Brain pacemaker delivers constant Deep-Brain Stimulation (DBS) for Alzheimer’s patients

Credit Image: Functional Neuromodulation

Once implanted into the brain, a pacemaker-like device delivering electrical stimulation could help improve the memory of Alzheimer’s patients. Technology Review reports.

Using electrodes, Deep-Brain Stimulation (DBS) is already used to treat patients with Parkinson’s, epilepsy, and obsessive-compulsive disorder.

In this Alzheimer’s trial, co-chaired by Constantine Lyketsos of Johns Hopkins, the device was placed into a region of the brain involved in learning and memory.

In Alzheimer’s patients, brain tissue atrophies and the reduction of memory and thinking skills increase over time.

According to the Johns Hopkins team, electrical shocks could stimulate critical neural networks disrupted by Alzheimer’s.

Recent trials for potential Alzheimer’s drugs have failed to halt or stave off cognitive decline.

Now, in a pilot study with these deep brain stimulators, after one year of constant stimulation, brain scans of six Alzheimer’s patients showed signs of increased neuron activity in areas involving learning and memory, although, it could be unlikely to actually reverse the effects or damage to the brain caused by Alzheimer’s disease.

The researchers are recruiting patients into the new trial initiated by Toronto-based Functional Neuromodulation. The trial will track patients who have the device for a year using doctor observations and brain scans.

[Via Technology Review]

PTSD and the erasure of disturbing Memories - YouTube

We’re all carrying around some cringe-inducing memories that we’d rather forget but for those suffering Post-Traumatic Stress Disorder (PTSD), recalling certain memories can provoke fearful, emotional experiences.

By the same token, some memories can remind those battling drug addiction of the rewarding effects of the drug and trigger a relapse.

Researchers at Canada’s Western University have found a way to effectively block these types of memories that could lead to better treatments for both conditions.

Using a rat model, neuroscientists at Western University’s Schulich School of Medicine & Dentistry found that they could completely prevent the recall of both aversive and reward-related memories by stimulating a sub-type of dopamine receptor called the “D1” receptor in the prefrontal cortex.

Importantly, unlike the process used in Eternal Sunshine of the Spotless Mind that permanently erased certain memories, the Western University team’s approach only controls the spontaneous recall of the aversive and reward-related memories, leaving the actual memory intact.

“The precise mechanisms in the brain that control how these memories are recalled are poorly understood, and there are presently no effective treatments for patients suffering from obtrusive memories associated with either PTSD or addiction,” says Nicole Lauzon, a PhD candidate in the laboratory of Steven Laviolette.

“If we are able to block the recall of those memories, then potentially we have a target for drugs to treat these disorders.”

Lauzon and Laviolette describe their findings, which appear in the journal Neuropharmacology, in the video below.

Source: Western University

Short-term memory is based on synchronized brain oscillations

In each of the two brain regions (IPF and V4) brain activity shows strong oscillations in a certain set of frequencies called the theta-band.

Credit: Stefanie Liebe, MPI for Biological Cybernetics

Holding information within one's memory for a short while is a seemingly simple and everyday task.

We use our short-term memory when remembering a new telephone number if there is nothing to write at hand, or to find the beautiful dress inside the store that we were just admiring in the shopping window.

Yet, despite the apparent simplicity of these actions, short-term memory is a complex cognitive act that entails the participation of multiple brain regions.

However, whether and how different brain regions cooperate during memory has remained elusive.

A group of researchers from the Max Planck Institute for Biological Cybernetics in Tübingen, Germany have now come closer to answering this question.

They discovered that oscillations between different brain regions are crucial in visually remembering things over a short period of time.

It has long been known that brain regions in the frontal part of the brain are involved in short-term memory, while processing of visual information occurs primarily at the back of the brain.

However, to successfully remember visual information over a short period of time, these distant regions need to coordinate and integrate information.

