Researchers can now make brain cells from the skin cells of patients with ALS, also known as Lou Gehrig’s disease, to better study the fatal disease.
The team used a genetic engineering technique to convert patients’ adult skin cells into “induced pluripotent stem cells,” which can then be coaxed into becoming brain cells.
“We make brain cells out of the patient’s own skin,” says Jeffrey Rothstein, professor of neurology, who directs the Brain Science Institute and the Robert Packard Center for ALS Research at Johns Hopkins University.
Researchers at Johns Hopkins Medicine have transformed skin cells from patients with Lou Gehrig’s disease, or amyotrophic lateral sclerosis (ALS), into brain cells affected by the progressive, fatal disease and deposited those human-made cells into...
A new study suggests that an investigational drug for multiple sclerosis (MS) may repair myelin, the fatty material that protects nerves and is damaged in MS, according to a study released today that will be presented at the American Academy of...
Duke University scientists have potentially discovered new avenues for Alzheimer's and dementia treatments.
They observed that in Alzheimer’s, immune cells that normally protect the brain instead begin to consume a vital nutrient called arginine.
By blocking this process with a drug, they were able to prevent the formation of ‘plaques’ in the brain that are characteristic of Alzheimer’s disease, and also halted memory loss in the mice.
What's more is that they were researching with a drug that has already begun human trials for cancer treatments—possibly paving the way for clinical trials in the near future.
While no technique that is tested in an animal can be guaranteed to work the same way in humans, the findings are particularly encouraging because, until now, the exact role of the immune system and arginine in Alzheimer’s was completely unknown. The drug that was used to block the body’s immune response to arginine – known as difluoromethylornithine (DFMO) – is already being investigated in drug trials for certain types of cancer and may be suitable for testing as a potential Alzheimer’s therapy.
This follows on the heels of other recent breakthroughs in possible "plaque fighting" techniques for Alzheimer's patients.
Fast synaptic communication in the brain requires synchronous vesicle fusion that is evoked by action potential-induced Ca2+ influx. However, synaptic terminals also release neurotransmitters by spontaneous vesicle fusion, which is independent of presynaptic action potentials. A functional role for spontaneous neurotransmitter release events in the regulation of synaptic plasticity and homeostasis, as well as the regulation of certain behaviours, has been reported. In addition, there is evidence that the presynaptic mechanisms underlying spontaneous release of neurotransmitters and their postsynaptic targets are segregated from those of evoked neurotransmission. These findings challenge current assumptions about neuronal signalling and neurotransmission, as they indicate that spontaneous neurotransmission has an autonomous role in interneuronal communication that is distinct from that of evoked release.(...) - by Ege T. Kavalali,, Nature Reviews Neuroscience, 16, 5–16 (2015)
In a group of children and young adults with the most intractable forms of epilepsy, a liquid form of marijuana called cannabidiol reduced seizures by more than 50% without causing the drug's usual "high," researchers said.
Scientists have modeled the stunning structure of the receptor in our bodies that jolts our senses when we eat sushi garnished with spicy wasabi -- and it turns out that this so-called 'wasabi receptor' may hold clues for developing new pain treatments.
The receptor, a protein called TRPA1, resides in the cellular membrane of our sensory nerve cells. Not only does it detect certain chemical agents outside of our bodies -- from wasabi to tear gas -- but it also gets triggered by pain-inducing signals within our bodies from itches and inflammation.
“The pain system is there to warn us when we need to avoid things that can cause injury, but also to enhance protective mechanisms,” Dr. David Julius, professor and chair of the physiology department at the University of California, San Francisco, and senior co-author of the new study, said in a written statement. “Of course, this information may also help guide the design of new analgesic drugs.”
The researchers built the new detailed 3D model using an advanced imaging technique known as electron cryo-microscopy, Science magazine reported. Using the model, the researchers discovered a spot in the receptor where wasabi chemical compounds bind, according to a video from UCSF about the research (see above). They noticed that when a receptor encounters such chemical compounds, it activates nerve fibers that then send pain signals to the brain.
There are already a few experimental drugs that target the wasabi receptor to alleviate pain, Smithsonian magazine reported, and the new model allows scientists to see the exact cleft in the protein where those drugs bind -- a discovery which may help guide the development of innovative pain medications.
"A dream of mine is that some of the work we do will translate into medicines people can take for chronic pain," Julius told NPR. "What the structure does is, it gives pharmaceutical firms sort of a map for either tweaking the drugs that they have... or for developing drugs that might have different properties."
Two types of touch information — the feel of an object and the position of an animal’s limb — have long been thought to flow into the brain via different channels and be integrated in sophisticated processing regions.
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