Posts tagged memory
Articles and news from the latest research reports.
Scripps Research Institute Scientists Uncover a New Pathway that Regulates Information Processing in the Brain
Scientists at The Scripps Research Institute (TSRI) have identified a new pathway that appears to play a major role in information processing in the brain. Their research also offers insight into how imbalances in this pathway could contribute to cognitive abnormalities in humans.
The study, published in the November 9, 2012 issue of the journal Cell, focuses on the actions of a protein called HDAC4. The researchers found that HDAC4 is critically involved in regulating genes essential for communication between neurons.
“We found that HDAC4 represses these genes, and its function in a given neuron is controlled by activity of other neurons forming a circuit,” said TSRI Assistant Professor Anton Maximov, senior investigator for the study.
Feel-good hormone helps to jog the memory
The feel-good hormone dopamine improves long-term memory. This is the finding of a team lead by Emrah Düzel, neuroscientist at the German Center for Neurodegenerative Diseases (DZNE) and the University of Magdeburg. The researchers investigated test subjects ranging in age from 65 to 75 years, who were given a precursor of dopamine. Treated subjects performed better in a memory test than a comparison group, who had taken a placebo. The study provides new insights into the formation of long lasting memories and also has implications for understanding why memories fade more rapidly following the onset of Alzheimer’s disease. The results appear in the Journal of Neuroscience.
Making Memories: Drexel Researchers Explore the Anatomy of Recollection
What was your high school mascot? Where did you put your keys last night? Who was the first president of the United States?
Groups of neurons in your brain are currently sending electromagnetic rhythms through established pathways in order for you to recall the answers to each of these questions. Researchers in Drexel’s School of Biomedical Engineering, Science and Health Systems are now getting a rare look inside the brain to discover the exact pattern of activity that produces a memory.
Dr. Joshua Jacobs, a professor in Drexel’s School of Biomedical Engineering, Science and Health Systems, is analyzing data accumulated from 60 epilepsy patients who have had electrodes implanted on their brains in order to determine the causes of their epileptic episodes.
"When performing seizure mapping, surgeons implant electrodes in many brain areas, while searching for seizure activity,” Jacobs said. “Thus, there many electrodes end up being in normal brain tissue, and they measure neuronal activity that reflects normal brain function – this is the function that we’re studying to learn about the nature of working memory."
Self-Imagination Can Enhance Memory in Healthy and Memory-Impaired Individuals
There’s no question that our ability to remember informs our sense of self. Now research published in Clinical Psychological Science, a journal of the Association for Psychological Science, provides new evidence that the relationship may also work the other way around: Invoking our sense of self can influence what we are able to remember.
Research has shown that self-imagination – imagining something from a personal perspective – can be an effective strategy for helping us to recognize something we’ve seen before or retrieve specific information on cue. And these beneficial effects have been demonstrated for both healthy adults and for individuals who suffer memory impairments as a result of brain injury.
These findings suggest that self-imagination is a promising strategy for memory rehabilitation. But no study has investigated the effect of self-imagination on what is perhaps the most difficult, and most relevant, type of memory: free recall.
Young brain develops activity peaks while it is still growing
After a short period of growth, cultured networks of neurons regularly exhibit major activity in the absence of external stimulation. These “bursts” are entirely related to growth. At this stage, they have little to do with learning behaviour, as the network is still too young to sustain a process of memory formation. This has now for the first time been simulated for networks ranging in size from 10,000 to 50,000 neurons. The simulations provide insight into the role of the growth process in initial activity. Researchers at the University of Twente’s MIRA Institute recently published details of this work in PLOS ONE.
How your brain likes to be treated at revision time
If you’re a student, you rely on one brain function above all others: memory.
These days, we understand more about the structure of memory than we ever have before, so we can find the best techniques for training your brain to hang on to as much information as possible. The process depends on the brain’s neuroplasticity, its ability to reorganise itself throughout your life by breaking and forming new connections between its billions of cells.
How does it work? Information is transmitted by brain cells called neurons. When you learn something new, a group of neurons activate in a part of the brain called the hippocampus. It’s like a pattern of light bulbs turning on.
Your hippocampus is forced to store many new patterns every day. This increases hugely when you are revising. Provided with the right trigger, the hippocampus should be able to retrieve any pattern. But if it keeps getting new information, the overworked brain might go wrong. That’s what happens when you think you’ve committed a new fact to memory, only to find 15 minutes later that it’s disappeared again.
So what’s the best way to revise? Here are seven top tips to get information into your brain and keep it there.
Multivitamin lifts brain activity
A daily multivitamin supplement may improve brain efficiency in older women, according to new research from Swinburne University of Technology.
Centre for Human Psychopharmacology researcher at Swinburne, Dr Helen Macpherson’s four month study of the commercial product Swisse Women’s Ultivite 50+ found some evidence that multivitamin supplements may influence cognitive function by altering electrical activity in the brain.