To better understand how this occurs, scientists from the Max Planck Institute of Biological Cybernetics in the department of Nikos Logothetis recorded electrical activity both in a visual area and in the frontal part of the brain in monkeys.

The scientists showed the animals identical or different images within short intervals while recording their brain activity. The animals then had to indicate whether the second image was the same as the first one.

The scientists observed that, in each of the two brain regions, brain activity showed strong oscillations in a certain set of frequencies called the theta-band.

Importantly, these oscillations did not occur independently of each other, but synchronized their activity temporarily: "It is as if you have two revolving doors in each of the two areas.

During working memory, they get in sync, thereby allowing information to pass through them much more efficiently than if they were out of sync," explains Stefanie Liebe, the first author of the study, conducted in the team of Gregor Rainer in cooperation with Gregor Hörzer from the Technical University Graz.

The more synchronized the activity was, the better could the animals remember the initial image. Thus, the authors were able to establish a direct relationship between what they observed in the brain and the performance of the animal. 

MIT Neuro-Scientists Prevent the Formation of Long-Term Memory

Neuroscientists at the Massachusetts Institute of technology (MIT) have found a way to "prevent the formation of long- term memory".They achieved this by deactivating Npas4, a memory gene.

When a person experiences a new event, his or her brain encodes it as a memory by altering the connections between the neurons, and the neurons turn on many genes.

The scientists found a way to control this process by deactivating the Npas4.

The MIT scientists conducted experiments on mice to achieve this. They sent the mice to a chamber. When the mice entered the chamber for the first time, they received a slight electric shock.

This frightened the mice, and the fear activated the Npas4. However, the scientists could prevent the formation of the long-term memory of this bad experience by deactivating the Npas4.

Yingxi Lin, a member of the Mc Govern Institute for Brain Research, who led the study, said that they had deactivated the gene by "deleting the gene from the genome".

"Our research showed that deletion of Npas4 prevents the formation of long-term memory. We don't have any data showing its role in memory erasure. Just want to clarify that," she said.

Her clarification came in the wake of some reports in the media which suggested that the MIT scientists had found a way to "erase memory".

When asked about how the method could be used in humans and its possible application in treating mental diseases, Lin said: "This is basic research. In the long run, it will help us understand the mechanisms of learning and memory in humans, which can potentially help treating mental disorders."

Brain function - A new way to measure the burden of aging

Cognitive function may be a better indicator of the impact of aging on an economy than age-distribution, with chronological age imposing less of a social and economic burden if the population is "functionally" younger, according to a study published today in the Proceedings of the National Academy of Sciences.

The study finds that one standardized indicator of cognitive ability - memory recall - is better in countries where education, nutrition, and health standards are generally higher.

Aging populations are of concern to many countries as it is often assumed that aging necessarily implies a greater cost to society in terms of aged care, age related disease, and reduced capacity to contribute to society.

However this research suggests that the effects of chronological aging are uneven across nations and that in some countries, particularly more affluent ones that are able to invest in early and sustained education and health programs, cognitive function and thus the ability to live healthy, productive lives, is maintained longer.

"Demographic indicators of the economic impact of an aging population typically rely on measures based on populations' age-distribution, expressed as the Old Age Dependency Ratio (OADR).

Whilst this is helpful measurement it does not include information on individual characteristics, other than age," says lead author Vegard Skirbekk from the International Institute for Applied Systems Analysis (IIASA).

"We believe cognitive function can provide a new and comparable measure of how a region or a nation's population may age. Such information can inform early intervention in the education and health systems to try and improve cognitive performance, ultimately reducing the burden of aging."

"For example, in northern Europe or the United States where there is a relatively large population over the age of 65, we found that cognitive function is higher for this age group than for the same age group in Mexico, India and China. Overall, even though Europe and the US may be chronologically older they are 'functionally' younger."

Cognitive ability levels are also good indicators of individual productivity and this has direct relevance to the economic and business activities within a country.

