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Brains, memory, and behavior


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#91 Futurist1000

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Posted 09 December 2007 - 05:11 AM

More about the interesting disorder called confabulation. Frontal lobe dysfunction is normally associated with this disorder. Confabulation is actually something that all humans do to a certain extent.
Confabulation
Self Deception

Various forms of confabulation, including denial of illness (e.g., paralysis, blindness), and conditions that often give rise to these disorders, such as cerebral disconnection, disinhibitory states, incomplete information reception, and"gap filling" are discussed. On the basis of clinical observation and a review of a number of studies, it appears that confabulatory states frequently are associated with cerebral damage that involves the right hemisphere, notably, the frontal (often bilaterally) and parietal lobes—areas intimately involved in arousal, attention, information regulation, and integration. With certain forms of injury, initially there appear disturbances in the organization, integration, and assimilation of ideas and associations, such that large gaps appear in the information transmitted to and received by the language axis of the left hemisphere. It is argued that in these instances, the language areas act so as to fill these"gaps"with information that, although inappropriate, is linked in some manner to the fragments received. In contrast, frontal lobe damage sometimes results in gross disinhibition and cortical over responsiveness and, thus, speech release due to the flooding of the language axis (and other cortical regions) with tangential, fantastical, and grandiose associations. Other forms of confabulation also are reviewed briefly.


A less common yet more extreme form of"lying,"or deception, is confabulation. Unlike self-deception, in which the individual resists admitting his true store of knowledge, the confabulator often appears to be unable to recognize the erroneous nature or absurdity of his statements even in the face of painfully (seemingly) apparent contradictory evidence. Hence, his replies to questions or statements may appear tangential, circumlocutious, irrelevant, and delusional. Moreover, rather than relinquishing an incorrect belief when confronted with contradictory information, these individuals may make further erroneous extrapolations or partially incorporate some aspects of the contradictory information within the confabulatory schema.


Inevitably, in order for an individual to confabulate, erroneous information must become integrated in some fashion so that the confabulated response can be expressed. When the frontal lobes are compromised, there is much flooding of the association and assimilation areas with tangential and irrelevant stimuli and information, much of which is amplified erroneously completely out of proportion to more salient details, and a proportion of which appears due to the disinhibition of impulses and ideations that normally are filtered out (or at least denied linguistic expression). Consequently, salient and irrelevant, highly arousing and fanciful information is expressed indiscriminately.


Edited by hrc579, 09 December 2007 - 05:14 AM.


#92 Futurist1000

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Posted 30 January 2008 - 04:58 PM

Deep stimulation 'boosts memory'

Electrical stimulation of areas deep within the brain could improve memory, early research suggests.

A team of doctors in Canada stumbled upon the finding while attempting to treat a morbidly obese man through deep brain stimulation (DBS). The electrical stimulation caused the patient to experience vivid memories. The findings, reported in the Annals of Neurology, potentially pave the way for electrical stimulation to treat disorders such as Alzheimer's disease. Lead researcher Professor Andres Lozano, of the Toronto Western Hospital, said: "This is a single case that was totally unexpected. "We knew immediately this was important. We are sufficiently intrigued to see if this could help people with memory disorders." The team had been trying to help a 50-year-old obese man with type 2 diabetes and sleeping disorders who had failed to respond to diet, medications and psychological help. He had refused gastric surgery, and doctors decided deep brain stimulation, although experimental, was his best option.

It has been found to have an impact on appetite in animal tests, but has not been widely tested as a treatment for obesity in humans. However, it has been used to treat Parkinson's disease, chronic pain, severe cluster headaches and even depression with some success. The technique involves implanting electrodes into the brain: in this case into an area in the limbic system called the hypothalamus, which is thought to control the appetite. When the electrodes were stimulated by electrical impulses the patient began to experience feelings of deja vu. He then had a sudden perception of being in a park with friends. He felt younger, thought he was around 20-years-old, and his girlfriend of the time was there. He was an observer, and saw the scene in colour. As the intensity of the stimulation increased, details in the scene became more vivid.

