Sunday, February 18, 2018

Scientists seek drug to ‘rewire’ adult brain after stroke

Adults who have experienced a stroke may one day be able to take a drug to help their brain “rewire” itself, so that tasks once carried out by now-damaged areas can be taken over by other regions, researchers have claimed.
The ability for the brain to rewire, so-called “brain plasticity”, is thought to occur throughout life; however, while children have a high degree of brain plasticity, adult brains are generally thought to be less plastic.

Research looking at children and young adults who had a stroke as a baby – a situation thought to affect at least one in 4,000 around the time of their birth – has highlighted the incredible ability of the young brain to rewire.

A professor of neurology, detailed a new study involving 12 such individuals, aged between 12 and 25.“What you see is the right hemisphere, which is never in control of language in anyone who is healthy, is apparently capable of taking over language if you lose left hemisphere,” said the Prof., who presented the findings at a meeting recently. “This does not happen in adults,” she added.

Using brain imaging the team found that the regions in the right hemisphere of the brain that took over were in the mirror image location to those used on the left side of the brain in healthy people. That, she said, emphasises that it is not just any area of the brain that takes over a function should a region become damaged.
The Prof. said that by understanding what underpins the brain plasticity seen in youngsters, scientists might be able to come up with ways to make the adult brain more plastic, potentially offering hope to adults who have had a stroke.

While less of a priority, the same kind of mechanisms that might help reorganise language areas in those who have had a stroke could work in healthy people to help them learn a second language, Newport admitted.

A Professor of molecular and cell biology, who was also speaking at the meeting, said that his research in mice showed that by blocking certain molecules in the adult brain that hinder plasticity, it was possible to increase its ability to rewire.

“The baseline of the brain is plastic, to rewire itself. Through evolution it is necessary to layer on brake-like factors to prevent too much rewiring from happening after a certain point,” he said. “This offers novel therapeutic possibilities. If we could judiciously lift the brakes later in life perhaps we could reopen this window.”
The Prof. is already working on possible therapeutics. He said that among the possibilities, drugs routinely used for mood disorders might show potential to increase plasticity in adults. His previous research has shown that adults given the drug valproate, used to treat bipolar disorder, regain the ability to learn perfect pitch – a skill that is usually only seen in children who began studying music before the age of six.

But he said there was cause for caution when it came to tinkering with the ability for the brain to change. “We have to consider though that the brain is well formed by then [adulthood] and has passed through its own critical period. The starting point is quite different,” he said. “We worry a lot about translating these results to humans. What would it mean to reopen the critical period a second time? Would we be wiping out your identity, who you’d become through all those years of development?”

But  a professor of clinical neurology and neurorehabilitation, said that it was not the case that adults recovering from a stroke could not use other parts of their brain to take over tasks. “Relatively well-recovered adult stroke patients tend to have different activity patterns compared with healthy people. Other parts of the language network might be used to support language recovery,” he said.

Ward also noted that it is thought, from animal models, that the stroke itself can increase brain plasticity in adults for a few months, meaning that timely rehabilitation and training are key.
“Drugs that keep the window open longer or reopen it would be good too,” said Ward. “It’s just that at the moment, services are being slashed and so the ‘dose’ of rehab is so low, no drug is going to help – doubling the effect of not very much rehab still gives you not very much rehab.” 
 
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Saturday, April 08, 2017

Researchers discover rescue protein that delays cell death

A team of researchers has discovered a rescue protein that delays the cell death and can offer a treatment for cancer, neurodegeneration and infection.

The study was published in journal Cell.The team has discovered how a set of proteins delays the "executioner" machinery that kills damaged or infected cells in a process called necroptosis.

The scientists believe these finding may have wide clinical implications if researchers can develop drugs to control the cellular rescue machinery.

Rescue treatments that prevent necroptosis in transplanted organs could reduce injury to the transplant caused by lack of oxygen, researchers said.