The authors suggest that the difference in cognitive function may be explained by the fact that seniors in some regions of the world experience better conditions during their childhood and adult life; including nutrition, duration and quality of schooling, exposure to disease, and physical and social activity.

ESA Mars Express: Fault causes observations to be temporarily suspended

Anomalies in the operation of the solid-state mass memory system on board Mars Express have caused science observations to be temporarily halted. A technical work-around is being investigated that will enable the resumption of a number of observations and should evolve into a long-term solution.

In mid-August, Mars Express autonomously entered safe mode, an operational mode designed to safeguard both the spacecraft itself and its instrument payload in the event of faults or errors.

The cause of entering the safe mode was a complex combination of events relating to reading from and writing to memory modules in the Solid-State Mass Memory (SSMM) system.

This is used to store data acquired by the instruments and housekeeping data from the spacecraft's subsystems, prior to its transmission to Earth, and is also used to store commands for the spacecraft that have been received from the ground stations, while awaiting execution.


Switch to spare memory controller
As the previous safe mode was three years ago and the current event looked like a 'normal' transition to safe mode, the flight control team executed the standard recovery procedure and restarted observations.

A few days later, another fairly similar set of SSMM problems occurred. The decision was then taken to switch over to the cold-redundant spare, or 'B-side', SSMM controller, as this was virtually the only subsystem common to the two events.

The decision to act was triggered by both the need to achieve stable science performance and the need to reduce the consumption of fuel caused by transitions to safe mode.

Molly Birnbaum - When all you can smell is your brain

In the summer of 2005 Molly Birnbaum was out jogging near her home in Brookline Massachusetts when she was hit by a car.

The impact fractured her skull and severed her olfactory nerves, leaving her without a sense of smell.

The prognosis was bad - Birnbaum was told she would never smell again. Depressed and deprived of her sense of smell, and therefore taste, she was forced to give up her place at culinary college and with it, her ambitions of becoming a chef.

Instead of resigning herself to living without scent, Birnbaum ended up on a quest to find out more about this mysterious sense, and eventually got her sense of smell back.

She tells this story in her book Season to Taste.

I started to get a few scents back one at a time, slowly but very attached to memory and emotion. As that went on I began to be very curious as to what was going on in my nose, in my brain, how come I didn't know anything about the sense of smell even though it so affected my life.

So I began to talk to scientists and doctors about the science of smell. I spoke with chefs and perfumers and I spent time in a flavour lab in New Jersey, I went to a perfume school in France, and spent time with neurologist Oliver Sacks and really tried to explore what it means to smell.

A little while after the accident I was helping my mother to cook dinner. I was chopping a bunch of fresh rosemary, and all of a sudden this smell hit me out of nowhere. It had been so long since I had smelt anything I was shocked. It was just this glorious scent of herbs and earthy rosemary and it reminded me of my childhood. It gave me a lot of hope.

At one point i became convinced i could smell my own brain. This was very disturbing. One common thing when people lose their sense of smell is to experience phantom smells - smells that don't actually exist from a concrete source in reality. I have met people who have had horrible ones - rotting smells, or garlic smells when they are trying to eat a fresh peach - but for me it was much more subtle.

Towards the beginning of my experience I could smell this one smell all the time. The only way I could make sense of it was that this smell was coming from within me, that it was probably my brain. It was one of the stories I told myself to make sense of this experience.

I think what I really lost was the emotional component to certain memories, the memories we have when we smell something familiar and are immediately transported back to a moment in our past - kind of like a punch in the gut emotion. When I couldn't smell I could still remember these events, I just didn't have that punch in the gut. And I worried about how, if I could never smell again, that would affect the memories that I should be making in the future.

How memory is lost — and re-found

A new study published July 27 in the journal Nature shows that the neural networks in the brains of the middle-aged and elderly have weaker connections and fire less robustly than in youthful ones.

Intriguingly, note the scientists, the research suggests that this condition is reversible.