Memory tests
Following surgery, the patient recovered for two months. But later when the electrodes were stimulated for a second time, he experienced a similar effect. After three weeks of constant electrical stimulation the patient performed better in memory tests than he had previously done. A year later he again performed well in memory tests when the electrodes were stimulated, but less well when they were switched off. The results suggest it might be possible to use deep brain stimulation directly to boost memory. "We hopefully have found a circuit in the brain which can be modulated by stimulation, and which might provide benefit to patients with memory disorders," said Professor Lozano.


Edited by hrc579, 30 January 2008 - 05:00 PM.


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#93 Lazarus Long

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Posted 02 February 2008 - 03:27 PM

In another of those accidental discoveries it appears that Canadian neurosurgeons applying deep brain electrostimulation for an entirely different purpose may have stumbled not only upon a method of retrieving memory and the means by which we store long term memories but have also it appears been able to duplicate the procedure to enhance learning ability.

Posted Image

Scientists discover way to reverse loss of memory
By Jeremy Laurance, Health Editor
Wednesday, 30 January 2008

Scientists performing experimental brain surgery on a man aged 50 have stumbled across a mechanism that could unlock how memory works.

The accidental breakthrough came during an experiment originally intended to suppress the obese man's appetite, using the increasingly successful technique of deep-brain stimulation. Electrodes were pushed into the man's brain and stimulated with an electric current. Instead of losing appetite, the patient instead had an intense experience of déjà vu. He recalled, in intricate detail, a scene from 30 years earlier. More tests showed his ability to learn was dramatically improved when the current was switched on and his brain stimulated. Scientists are now applying the technique in the first trial of the treatment in patients with Alzheimer's disease. If successful, it could offer hope to sufferers from the degenerative condition, which affects 450,000 people in Britain alone, by providing a "pacemaker" for the brain.

Three patients have been treated and initial results are promising, according to Andres Lozano, a professor of neurosurgery at the Toronto Western Hospital, Ontario, who is leading the research.

Professor Lozano said: "This is the first time that anyone has had electrodes implanted in the brain which have been shown to improve memory. We are driving the activity of the brain by increasing its sensitivity – turning up the volume of the memory circuits. Any event that involves the memory circuits is more likely to be stored and retained."

The discovery had caught him and his team "completely by surprise", Professor Lozano said. They had been operating on the man, who weighed 190kg (30st), to treat his obesity by locating the point in his brain that controls appetite. All other attempts to curb his eating had failed and brain surgery was the last resort.

The treatment for obesity was unsuccessful. But, while the researchers were identifying potential appetite suppressant points in the hypothalamus, the part of the brain associated with hunger, the man suddenly began to say that memory was flooding back. "He reported the experience of being in a park with friends from when he was around 20 years old and, as the intensity of stimulation increased, the details became more vivid. He recognised his girlfriend [from the time] ... The scene was in colour. People were wearing identifiable clothes and were talking, but he could not decipher what they were saying," the researchers write in Annals of Neurology, published today.

The man, who has not been identified, was also tested on his ability to learn lists of paired objects. After three weeks of continuous hypothalamic stimulation, his performance on two learning tests was significantly improved. He was also much more likely to remember a list of unrelated paired objects with the electrodes turned on than when turned off.

Speaking to The Independent yesterday, Professor Lozano said: "His performance improved dramatically. As we turned the current up, we first drove his memory circuits and improved his learning. As we increased the intensity of the current, we got spontaneous memories of discrete events. At a certain intensity, he would slash to the scene [in the park]. When the intensity was increased further, he got more detail but, when the current was turned off, it rapidly decayed."

The discovery surprised the scientists as the hypothalamus has not usually been identified as a seat of memory. The contacts that most readily produced the memories were located close to a structure called the fornix, an arched bundle of fibres that carries signals within the limbic system, which is involved in memory and emotions and is situated next to the hypothalamus.


Professor Lozano is a world authority on deep-brain stimulation who has undertaken 400 operations on Parkinson's disease sufferers and is developing the technique as a treatment for depression, for which he has performed 28 operations. He said the discovery of its role in stimulating memory had wide implications. "It gives us insight into which brain structures are involved in memory. It gives us a means of intervening in the way we have already done in Parkinson's and for mood disorders such as depression, and it may have therapeutic benefit in people with memory problems," he said.