"The main finding of the study was that 16 weeks supplementation with the Swisse Women’s 50+ multivitamin modulated brain activity," Dr Macpherson said.
"This is an important result as it shows there are direct effects of multivitamins on the brain.
"Previous research has used measures of behaviour to determine whether multivitamins can affect brain function, but this is the first trial to directly measure brain activity."
The study was conducted over 16 weeks with 56 women aged between 64 and 79 who were concerned about their memory or experiencing memory difficulties. They were randomly assigned to take the multivitamin supplement or a placebo daily.
Volunteers underwent a recording of their brain electrical activity whilst performing a spatial working memory task.
The research was published in Physiology and Behavior.
A previous paper published in Psychopharmacology reported that multivitamin supplementation improved behavioural performance on a similar task, in the same group of participants.
The study concluded that 16 weeks of supplementation with a combined multivitamin, mineral and herbal formula may benefit memory, by enabling the brain to work in a more efficient way.
"When considered with our other findings of benefits to memory performance, there is increasing evidence that multivitamins may be useful to combat cognitive decline in the elderly," Dr Macpherson said.
(Source: swinburne.edu.au)
Making a Game Out of Improving the ‘Sticky’ Brain
UCSF neuroscientists have found that by training on attention tests, people young and old can improve brain performance and multitasking skills.
Anyone who tries to perform two tasks at once is likely to do worse on both. Why that is so at the neurological level has largely been terra incognita. But research now is starting to reveal the impact of multitasking on short-term memory and attention.
Adam Gazzaley, MD, PhD, associate professor of neurology, physiology and psychiatry, and researchers at the UCSF Neuroscience Imaging Center use EEG, MRI and other non-invasive tools to study cognitive processes while people try their best on drills that test short-term memory.
LSUHSC research identifies new therapeutic target for Alzheimer’s disease
Research led by Chu Chen, PhD, Associate Professor of Neuroscience at LSU Health Sciences Center New Orleans, has identified an enzyme called Monoacylglycerol lipase (MAGL) as a new therapeutic target to treat or prevent Alzheimer’s disease. The study was published online November 1, 2012 in the Online Now section of the journal Cell Reports.
The research team found that inactivation of MAGL, best known for its role in degrading a cannabinoid produced in the brain, reduced the production and accumulation of beta amyloid plaques, a pathological hallmark of Alzheimer’s disease. Inhibition of this enzyme also decreased neuroinflammation and neurodegeneration, and improved plasticity of the brain, learning and memory.
"Our results suggest that MAGL contributes to the cause and development of Alzheimer’s disease and that blocking MAGL represents a promising therapeutic target," notes Dr. Chu Chen, who is also a member of the Department of Otolaryngology at LSU Health Sciences Center New Orleans.
The researchers blocked MAGL with a highly selective and potent inhibitor in mice using different dosing regimens and found that inactivation of MAGL for eight weeks was sufficient to decrease production and deposition of beta amyloid plaques and the function of a gene involved in making beta amyloid toxic to brain cells. They also measured indicators of neuroinflammation and neurodegeneration and found them suppressed when MAGL was inhibited. The team discovered that not only did the integrity of the structure and function of synapses associated with cognition remain intact in treated mice, but MAGL inactivation appeared to promote spatial learning and memory, measured with behavioral testing.
Alzheimer’s disease is a neurodegenerative disorder characterized by accumulation and deposition of amyloid plaques and neurofibrillary tangles, neuroinflammation, synaptic dysfunction, progressive deterioration of cognitive function and loss of memory in association with widespread nerve cell death. The most common cause of dementia among older people, more than 5.4 million people in the United States and 36 million people worldwide suffer with Alzheimer’s disease in its various stages. Unfortunately, the few drugs that are currently approved by the Food and Drug Administration have demonstrated only modest effects in modifying the clinical symptoms for relatively short periods, and none has shown a clear effect on disease progression or prevention.
"There is a great public health need to discover new therapies to prevent and treat this devastating disorder," Dr. Chen concludes. The research was supported by grants from the National Institutes of Health. In addition to scientists from LSU Health Sciences Center New Orleans, the research team also included investigators from the Massachusetts Institute of Technology.
(Source: eurekalert.org)
Of noise and neurons: Sensory coding, representation and short-term memory
While much is known about the limiting effect of neural noise on the fidelity of sensory coding representation, knowledge about the impact of noise in short-term memory and integrator networks has remained more elusive. (Integrator networks are networks of nodes – in this case neurons in a biological network – often recurrently connected, whose time dynamics settle to stable stationary, cyclic, or chaotic patterns, that can integrate or store memories of external inputs.)
Recently, however, scientists at The Hebrew University of Jerusalem, Harvard University and University of Texas, Austin used statistical and dynamical approaches to investigate how neural noise interacts with neural and network parameters to limit memory. They derived a series of unanticipated results – including the implications that short-term memory may be co-localized with sensory representation – by establishing a fundamental limit on the network’s ability to maintain a persistent neural state.