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Protective exposure of radiation on brain reduces risk of memory loss

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Protecting specific area of the brain during a radiation therapy substantially reduces memory loss in the cancer patients, a new study shows.

According to the study, protecting the stem cells that reside in and around the hippocampus substantially reduces the rate of memory loss in the cancer patients during whole-brain radiotherapy without a significant risk of recurrence in that area of the brain.

Hippocampus are C-shaped area in the temporal lobe on both sides of the brain that are associated with the ability to form and store memories.

“Memory loss, especially short-term recall, is an important consideration for patients receiving whole-brain radiotherapy,” says the study’s co-principal investigator, Minesh P. Mehta, M.B., Ch.B., professor of radiation oncology at the University of Maryland School of Medicine. “We found that reducing the radiation dose to the stem-cell niches surrounding the hippocampus during treatment was clearly associated with memory preservation without an inordinate risk of relapse in that portion of the brain. The findings far exceeded our expectations.”

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Study

A total of 113 patients were recruited between 2011 and 2013; investigators were able to evaluate 42 patients at four months and 29 patients at six months.

Patients in the study, the majority of them with lung cancer that had spread to the brain, were treated with intensity-modulated radiation therapy (IMRT), which enabled doctors to shape the radiation beams to avoid the hippocampus.

Researchers used a standardized cognitive function assessment — the Hopkins Verbal Learning Test (HVLT) — to measure patients’ baseline memory, such as their ability to recall information immediately or after a delay, with follow-up at two, four and six months.

Dr. Mehta says that the radiation affects cognitive function by damaging nerve cells as well as stem cells, which help to regenerate nerve cells that support memory formation. “These stem-cell niches are exquisitely sensitive to radiation and are involved in neurogenesis — the process of generating new neurons, or nerve cells. Although we call it hippocampal-avoidance radiotherapy, we really are targeting the stem-cell niches in and around the hippocampus,” Dr. Mehta says.

Always online? You may suffer from short-term memory

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The trend of social networking, chatting, tweating is growing among internet users especially teens. But scientists recommend you to take a break.

According to a new study, people who spend too much time browsing social media could be squandering their memories or losing important information.

The researchers from Stockholm’s KTH Royal Institute of Technology say, an idle brain is in fact doing important work – and in the age of constant information overload, it’s a good idea to go offline on a regular basis.

Erik Fransen, whose research focuses on short-term memory and ways to treat diseased neurons, finds too much social networking not good for your brain as it leads to overload. He said that a brain exposed to a typical session of social media browsing can easily become hobbled by information overload. The result is that less information gets filed away in your memory.

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“Working memory enables us to filter out information and find what we need in the communication. It enables us to work online and store what we find online, but it’s also a limited resource,” he said.

“When you are on Facebook, you are making it harder to keep the things that are ‘online’ in your brain that you need. So you are reducing your own working memory capacity,” Fransen said.

He further said, “The brain is made to go into a less active state, which we might think is wasteful; but probably memory consolidation, and transferring information into memory takes place in this state. Theories of how memory works explain why these two different states are needed. When we max out our active states with technology equipment, just because we can, we remove from the brain part of the processing, and it can’t work.”

 

Scientists find Alzheimer’s cure in diabetes way

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Scientists have discovered a link between diabetes drugs and Alzheimer’s cure.

A new study suggests, a commonly prescribed diabetes drug can reverse memory loss and the build-up of plaques in the brain linked to Alzheimer’s disease.

The study, led by Professor Christian Holscher at Lancaster University, found that the drug liraglutide commonly used by diabetics, may be able to reverse some of the damages caused by Alzheimer’s. They are even effective in the later stages of the condition. If successful in clinical trials this will be the first new dementia treatment in a decade.

Alzheimer’s disease is the most common form of dementia. The condition is characterised by the slow death of brain cells. It is progressive, ultimately terminal and there is yet no cure.

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Study

The researchers carried study on mice with late-stage Alzheimer’s. They were given the diabetic drug. The scientists found that they performed significantly better on an object recognition test and their brains showed a 30 percent reduction in the build-up of toxic plaques.