The researchers are testing the approach in six Alzheimer's patients in a Phase 1 safety study. Three have so far had electrodes surgically implanted. The electrodes are attached via a cable that runs below the skull and down the neck to a battery pack stitched under the skin of the chest. The "pacemaker" delivers a constant low-level current that stimulates the brain but cannot be perceived by the patient. Professor Lozano said: "It is the same device as is used for Parkinson's disease. We have placed the electrodes in exactly the same area of the hypothalamus because we want to see if we can reproduce the findings in the earlier experiment. We believe the memory circuits we are stimulating are close by, physically touching the hypothalamus.

"It is a very effective treatment for the motor problems associated with Parkinson's disease and it has been used on 40,000 people. We are in the early stages of using it with Alzheimer's patients and we don't know if it will work. We want to assess if we can reach the memory circuits and drive improvement. It is a novel approach to dealing with this problem."

British researchers welcomed the discovery. Andrea Malizia, a senior lecturer in psychopharmacology at the University of Bristol who is studying deep-brain stimulation as a treatment for depression, said: "If they had said let's stick an electrode in the hypothalamus to modify Alzheimer's disease, I would have said 'Why start there?' But, if they have had a serendipitous finding, then that is as good. Serendipitous findings are how a lot of discoveries in science have been made."

Ayesha Khan, a scientific liaison officer at the Alzheimer's Disease Society, said: "This is very cutting-edge research. It is exciting, but the initial result is in one person. It will need much further investigation."


How deep-brain stimulation works

Deep -brain stimulation has been used for more than a decade to treat a range of conditions including depression, chronic pain, Parkinson's disease and other movement disorders. It has been so successful in treating Parkinson's that 40,000 patients worldwide now have electrodes implanted in their brains driven by pacemakers stitched into their chests. As the devices become smaller, requiring less risky surgery, and the target areas of the brain requiring stimulation are more precisely identified, demand for the treatment is expected to leap. Although it is expensive, the potential savings in care and treatment costs are immense. It does not lead to dependence on drugs and is reversible.

The electrodes are implanted under local anaesthesia while the patient is awake. Before the operation, the neurosurgeon performs an MRI scan and establishes the target location for the electrodes. He then carries out a craniotomy – lifting a section of the skull – and inserts the electrodes and leads. By stimulating the electrodes and checking the patient's response, the surgeon can check that they are positioned in the right place.

Different areas of the brain are targeted for different conditions. For Parkinson's disease, they are placed in the subthalamic nucleus; for depression, in area 25 of the cingulate cortex.

Deep-brain stimulation was developed in France and first licensed by the Food and Drug Administration in the US in 1997 as a treatment for tremor. In the UK, the surgery is performed at the National Hospital for Neurology and Neurosurgery in London, in Bristol, in Oxford and at a handful of other centres. The name of the procedure is in some ways a misnomer as it often involves inhibiting electrical activity in an area of the brain rather than stimulating it. The technique is as much about restoring balance between competing brain areas which leads to the tremor characteristic of some types of Parkinson's disease.



#94 Mind

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Posted 18 March 2008 - 10:05 PM

ScienceDaily (Mar. 18, 2008) — More than a third of people over age 70 have some form of memory loss according to a national study by a team of researchers at Duke University Medical Center, the University of Michigan, the University of Iowa, the University of Southern California and the RAND Corporation. The group performed the first population-based study to determine the number of people who have some form of cognitive impairment, with and without dementia.

While an estimated 3.4 million Americans have dementia, defined as a loss of the ability to function independently, the researchers estimate that another 5.4 million over age 70 have memory loss that disrupts their regular routine but is not severe enough to affect their ability to complete daily activities.

"These findings illustrate that nearly every family will be faced with the challenges of caring for a family member with some form of memory impairment," said Brenda Plassman, Ph.D., associate research professor of psychiatry at Duke and the study's lead author. "Even among the people age 71-79, a sizeable number had cognitive impairment. This is an age at which most people expect to have many productive years ahead."


read the full article here

#95 Unregistered

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Posted 19 March 2008 - 06:32 AM

These sort of things, studies and the like(age related deaths), reaffirm that ageing(speaking of Biological Aging) is something that should be given the highest priority to be conquered. It is disheartening the vast majory, as we all know, do not have knowledge about what is being done about this vile enemy, aging.