Drugs to rescue cells from necroptosis could also help prevent injuries to tissue deprived of blood by heart attack and stroke. In such cases, restoring blood flow and oxygenation triggers inflammation that kills tissue.

The scientists said cell-rescuing drugs could also thwart cancer spread by protecting blood vessel cells from being killed by tumor cells.

Tumor cells escape the bloodstream to spread in the body by killing blood vessels. Blocking the rescue machinery might also prove useful in treating cancers, by enhancing death of cancer cells by necroptosis.

In treating neurodegenerative disorders such as ALS--also known as Lou Gehrig`s Disease--activating the rescue machinery could help prevent death of brain cells.

In treating viral infections such as influenza, rescue treatment could extend the life of cells infected by the virus, so that the body`s immune system would be more strongly alerted to fight the infection.

Scientists knew that the "executioner" in necroptosis was a protein called MLKL.When MLKL is activated by the necroptosis machinery, it triggers a piercing of the plasma membrane surrounding the cell, ultimately killing it.

However, the scientists discovered how cells could survive necroptosis.Researchers showed the plasma membrane could repair itself by forming "bubbles" of broken plasma membrane that would shed from the cell to repair the holes.

Experiments showed the set of proteins called ESCRT-III was responsible for forming the repair bubbles. The research also revealed that ESCRT-III delayed or prevented necroptosis by repairing breaks in the plasma membrane.

The delay gave the dying cells time to release signals to alert surrounding cells to the presence of a viral infection.The investigators also discovered that activating MLKL is not a point of no return for cell survival, and that ESCRT-III could resuscitate damaged cells.In experiments relevant to transplantation, the researchers measured levels of activated MLKL protein in tissue samples from kidneys used in transplants.

Such cells experience stress during the transplantations, and researchers suspected the cells would show signs of necroptosis.The scientists found that although MLKL was activated in the kidney cells after transplantation, the cells did not die, and this protection correlated with an increase in the levels of the ESCRT-III machinery necessary for rescue of cells with active MLKL.

Douglas Green, Ph.D., chair of the St. Jude Department of Immunology emphasized that the current findings are only "suggestive" at this point, because the experiments were done in cell cultures and tissue samples. Further studies are needed to establish that the rescue machinery functions in whole organs.

The research by Green and his colleagues will also aim at discovering the biological signals regulating ESCRT-III, to enable more precise control of the rescue machinery."Those studies could yield drugs to regulate the rescue process," Green said.

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Saturday, January 07, 2017

Fasting / Ekadasi ‘upavasam’ and Nobel Prize! what is the connection? read---

This year’s Nobel prize for medicine has gone to a Japanese scientist Dr. Yoshinori Ohsumi for his research on autophagy.

Autophagy means to “self eat”. In other words, the process by which the human body eats it own damaged cells and unused proteins. Autophagy is a natural process and also one which occurs in cases of starvation. The failure of autophagy is one of the main reasons for accumulation of damaged cells which eventually leads to various diseases in the body. Autophagy is important to prevent/fight cancer and also plays a vital role in degrading and ‘consuming’ cells infected by bacteria and viruses.


We have to observe here that ancient India had recommended a practice of fasting (‘EkAdasi upavAsam’) one day in a fortnight. Many of us religiously follow this practice to this day as a penance for spiritual progress without any idea of the biological and therapeutic benefits of this practice. Through this process of fasting induced autophagy, our body repairs its damaged and degenerated cells or use up the proteins of the damaged cells for its survival.
Whenever modern science conquers a frontier in any field, it somehow relates back to a quaint spiritual practice followed in India for generations.


A day in a fortnight spent in prayer and divine contemplation was a tonic for the mind and soul while the practice of fasting ensured that the body would heal and rejuvenate itself.


Clearly, our ancients believed in a process of holistic healing of both the body and the mind. They were able to connect, quite remarkably, the yearning for spiritual progress in a human being with the biological necessity of the human body. We cannot but marvel and bow our heads with admiration and reverence at their wisdom and deep scientific understanding of the body and the mind.


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