“Age-related cognitive deficits can have a serious impact on our lives in the Information Age, as people often need higher cognitive functions to meet even basic needs, such as paying bills or accessing medical care,” says Amy Arnsten, professor of neurobiology and psychology and a member of the Kavli Institute for Neuroscience.

“These abilities are critical for maintaining demanding careers and being able to live independently as we grow older.”

Arnsten and her team studied the firing of prefrontal cortical neurons in young, middle-aged and old animals as they performed a working memory task. Neurons in the prefrontal cortex of the young animals were able to maintain firing at a high rate during working memory, while neurons in older animals showed slower firing rates.

However, when the researchers adjusted the neurochemical environment around the neurons to be more similar to that of a younger subject, the neuronal firing rates were restored to more youthful levels.

Arnsten says that the aging prefrontal cortex appears to accumulate excessive levels of a signaling molecule called cAMP, which can open ion channels and weaken prefrontal neuronal firing. Agents that either inhibited cAMP or blocked cAMP-sensitive ion channels were able to restore more youthful firing patterns in the aged neurons.

One of the compounds that enhanced neuronal firing was guanfacine, a medication that is already approved for treating hypertension in adults and prefrontal deficits in children, suggesting that it may be helpful in the elderly as well, note the researchers.

Arnsten’s finding is already moving to the clinical setting. Christopher vn Dyck of the Yale School of Medicine is enrolling subjects in a clinical trial testing guanfacine’s ability to improve working memory and executive functions in elderly subjects who do not have Alzheimer’s disease or other dementias.

Information about the clinical trial can be found online,

Shuttle Memories: Bernard Harris

Shuttle Memories: Bernard Harris

NASA Shuttle Atlantis: Last Flight's Secret Souvenir Cargo

Various U.S., military and country flags, as well as assorted space shuttle mission patches are among the mementos packed aboard Atlantis for the final space shuttle mission.

CREDIT: collectSPACE/NASA

The final astronaut crew to fly on a space shuttle has a secret in store for everyone watching when the astronauts pause during their mission to offer a tribute to NASA's 30-year shuttle program.

The four crewmembers have some special souvenirs packed on shuttle Atlantis, but what they are, they aren't saying.

"Our commander wants to keep a lot of that a surprise for the day that we do those things," said Atlantis' pilot Doug Hurley in a pre-flight interview. "Obviously, there may be some mementos involved before we leave the space station for the last time."

Researchers turn long-term memories on and off with the flip of a switch

Using electrical probes embedded into the brains of rats, scientists have managed to replicate the brain function associated with long-term behaviour and found a way to literally turn memories on and off with the flip of a switch.

The scientists hope their research will eventually lead to a neural prosthesis to help people suffering Alzheimer's disease, the effects of stroke or other brain injury to recover long-term memory capability.

For their experiments, the research team from the University of Southern California (USC) Viterbi School of Engineering's Department of Biomedical Engineering, working with scientists from Wake Forest University, had rats learn which of one of two levers to press to receive a reward.

Building on their previous work showing that the hippocampus is responsible for converting short-term memory into long-term memory, the researchers used embedded electrical probes to record the rat's brain activity between two major internal divisions of the hippocampus as they were learning.

These divisions, which are known as subregions CA3 and CA1, had previously been shown to interact to create long-term memory.

"No hippocampus," says USC's Theodore Berger, "no long-term memory, but still short-term memory."

The researchers then drugged the rats to block the normal neural interactions between CA3 and CA1. The rats that had previously been trained to choose the correct lever no longer displayed the long-term learned behaviour.

"The rats still showed that they knew 'when you press left first, then press right next time, and vice-versa,'" Berger said. "And they still knew in general to press levers for water, but they could only remember whether they had pressed left or right for 5-10 seconds."

The next step of the experiment involved creating an artificial hippocampial system that could duplicate the pattern of interaction between CA3-CA1 interactions. When the team activated the electronic device programmed to duplicate the memory-encoding function, long-term memory capability returned to the pharmacologically blocked rats.