#96 Unregistered

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Posted 21 March 2008 - 06:03 AM

Edit: "majory" is misspelt. I ment "majority", "majority of people".

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#97 Rags847

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Posted 07 July 2008 - 11:22 PM

Recent press on this:
http://www.theheart....ticle/878971.do
http://www.webmd.com...-to-memory-loss
http://www.medscape....warticle/576972

Interesting editorial caution on causality:

Editorial cautious (from http://www.theheart....icle/878971.do)

In an accompanying editorial [2], Drs Anatol Kontush and John Chapman (INSERM and University Pierre and Marie Curie, Paris, France) note that the association between low plasma concentrations of HDL-C and dementia have been repeatedly reported. They also note that high HDL-C levels, possibly mediated by low cholesteryl-ester-transfer-protein (CETP) activity, have been linked to longevity, improved cognition, and dementia-free survival and that CETP polymorphisms resulting in low HDL-C are prevalent in people with Alzheimer's disease.

But the editorialists point out that none of these studies suggests causality, because plasma lipid levels can change considerably during the development of dementia, making the time point of the measurement critically important.

They report that there are many complex and variable biochemical mechanisms potentially linking HDL-C to Alzheimer's disease, adding that it is "tempting to speculate that increasing levels of HDL-C might protect our good memories." However, they note that "we should remain extremely cautious when proposing therapeutic intervention on the basis of observational studies that do not imply causation. This is particularly true for a study with a number of important limitations, such as that of Singh-Manoux et al.

"Thus, HDL-C remains a potentially promising but still remote target in the prevention of dementia and memory loss. Nonetheless, these studies demand that we focus more effort on research at the interface between HDL-C and brain function," they conclude.

Edited by Rags847, 07 July 2008 - 11:23 PM.


#98 Mind

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Posted 31 July 2008 - 07:56 PM

Brain's Sleep-Time Memory Storage Gets Muddled with Age

University of Arizona in Tucson researchers report in The Journal of Neuroscience that forgetfulness may, at least in part, stem from a breakdown in the brain's ability to store or consolidate memories, a process that involves "replaying" and filing away events while we snooze.

In a study of rats, the scientists found that when the animals were at rest there were repeating patterns of neuronal (nerve cell) activity believed to be involved in moving information from short-term to long-term memory vaults in the brain. The process, however, was disrupted in the older rats.

The new work is the first to show that an animal's ability to store memories may be linked to the crispness of its recollections. Among the older rats, replay occurred, but their brains scrambled the sequences in which the neurons fired (transmitted electrical impulses to communicate with neighboring cells).



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Posted 03 August 2008 - 11:49 PM

I have studied molecular biology for four years untill know I have learned almost nothing about genes that are brain specific. I would like some information about brain specific genes if you have some. Suppose you create a model in a computer of all protein and chemical interactions in the brain, have you then created a new artificial brain?? I guess so..


I would say it is not so much the genes but the epigenetics, yes?

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Posted 03 August 2008 - 11:54 PM

FASEB J. 2004 Jan 8
Prenatal choline supplementation advances hippocampal development and enhances MAPK and CREB activation.

Mellott TJ, Williams CL, Meck WH, Blusztajn JK.

Choline is an essential nutrient for animals and humans. Previous studies showed that supplementing the maternal diet with choline during the second half of gestation in rats permanently enhances memory performance of the adult offspring. Here we show that prenatal choline supplementation causes a 3-day advancement in the ability of juvenile rats to use relational cues in a water maze task, indicating that the treatment accelerates hippocampal maturation. Moreover, phosphorylation and therefore activation of hippocampal mitogen-activated protein kinase (MAPK) and cAMP-response element binding protein (CREB) in response to stimulation by glutamate, N-methyl-D-aspartate, or depolarizing concentrations of K(+) were increased by prenatal choline supplementation and reduced by prenatal choline deficiency. These data provide the first evidence that developmental plasticity of the hippocampal MAPK and CREB signaling pathways is controlled by the supply of a single essential nutrient, choline, during fetal development and point to these pathways as candidate mechanisms for the developmental and long-term cognitive enhancement induced by prenatal choline supplementation.