Most of the drugs available for dementia are generally effective in early stages. But these drugs were found effective even in later stage of the disease.

Liraglutide is a member of a class of drugs known as a GLP-1 analogue. The drug is used to stimulate insulin production in diabetes, but research shows it can also pass through the blood brain barrier and have a protective effect on brain cells.

“This exciting study suggests that one of these drugs can reverse the biological causes of Alzheimer’s even in the late stages and demonstrates we’re on the right track,” said Dr Doug Brown, Director of Research and Development at Alzheimer’s Society.

The study was published in the journal Neuropharmacology.

Scientists find proteins ‘Wnts’ responsible for long-term memory

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Scientists have found a group of proteins that they claim are essential for the formation of long-term memories in humans.

The Researchers at The Scripps Research Institute (TSRI) in Florida studied a family of proteins called Wnts that are responsible for memories in humans.

These proteins send signals from the outside to inner part of a cell, inducing a cellular response crucial for many aspects of embryonic development, including stem cell differentiation and normal functioning of the adult brain.

“By removing the function of three proteins in the Wnt signalling pathway, we produced a deficit in long-term but not short-term memory,” said Ron Davis, chair of the TSRI Department of Neuroscience.

“The pathway is clearly part of the conversion of short-term memory to the long-term stable form, which occurs through changes in gene expression,” Davis said.

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Study

The scientists carried study on Drosophila, the common fruit fly – a widely used doppelganger for human memory studies, to probe the role of Wnt.

Scientists inactivated the expression of several Wnt signalling proteins in the mushroom bodies of adult flies – part of the fly brain that plays a role in learning and memory.

According to the researchers, the resulting memory disruption suggests that Wnt signalling participates actively in the formation of long-term memory, rather than having some general, non-specific effect on behaviour.

“What is interesting is that the molecular mechanisms of adult memory use the same processes that guide the early development of the organism, except that they are repurposed for memory formation,” Davis said.

“One difference, however, is that during early development the signals are intrinsic, while in adults they require an outside stimulus to create a memory,” he said.

The study was published in the journal Cell Reports.

Omega-3 fish oil may cut alcohol-related dementia risk

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Scientists have uncovered another health benefit of omega-3 fish oil. According to a new study, this enriched oil may help protect against alcohol-related dementia.

The long-term use of alcohol increases the risk of dementia, scientists say.

Small amounts of alcohol are likely to make brain cells more fit. Alcohol in moderate amounts stresses cells and thus toughens them up to cope with major stresses down the road that could cause dementia. However, too much alcohol overwhelms the cells, leading to inflammation and cell death.

Study

Researchers at Loyola University Chicago Stritch School of Medicine carried study on brain cells of rats exposed to high levels of alcohol.

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An earlier analysis by Michael A Collins and colleague Edward J Neafsey, which pooled the results of 143 studies, found that moderate social drinking may reduce the risk of dementia and cognitive impairment. Notably, moderate drinking is defined as a maximum of two drinks per day for men and 1 drink per day for women.

Collins and colleagues exposed cultures of adult rat brain cells to amounts of alcohol equivalent to more than four times the legal limit for driving in the US. These cell cultures were compared with cultures of brain cells exposed to the same high levels of alcohol, plus a compound found in fish oil called omega-3 docosahexaenoic acid (DHA).

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Findings

There was about 90 percent less neuroinflammation and neuronal death in the brain cells exposed to DHA and alcohol than in the cells exposed to alcohol alone.

“Fish oil has the potential of helping preserve brain integrity in abusers. At the very least, it wouldn’t hurt them,” Collins said.

Down syndrome to decode Alzheimer’s disease, say scientists

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Alzheimer’s are evident as the most common disease among the elderly people. In a significant study, scientists have discovered a link between Down syndrome and Alzheimer’s, saying that understanding the former may help in decoding the latter.

This has been known for decades that people with Down syndrome were at increased risk of developing Alzheimer’s disease, but some researchers now believe that understanding the connection between the two conditions might help us unravel the Alzheimer’s puzzle and point towards therapies that might slow, or even halt, the dreaded disease.