Additionally, when the team applied the same technique to rats with a normal, functioning hippocampus, the device actually strengthened the memory being generated internally in the brain to enhance their memory capability.

The researchers are now looking to duplicate the results in monkeys, with the aim of creating prostheses that can return long-term memory function to human victims of Alzeimer's disease, stroke or other types of brain injury.

The research team's paper entitled "A Cortical Neural Prosthesis for Restoring and Enhancing Memory," appears in the Journal of Neural Engineering.

Turing Machine: Scrap metal and wood

A mechanical machine that can solve the same algorithms as a modern computer has now been built out of wood and scrap metal.

Created by software engineer Jim MacArthur it works by using levers and cams and only requires electricity to power a small motor (see video above).

The machine is a close physical model of the theoretical Turing machine - a device first described by Alan Turing in 1937 as a thought experiment to understand the limits of mechanical computation.

According to the theory, the machine performs calculations using a set of rules to manipulate symbols on an infinite strip of tape.

Instead of using tape, this machine's memory uses ball bearings placed on a steel grid. A ball can represent one of five different symbols based on its position on the grid.

The machine reads and writes data by repositioning the balls into different cells. It does this by moving along the grid, lifting ball bearings with magnets and then depositing them into a new position based on a set of rules.

A true Turing machine requires an infinite track or tape to run on but according to MacArthur, his machine is as close as you can get to a physical replica.

It has no practical computing applications and would take months to add a few numbers together but MacArthur says it was fun to build. "Since you can see this computer working, it could be useful for educational purposes," he says.

Mechanism Boasts Memory: Neuropeptide S

In collaboration with scientists at Germany's University of Munster, the UC Irvine team found that a small protein called neuropeptide S can strengthen and prolong memories of everything from negative events to simple objects.

According to study leader Rainer Reinscheid, UCI associate professor of pharmaceutical sciences, the discovery could provide important clues about how the brain stores memories and also lead to new treatments for Alzheimer's disease, dementia and other cognitive impairments.

"Additionally, it may help us better understand post-traumatic stress disorder, which involves exaggerated memories of traumatic events," he said.

In tests on mice, the researchers observed that if neuropeptide S receptors in the brain were activated immediately after a learning experience, it could be recalled for much longer and with much greater intensity.

This memory enhancement lasted up to a week, Reinscheid said, but when NPS receptor activation was disrupted, the mice didn't remember events as strongly -- if at all -- when tested just a day or two later.

Study results, which appear in the journal Neuro-psycho-pharmacology, are in accordance with Reinscheid's previous findings that NPS causes wakefulness and has a calming effect.

"It appears that the combination of increased alertness and reduced anxiety produced by NPS prepares the animals to learn much better," he said. "Memory is remarkably improved after activation of their NPS system, and the effects are long-lasting, independent of content."

Naoe Okamura, Celia Garau, Dee Duangdao and Stewart Clark of UCI as well as Kay Jungling and Hans-Christian Pape of the University of Munster contributed to the study, which was funded in part by the National Institute of Mental Health.

Gene switch rejuvenates failing mouse brains

Gene switch rejuvenates failing mouse brains

Step aside, Sudoku. A genetic switch that causes memory impairment in ageing mice when it goes into "off" mode has been flicked on, restoring failing brains to a more youthful state.

If a similar switch can be found in people, it might provide a new way to keep ageing human brains young.
Cognitive decline, particularly memory impairment, is a normal part of ageing in humans and animals. Yet why this happens, and how we can prevent it, is largely unknown, says David Sweatt at the University of Alabama, Birmingham, who was not involved in the new work.

André Fischer of the European Neuroscience Institute in Göttingen, Germany, and colleagues forced 3-month-old mice to find their way around a new environment and assessed them on their ability to associate an electric shock with a particular environment.