http://www.ncbi.nlm....p;dopt=Abstract


Resveratrol Mediated Activation of CREB Through Adenosine A3
Receptor by Akt -Dependent and –Independent Pathways
http://jpet.aspetjou...05.084285v1.pdf

The sirtuin activating compound resveratrol decreases GH transcription
http://www.endocrine.../ea0016p542.htm

#101 Rags847

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Posted 04 August 2008 - 02:34 AM

I've been frustrated way too many times by the same thing you found that suddenly.. you have to pay money to get an article that is free... or worse.. that the article has been removed, never to be found again.


Can always put it in your Google Documents, and open access to it to anyone, and then post a link to the specific Google Document page. It would be there forever. Can even put an entire 27 page study in there.
Google Rocks!

Edited by Rags847, 04 August 2008 - 02:35 AM.


#102 jacksen

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Posted 24 September 2008 - 10:46 PM

In early childhood can produce radical behavioral changes that last a lifetime. They also note that we're not surprised when treatments like early visual deprivation impact the visual system in the adult brain.To get at the question more directly, they point to a relatively simple model system: maternal grooming of pups in rodents. Maternal care is one of the more complex behaviors in rodents, and different strains of mice are available that provide their young with different levels of attention. Attention they give their young in the first week after birth, however, has a profound impact,various tests suggest that those given more attention by their mothers wind up better able to deal with stress and handle memory-based task
-------------------------
jacksen


SMO

#103 Lazarus Long

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Posted 16 December 2008 - 02:10 PM

In an interesting finding it appears that as we age our brains process and retain information through different mechanisms. We do not know why but now it appears it is another question we should ask in respect to aging theory and not stop till the answer is found.

http://www.eurekaler...c-oay121508.php

Public release date: 16-Dec-2008
Contact: Mary Jane Gore
mary.gore@duke.edu
919-660-1309

Duke University Medical Center

Old and young brains rely on different systems to remember emotional content

DURHAM, N.C.—Neuroscientists from Duke University Medical Center have discovered that older people use their brains differently than younger people when it comes to storing memories, particularly those associated with negative emotions.

The study, appearing online in the January issue of Psychological Science, is a novel look at how brain connections change with age.

Older adults, average age 70, and younger adults, average age 24, were shown a series of 30 photographs while their brains were imaged in a functional MRI (fMRI) machine. Some of the photos were neutral in nature and others had strong negative content such as attacking snakes, mutilated bodies and violent acts. While in the fMRI machine, the subjects looked at the photos and ranked them on a pleasantness scale. Then they completed an unexpected recall task following the fMRI scan to determine whether the brain activity that occurred while looking at the pictures could predict later memory. The results were sorted according to the numbers of negative and neutral pictures that were remembered or missed by each group.

The scientists found that older adults have less connectivity between an area of the brain that generates emotions and a region involved in memory and learning. But they also found that the older adults have stronger connections with the frontal cortex, the higher thinking area of the brain that controls these lower-order parts of the brain.

Young adults used more of the brain regions typically involved in emotion and recalling memories.

"The younger adults were able to recall more of the negative photos," said Roberto Cabeza, Ph.D., senior author and Duke professor in the Center for Cognitive Neuroscience. If the older adults are using more thinking than feeling, "that may be one reason why older adults showed a reduction in memory for pictures with a more negative emotional content."

"It wasn't surprising that older people showed a reduction in memory for negative pictures, but it was surprising that the older subjects were using a different system to help them to better encode those pictures they could remember," said lead author Peggy St. Jacques, a graduate student in the Cabeza laboratory.

The emotional centers of the older subjects were as active as those of younger subjects -- it was the brain connections that differed.

