer part of the brain) to sensory input is more than typical. Cortical hyperexcitability has also been observed in the broader category of autism spectrum disorder, as well as migraine or after a stroke.
At Emory, graduate student Pernille Bülow forged a collaboration between Peter Wenner, PhD and Gary Bassell, PhD. Wenner, interested in homeostatic plasticity, and Bassell, an expert in fragile X neurobiology, wanted to investigate why a mechanism called homeostatic intrinsic plasticity does not compensate for the changes in the brain brought about in fragile X syndrome. More here.