New neurons
The result was increased activity of a cluster of over 1500 genes which are known make proteins that are needed for the creation of new neurons – a process that is necessary for learning in humans and mice.

This boost in gene expression did not occur in 16-month-old mice given the same tasks: the activity of their genes changed only slightly. The mice also did worse than the young ones at spatial learning and memory tasks.

To uncover what prevents elderly mice getting this genetic boost, Fischer analysed the DNA found in neurons in the hippocampus of both old and young mice.

They found that when young mice are learning, a molecular fragment known as an acetyl group binds to a particular point on the histone protein that DNA wraps itself around – with the result that the cluster of learning and memory genes on the surrounding DNA ends up close to the acetyl group.

DNA 'on' switch
This acetyl "cap" was missing in the older mice that had been set the same tasks. From this, the team concludes that the cap acts as an "on" switch for the cluster of learning and memory genes: removing the cap switches off the genes.

Next, by injecting an enzyme known to encourage caps to bind to any kind of histone molecule, Fischer's team artificially flipped the switch to the on position in old mice. The acetyl group returned to the histone molecule and the mice's learning and memory performance became similar to that of 3-month-old mice.

Memory Magic: What's in Store?

Read more about the expansion of computer memory. It's always refreshing!...................

ESA: SMOS satellite instrument comes alive

Click here to see animation.........

The MIRAS instrument on ESA's SMOS satellite, launched earlier this month, has been switched on and is operating normally. MIRAS will map soil moisture and ocean salinity to improve our understanding of the role these two key variables play in regulating Earth’s water cycle.

"Following the switch-on, MIRAS is working beautifully well with all key subsystems, including all of the receivers, the optical fibres and the correlator unit, in perfect functioning condition," said ESA’s Manuel Martin-Neira, SMOS Instrument Principal Engineer. "We have been able to produce reasonable test data even without in-orbit calibration."

MIRAS (Microwave Imaging Radiometer using Aperture Synthesis) is an L-band radiometer with 69 receivers mounted on three deployed arms to measure the radiation coming from Earth.
In order to measure accurately, the receivers must be within a +/-3°C temperature range of each other, with the optimal operating temperature at 22°C. Heaters are installed on the satellite to achieve the temperature needed.

First MIRAS signal received
Switching on the instrument begins with activating the central payload computer, which controls many of the instrument’s subsystems and gives instructions to the distributed command and monitoring modes on each arm.

To assess the electrical performance of the instrument after switch-on while limiting the consumption of heater power, the physical temperature for start up was set to 10°C.

"The active thermal control is now in operation and is keeping the instrument well within the expected temperature range," Mr Martin-Neira said. "Tomorrow we expect to assess the payload at the final 22°C temperature."

The central payload computer also controls the 'mass memory', which collects all the science data from the receivers and sends them to receiving stations on the ground. The high-speed downlink, which transmits the data to the ground station, was switched on, and data have been transmitted to ESA’s European Space Astronomy Centre (ESAC), in Villafranca, Spain. The data acquisition and processing systems located at ESAC are also working well, and the first test of the product generation system has been successful.

"With the critical launch and early orbit phase completed, the engineers can now evaluate the quality of the downlinks and concentrate on the calibration of the instrument," SMOS Project Manager Achim Hahne said.

Alzheimer's disease: Memory Jogging Camera

Originally invented to help jog the memories of people with Alzheimer's disease, it might one day be used by consumers to create "lifelogs" that archive their entire lives.

Worn on a cord around the neck, the camera takes pictures automatically as often as once every 30 seconds. It also uses an accelerometer and light sensors to snap an image when a person enters a new environment, and an infrared sensor to take one when it detects the body heat of a person in front of the wearer. It can fit 30,000 images onto its 1-gigabyte memory.

The ViconRevue was originally developed as the SenseCam by Microsoft Research Cambridge, UK, for researchers studying Alzheimer's and other dementias. Studies showed that reviewing the events of the day using SenseCam photos could help some people improve long-term recall.