"If using the frontal regions to perform a memory task was always beneficial, then the young people would use that strategy, too," Cabeza said. "Each way of doing a task has some trade-offs. Older people have learned to be less affected by negative information in order to maintain their well being and emotional state – they may have sacrificed more accurate memory for a negative stimulus, so that they won't be so affected by it."

"Perhaps at different stages of life, there are different brain strategies," Cabeza speculated. "Younger adults might need to keep an accurate memory for both positive and negative information in the world. Older people dwell in a world with a lot of negatives, so perhaps they have learned to reduce the impact of negative information and remember in a different way." According to Cabeza, the results of the study are consistent with a theory about emotional processes in older adults proposed by Dr. Laura Carstensen at Stanford University, an expert in cognitive processing in old age.

"One thing we might do in the future is to ask subjects to try to actively regulate their emotions as they look at the pictures," St. Jacques said. "Would there be a shift in the neural networks for processing the negative pictures when we asked younger people to regulate their emotional responses? How would that affect their later recall of the negative pictures?"

###

The other author on the study was Florin Dolcos, who is now at the Department of Psychiatry, University of Alberta, in Edmonton, Canada. The study was funded by the National Institutes of Health, a postdoctoral fellowship from the Natural Sciences and Engineering Research Council of Canada, an award from the Canadian Psychiatric Research Foundation, and a Young Investigator Award from the U.S. National Alliance for Research on Schizophrenia and Depression.

--------------------------------------------------------------------------------



#104 suspire

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Posted 01 January 2009 - 08:09 AM

"Spikes in blood sugar can take a toll on memory by affecting the dentate gyrus, an area of the brain within the hippocampus that helps form memories, a new study reports.

Researchers said the effects can be seen even when levels of blood sugar, or glucose, are only moderately elevated, a finding that may help explain normal age-related cognitive decline, since glucose regulation worsens with age."
: http://www.nytimes.c...1memory.html?em

Maybe another nudge in favor of the paleo-diet folks.

#105 Declmem

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Posted 19 January 2009 - 07:52 PM

As someone who is having memory problems currently, I found this very interesting:

http://scienceblogs...._loss_in_br.php

These experiments suggest that many lost memories are in fact not lost at all, but misplaced. The dead neurons take important connections with them and the survivors, though incommunicado, still retain latent traces of memory. When they are jolted into action and form new networks, these trace memories are reinstated. And that provides genuine hope for people affected by dementia, Alzheimer's and other conditions.

It would be a touch silly to suggest putting such people in the equivalent of a large playpen. But Fischer also found a group of drugs called HDAC inhibitors that have the same effect - the molecular equivalent of a stimulating environment.

HDACs or histone deacetylases control whether genes are switched on or off by altering other proteins called histones. DNA winds around histones like spools, which serves to package this long and unwieldy molecule into a compact and more manageable form.

HDACs change the histones so that they wrap more tightly around DNA and render its genetic code unreadable. Any genes contained in these stretches of DNA are silenced. Drugs like sodium butyrate (SB) neutralise HDACs, freeing DNA from the repressive grip of histones.

Any silenced genes can now be freely switched on and among these, are genes that allow the brain's neurons to sprout new synapses. The details still need to be ironed out, but the results are clear - just like mice housed in fun cages, those treated with SB regained lost memories.


I have noticed my memory improves significantly when I'm learning something new - even memories that aren't particularly related to the task at hand. Unfortunately these days I don't have a lot of extra time. A drug like the one mentioned in the article does sound appealing :)

#106 Lazarus Long

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Posted 26 January 2009 - 04:46 PM

Now it appears that individual cells can hold what amounts to a RAM memory function. This lends more support to cryonicists that claim the memory of a cryo patient is preserved while in stasis assuming the procedure can be applied before severe cellular damage occurs. But I also suggest it implies that a chemical memory signature might be preservable in other ways than frozen cells.


Single cell 'can store memories'

http://news.bbc.co.u...lth/7846531.stm
BBC, Monday, 26 January 2009

Just one brain cell is capable of holding fleeting memories vital for our everyday life, according to US scientists. A study of mouse brain cells revealed how they could keep information stored for as long as a minute. A UK specialist said that understanding these short-term memories might help unlock the secrets of Alzheimer's Disease. The finding was reported in the journal Nature Neuroscience.

