Health and Medical News and Resources

General interest items edited by Janice Flahiff

Recalling happier memories can reverse depression

Recalling happier memories can reverse depression 

From the 17 June 2015 MIT news release

MIT neuroscientists have shown that they can cure the symptoms of depression in mice by artificially reactivating happy memories that were formed before the onset of depression.

The findings, described in the June 18 issue of Nature, offer a possible explanation for the success of psychotherapies in which depression patients are encouraged to recall pleasant experiences. They also suggest new ways to treat depression by manipulating the brain cells where memories are stored. The researchers believe this kind of targeted approach could have fewer side effects than most existing antidepressant drugs, which bathe the entire brain.

“Once you identify specific sites in the memory circuit which are not functioning well, or whose boosting will bring a beneficial consequence, there is a possibility of inventing new medical technology where the improvement will be targeted to the specific part of the circuit, rather than administering a drug and letting that drug function everywhere in the brain,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, director of the RIKEN-MIT Center for Neural Circuit Genetics at MIT’s Picower Institute for Learning and Memory, and senior author of the paper.

Memory control

In 2012, Tonegawa, former MIT postdoc Xu Liu, Ramirez, and colleagues first reported that they could label and reactivate clusters of brain cells that store specific memories, which they called engrams. More recently, they showed that they could plant false memories, and that they couldswitch the emotional associations of a particular memory from positive to negative, and vice versa.

In their new study, the researchers sought to discover if their ability to reactivate existing memories could be exploited to treat depression.

To do this, the researchers first exposed mice to a pleasurable experience. In this case, all of the mice were male and the pleasurable experience consisted of spending time with female mice. During this time, cells in the hippocampus that encode the memory engram were labeled with a light-sensitive protein that activates the neuron in response to blue light.

After the positive memory was formed, the researchers induced depression-like symptoms in the mice by exposing them to chronic stress. These mice show symptoms that mimic those of human sufferers of depression, such as giving up easily when faced with a difficult situation and failing to take pleasure in activities that are normally enjoyable.

However, when the mice were placed in situations designed to test for those symptoms, the researchers found that they could dramatically improve the symptoms by reactivating the neurons that stored the memory of a past enjoyable experience. Those mice began to behave just like mice that had never been depressed — but only for as long as the pleasant memory stayed activated.

July 17, 2015 Posted by | Medical and Health Research News, Psychiatry, Psychology, Uncategorized | , , , , , , , , | Leave a comment

[Press release] Model predicts public response to disease outbreaks

Model predicts public response to disease outbreaks

From the 14 January 2015  press release

David L. Chandler | MIT News Office
January 14, 2015

Sometimes the response to the outbreak of a disease can make things worse — such as when people panic and flee, potentially spreading the disease to new areas. The ability to anticipate when such overreactions might occur could help public health officials take steps to limit the dangers.

Now a new computer model could provide a way of making such forecasts, based on a combination of data collected from hospitals, social media, and other sources. The model was developed by researchers at MIT, Draper Laboratory, and Ascel Bio, and is described in a paper published in the journal Interface.

The research grew out of earlier studies of how behavior spreads through social networks, explains co-author Marta Gonzalez, an assistant professor of civil and environmental engineering at MIT. The spread of information — and misinformation — about disease outbreaks “had not been studied, and it’s hard to get detailed information on the panic reactions,” Gonzalez says. “How do you quantify panic?”

One way of analyzing those reactions is by studying news reporting on outbreaks, as well as messages posted on social media, and comparing those with data from hospital records about the actual incidence of the disease.

In many cases, the reaction to an outbreak can cause more harm than the disease itself: For example, the researchers say, curtailing travel and distribution of goods can create economic damage, or even lead to rioting and other behavior that can exacerbates a disease’s spread. Wide publicity of an outbreak can also cause health care facilities to be overrun by people concerned about minor symptoms, potentially making it difficult for those affected by the disease to obtain the care they need, the researchers add.

To study the phenomenon, the team looked at data from three disease outbreaks: the 2009 spread of H1N1 flu in both Mexico and in Hong Kong, and the 2003 spread of SARS in Hong Kong. The model they developed could accurately reproduce the population-level behavior that accompanied those outbreaks.

In these cases, public response was often disproportionate to actual risk; in general, the research showed, diseases that are rare or unusual frequently receive attention that far outpaces the true risk. For example, the SARS outbreak in Hong Kong produced a much stronger public response than H1N1, even though the rate of infection with H1N1 was hundreds of times greater than that of SARS.

This analysis did not specifically address the ongoing Ebola epidemic in West Africa — but once again, Gonzalez says, “The response [is] just not justified by the extent of the disease.”

 

January 27, 2015 Posted by | Public Health | , , , , , , , | Leave a comment

   

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