In 1953, a young man named Henry Molaison underwent an experimental operation that doctors hoped would control his frequent epileptic seizures. When the surgeon could not locate the origin of Molaison’s seizures, he removed a structure known as the hippocampus from both sides of his brain.
Soon after the surgery, Molaison’s doctors realized that the procedure had had a dramatic and unintended consequence: Molaison could no longer form new memories. This tragic loss for Molaison and his family turned him into one of the most important patients in the history of neuroscience. In fact, his case answered more questions about how memory works than the entire previous century of research, writes Suzanne Corkin, MIT professor of neuroscience emerita, in her new book, “Permanent Present Tense.”
Prometheus, the mythological figure who stole fire from the gods, was punished for this theft by being bound to a rock. Each day, an eagle swept down and fed on his liver, which then grew back to be eaten again the next day.
Modern scientists know there is a grain of truth to the tale, says MIT engineer Sangeeta Bhatia: The liver can indeed regenerate itself if part of it is removed. However, researchers trying to exploit that ability in hopes of producing artificial liver tissue for transplantation have repeatedly been stymied: Mature liver cells, known as hepatocytes, quickly lose their normal function when removed from the body.
Researchers at the Stanford University School of Medicine have found that a naturally occurring protein secreted only in discrete areas of the mammalian brain may act as a Valium-like brake on certain types of epileptic seizures.
The protein is known as diazepam binding inhibitor, or DBI. It calms the rhythms of a key brain circuit and so could prove valuable in developing novel, less side-effect-prone therapies not only for epilepsy but possibly for anxiety and sleep disorders, too. The researchers’ discoveries were published May 30 in Neuron.
“This is one of the most exciting findings we have had in many years,” said John Huguenard, PhD, professor of neurology and neurological sciences and the study’s senior author. “Our results show for the first time that a nucleus deep in the middle of the brain generates a small protein product, or peptide, that acts just like benzodiazepines.” This drug class includes not only the anti-anxiety compound Valium (generic name diazepam), first marketed in 1965, but its predecessor Librium, discovered in 1955, and the more recently developed sleep aid Halcyon.
If you are one of the 20% of healthy adults who struggle with basic arithmetic, simple tasks like splitting the dinner bill can be excruciating. Now, a new study suggests that a gentle, painless electrical current applied to the brain can boost math performance for up to 6 months. Researchers dont fully understand how it works, however, and there could be side effects.
A new flu, H7N9, has killed 36 people since it was first found in China two months ago. A new virus from the SARS family has killed 22 people since it was found on the Arabian Peninsula last summer.
In past years, this might have been occasion for panic. Yet chicken and pork sales have not plummeted, as they did during flus linked to swine and birds. Travel to Shanghai or Mecca has not been curtailed, nor have there been alarmist calls to close national borders.
Is this relatively calm response in order? Or does the simultaneous emergence of two new diseases suggest something more dire?
Actually, experts say, the answer to both questions may well be yes.
CoQ10 is the first medication to improve survival in chronic heart failure since ACE inhibitors and beta blockers more than a decade ago and should be added to standard heart failure therapy.
Lisbon, 25 May 2013: Coenzyme Q10 decreases all cause mortality by half, according to the results of a multicentre randomised double blind trial presented today at Heart Failure 2013 congress. It is the first drug to improve heart failure mortality in over a decade and should be added to standard treatment, according to lead author Professor Svend Aage Mortensen (Copenhagen, Denmark).
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Activating an enzyme known to play a role in the anti-aging benefits of calorie restriction delays the loss of brain cells and preserves cognitive function in mice, according to a study published in the May 22 issue of The Journal of Neuroscience. The findings could one day guide researchers to discover drug alternatives that slow the progress of age-associated impairments in the brain.
Li-Huei Tsai — director of the Picower Institute for Learning and Memory and Picower Professor of Neuroscience at MIT — along with postdoc Johannes Gräff and others at MIT tested whether reducing caloric intake would delay the onset of nerve cell loss that is common in neurodegenerative disease, and if so, whether SIRT1 activation was driving this effect. The group not only confirmed that caloric restriction delays nerve cell loss, but also found that a drug that activates SIRT1 produces the same effects.