The difference between the brain's long-term and short-term memory has been likened to the RAM of a computer and the hard-drive. To perform normal functions, we need the ability to store, quickly and reliably, large amounts of data, but only a small amount of this needs to be retained in the longer term.

Scientists have spent decades working out which parts of the brain are responsible for these functions, and how cells manage this feat. Original theories suggested the memories were retained by multiple cells forming "circuits" around which electrical impulses were fired for the necessary period.

More recent ideas have centred around the concept that even an individual cell could somehow hold on to information. Researchers from the University of Texas Southwestern looked at brain cells taken from mice using tiny electrodes to measure their function. They found that a particular component of the cells in question, a chemical receptor, which, when switched on, tells the cell to start an internal signal system that holds the "memory" in place.


Drug boost

The next step, they say, is to find out more about this internal system so that it could be targeted by drugs with the aim of improving memory.

Dr Don Cooper, the lead researcher, said: "If we can identify and manipulate the molecular components of memory, we can develop drugs that boost the ability to maintain this memory trace to hopefully allow a person to complete tasks without being distracted."

He said that this could potentially help people addicted to drugs, by improving the ability of their brain to ignore impulses.

Professor Ian Forsythe, from the University of Leicester, said that the information shed on the brain's ability to retain short-term information was important in understanding the laying down of longer-term memories - and perhaps to understand how to help people for whom that was a problem.

He said: "Probably the most interesting thing will be to get to grips with the memory problems involved in Alzheimer's Disease. "If you've got no short term memory, you've got no chance of longer-term memories."

Alison Cranage, from the Alzheimer's Research Trust, said, "By understanding memory formation, scientists may be able to discover ways to enhance it. "Memory loss can be an early sign of dementia, and we desperately need to fund more research in order to find a cure for this devastating disease."



#107 Immotalas

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Posted 26 February 2009 - 11:07 PM

I recently learned that your brain prunes old memories, removing memory clusters that haven't had any use, or aren't important. I think this might be troublesome after about 500 years. It might be necessary for nanomachines to take up this process. This might make the brain, not only able to store more memories, but also swifter and more efficient.

#108 Mind

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Posted 01 March 2009 - 02:25 AM

Maybe they were working too long of hours.

The Finnish-led study was based on analysis of 2,214 middle-aged British civil servants.

It found that those working more than 55 hours a week had poorer mental skills than those who worked a standard working week.

The American Journal of Epidemiology study found hard workers had problems with short-term memory and word recall.

This should say to employers that insisting people work long hours is actually not good for your business.

Lead researcher Dr Marianna Virtanen, from the Finnish Institute of Occupational Health, said: "The disadvantages of overtime work should be taken seriously."

It is not known why working long hours might have an adverse effect on the brain.

However, the researchers say key factors could include increased sleeping problems, depression, an unhealthy lifestyle and a raised risk of cardiovascular disease, possibly linked to stress.

The civil servants who took part in the study took five different tests of their mental function, once between 1997 and 1999, and again between 2002 and 2004.

Those doing the most overtime recorded lower scores in two of the five tests, assessing reasoning and vocabulary.



#109 Mind

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Posted 04 July 2009 - 04:49 PM

http://www.sciencema...act/325/5936/87

Using the protein regulator of G protein signaling–14 (RGS-14) as a tool, we found that the expression of this protein into layer 6 neurons of rat-brain area V2 promoted the conversion of a normal short-term ORM that normally lasts for 45 minutes into long-term memory detectable even after many months.


Another write-up about the research.

Imagine if you could look at something once and remember it forever. You would never have to ask for directions again. Now a group of scientists has isolated a protein that mega-boosts your ability to remember what you see.

A group of Spanish researchers reported today in Science that they may have stumbled upon a substance that could become the ultimate memory-enhancer. The group was studying a poorly-understood region of the visual cortex. They found that if they boosted production of a protein called RGS-14 (pictured) in that area of the visual cortex in mice, it dramatically affected the animals' ability to remember objects they had seen.



#110 unsleepable

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Posted 07 July 2009 - 02:53 AM

http://www.sciencema...act/325/5936/87



Another write-up about the research.