“It’s a tantalizing and provocative question: Do people with Down syndrome hold the key to the mystery of Alzheimer’s development?” Dr. Brian Skotko, co-director of the Down Syndrome Program at the Massachusetts General Hospital in Boston, said while adding, “And what can we learn from those with Down syndrome that will benefit the rest of the population?”

Alzheimer’s disease affects more than 26 million people worldwide. It is predicted to skyrocket as boomers age — nearly 106 million people are projected to have the disease by 2050.

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Researchers say, not only do more people with Down syndrome develop Alzheimer’s, but they also develop it at a much younger age. By age 40, a full 40 percent of people with Down syndrome will develop the disease, and by age 50 that rises to 50 percent.

While not everyone with Down syndrome develops dementia, all develop changes in their brains that are found in Alzheimer’s patients, scientists stressed.

“We’ve learned that prevention and treatment in the earliest stages is probably our best way to battle this disease,” Lemere said.

“And we know that everybody with Down syndrome will eventually develop Alzheimer’s disease – or at least the changes in the brain. So we know that this is now another population where we can perhaps go in and test therapies very early in the disease as a prevention,” she added.

Video games can act as therapeutic tool for memory loss patients: Study

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With age the activity of brain declines. Memory loss or short term memory are the common problems witnessed in this age. But here is a good news for octogenarians. A new study has found that video games help elderly people keep their brain sharp.

Video games like car racing, shooting etc provide a good opportunity for brain to engage in exercise. Like kids, elderly people also gets chance to grasp new m moments and keep a track of events in their minds.

Scientists have discovered that swerving around cars while simultaneously picking out road signs in a video game can improve the short-term memory and long-term focus of older adults.

A team at the University of California San Francisco, led by Adam Gazzaley, associate professor of neurology, physiology and psychiatry, has tried to tackle the memory loss problem using a video game.

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They tested a group of older adults with a 3D driving game that involved hitting a button when the participant saw a specific sign. It turned out that playing the game really did improve a person’s multitasking skills.

The researchers looked at the performance of a group of 16 people aged 60 to 85. They found that just 12 hours of training spread over a month dramatically improved the ability of the individuals in the group to pick out the right signs. Some people even did as well or better than 20-year-olds playing for the first time.

To make sure it was the game that was doing it, the team tested two other similarly sized groups of elderly people. One played a game where only driving or picking the sign was involved, while another didn’t play at all. Neither of the other two groups improved.

Gazzaley said, “This technique may act as a therapeutic tool in curing patients of memory loss.”

The findings were published in the latest issue of the journal Nature.

Protein that leads you to Alzheimer’s discovered

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US scientists have found a stress-related protein that is responsible for accelerating Alzheimer’s disease.

These proteins are genetically linked to depression, anxiety and other psychiatric disorders leading to Alzheimer‘s disease, the study has found.

Researchers at the University of South Florida found when the stress-related protein FKBP51 partners with another protein known as Hsp90 it prevents the clearance from the brain of the toxic tau protein associated with Alzheimer‘s disease.

Hsp90 is a chaperone protein, which supervises the activity of tau inside nerve cells. Chaperone proteins typically help ensure that tau proteins are properly folded to maintain the healthy structure of nerve cells.

The stress-related protein partners with Hsp90 to make tau more deadly to the brain cells involved in memory formation, scientists said.

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However, as FKBP51 levels increases with age, they usurp Hsp90’s beneficial effect to promote tau toxicity.

“We found that FKB51 commandeers Hsp90 to create an environment that prevents the removal of tau and makes it more toxic,” said the study’s principal investigator Chad Dickey, associate professor of molecular medicine at the USF Health Byrd Alzheimer‘s Institute.

Under normal circumstances, tau helps make up the skeleton of our brain cells.

The study was done using test tube experiments, mice genetically engineered to produce abnormal tau protein like that accumulated in the brains of people with Alzheimer‘s disease, and post-mortem human Alzheimer‘s brain tissue.

The study was published in the Journal of Clinical Investigation.

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