I just read this article, very exciting potential!

#111 lucy robert

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Posted 21 July 2009 - 09:42 AM

Thanks for giving such a new information.
yeast infetions

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Researchers studying how memories are made have discovered a protein that is critical to the process. They have also found that the protein works in an unusual way that may help neurons store memories for days or even weeks.

The protein changes its shape in a way similar to the prion protein that has been linked to mad cow disease. But unlike the prion protein, which in its altered state causes brain disease in cows, sheep, and humans, the newly discovered protein does a good thing, by helping nerve cells connect to each other.

Eric Kandel and his coworkers at Columbia University in New York City use a sea slug species known as Aplysia to study memory. The ugly slug uses a relatively simple system of neurons to remember certain stimuli and react to them. For example, the slugs can remember being pinched in the gill, and they learn to react by withdrawing the gill.

By the same token, in the brain, the trick to storing memories is to strengthen a specific synapse, a small gap between connecting neurons.

Kandel already knew that once a neuron receives a signal through one of its many synapses, that the synapse is somehow "marked." But he didn't know whether the proteins and protein precursors needed to strengthen the connection know which synapses to go to--or whether they go to all synapses but are used only where needed.

In new studies reported in Cell, Kausik Si, a member of Kandel's lab, and his colleagues find that a protein called CPEB gets sent to all the synapses in a neuron. But at synapses that have been stimulated, the protein wakes up other molecules already there to produce new proteins that help strengthen the connection.

"New growth of synapses occurs in front of your eyes over the course of a day," says Kandel.

For a long-term memory—one that lasts days and not hours—those connections must be maintained. But how does CPEB maintain the synaptic connection?

The researchers noticed that the protein has an unusual structure, similar to a yeast version of the prion protein. They found that when the slug memory protein is produced in yeast, it undergoes a similar change in shape.

"Usually, when these kinds of proteins change shape, they aggregate, and that can cause disease," says Kandel. "But we found that it is the altered shape of the protein that is active. That was a surprise."

The CPEB protein is also found in the neurons of humans, mice and fruit flies. Kandel hopes the studies will help researchers eventually understand how humans store long-term memories.
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For a great review on molecular processes (for what we know so-far) behind memory formation...

STRUCTURAL PLASTICITY AND MEMORY

PM me for any questions :) )
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Edited by lucy robert, 21 July 2009 - 09:44 AM.


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#112 Lazarus Long

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Posted 29 July 2009 - 03:47 PM

Here is another new model for brain function, which is taking a more comprehensive approach addressing not merely the size of specific aspects but the the complexity and integration of neural components.

http://www.livescien...-potential.html

Brain's Potential Explained by Big New Idea

By Rachael Rettner, LiveScience Staff
posted: 28 July 2009 10:13 am ET

Different species and individuals have limits as to what they can learn. For instance, you can't teach your dog to read. But what sets these boundaries?

According to a new hypothesis, components of an organism's brain cortex may help determine how well that organism — be it dog, monkey or human — learns and improves its cognitive skills.
The cortex is your brain's outer layer — the exterior part you can see if you look at a picture of the whole organ.

The new idea posits that small sets of neuronal cells in the cortex, called cortical modules, determine our "cognitive plasticity," that is, our capacity to learn new ways of thinking, or improve upon old ones.

"What [constrains] an individual organisms' ability to learn cognitive skills is essentially the diversity and number of [cortical] modules they have," said Eduardo Mercado III, a psychologist at the University at Buffalo in New York. "So, if you think about it like a set of Legos, if you have more Legos, you can build a wider variety of things."


Quality, not size, matters

These cortical modules are very spatially distinct, like circles in a honeycomb-pattern layered over a brain, Mercado said.

Past studies have shown that, in general, the larger the cortex, the higher an organism's intellectual level will be. However, with Mercado's hypothesis, it is not necessarily the size, but rather, the variety and quantity of cortical modules that matter. A larger cortex simply provides space for lots of diverse modules.

His idea may explain why rats are thought to have a greater cognitive plasticity than cows, even though cows have a larger cortex. (excerpt)






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