Memory Strategy May Help Depressed People Remember the Good Times

New research highlights a memory strategy that may help people who suffer from depression in recalling positive day-to-day experiences. The study is published in Clinical Psychological Science, a journal of the Association for Psychological Science.

Previous research has shown that being able to call up concrete, detailed memories that are positive or self-affirming can help to boost positive mood for people with a history of depression. But it’s this kind of vivid memory for everyday events that seems to be dampened for people who suffer from depression.

Researcher Tim Dalgleish of the Medical Research Council Cognition and Brain Sciences Unit and colleagues hypothesized that a well-known method used to enhance memory — known as the “method-of-loci” strategy — might help depressed patients to recall positive memories with greater ease.

The method-of-loci strategy consists of associating vivid memories with physical objects or locations — buildings you see on your commute to work every day, for instance. To recall the memories, all you have to do is imagine going through your commute.

In the study, depressed patients were asked to come up with 15 positive memories. One group was asked to use the method-of-loci strategy to create associations with their memories, while a control group was asked to use a simple “rehearsal” strategy, grouping memories based on their similarities.

After practicing their techniques, the participants were asked to recall as many of their 15 positive memories as they could.

The two methods were equally effective on the initial memory test conducted in the lab — both groups were able to recall nearly all of the 15 memories.

But the strategies were not equally effective over time.

After a week’s worth of practice at home, the participants received a surprise phone call from the researchers, who asked them to recall the memories one more time.

Participants who used the method-of-loci technique were significantly better at recalling their positive memories when compared to those who used the rehearsal technique.

These data suggest that using the method-of-loci technique to associate vivid, positive memories with physical objects or locations may make it easier for depressed individuals to recall those positive memories, which may help to elevate their mood in the long-term.

Small groups of brain cells store concepts for memory formation– from Luke Skywalker to your grandmother

Concepts in our minds – from Luke Skywalker to our grandmother - are represented by their own distinct group of neurons, according to new research involving a University of Leicester neuroscientist.

The research, by neuroscientist Professor Rodrigo Quian Quiroga from the University of Leicester Centre for Systems Neuroscience together with Professor Itzhak Fried, of the UCLA David Geffen School of Medicine, Tel Aviv Sourasky Medical Center and Tel Aviv University, and Professor Christof Koch, of the California Institute of Technology and Allen Institute for Brain Science, Seattle, is featured in a recent article of the prestigious Scientific American magazine.

Recent experiments during brain surgeries have shown that small groups of brain cells are responsible for encoding memories of specific people or objects.

These neurons may also represent different variations of one thing – from the name of a person to their appearance from many different viewpoints.

The researchers believe that single concepts may be held in as little as thousands of neurons or less – a tiny fraction of the billion or so neurons contained in the medial temporal lobe, which is a memory related structure within the brain.

The group were able to monitor the brain activity of consenting patients undergoing surgery to treat epilepsy. This allowed the team to monitor the activity of single neurons in conscious patients while they looked at images on laptop screens, creating and recalling memories.

In previous experiments, they had found that single neurons would ‘fire’ for specific concepts – such as Luke Skywalker – even when they were viewing images of him from different angles or simply hearing or reading his name.

They have also found that single neurons can also fire to related people and objects – for instance, the neuron that responded to Luke Skywalker also fired to Yoda, another Jedi from Star Wars.

They argue that relatively small groups of neurons hold concepts like Luke Skywalker and that related concepts such as Yoda are held by some but not all of the same neurons. At the same time, a completely separate set of neurons would hold an unrelated concept like Jennifer Aniston.

The group believes this partially overlapping representation of related concepts are the neural underpinnings of encoding associations, a key memory function.

Professor Quian Quiroga said: “After the first thrill when finding neurons in the human hippocampus with such remarkable firing characteristics, converging evidence from experiments we have been carrying out in the last years suggests that we may be hitting one of the key mechanisms of memory formation and recall.

“The abstract representation of concepts provided by these neurons is indeed ideal for representing the meaning of the sensory stimuli around us, the internal representation we use to form and retrieve memories. These concepts cells, we believe, are the building blocks of memory functions.”

Scientists make older adults less forgetful in memory tests

Scientists at Baycrest Health Sciences’ Rotman Research Institute (RRI) and the University of Toronto’s Psychology Department have found compelling evidence that older adults can eliminate forgetfulness and perform as well as younger adults on memory tests.

Scientists used a distraction learning strategy to help older adults overcome age-related forgetting and boost their performance to that of younger adults. Distraction learning sounds like an oxymoron, but a growing body of science is showing that older brains are adept at processing irrelevant and relevant information in the environment, without conscious effort, to aid memory performance.

“Older brains may be be doing something very adaptive with distraction to compensate for weakening memory,” said Renée Biss, lead investigator and PhD student. “In our study we asked whether distraction can be used to foster memory-boosting rehearsal for older adults. The answer is yes!”

“To eliminate age-related forgetfulness across three consecutive memory experiments and help older adults perform like younger adults is dramatic and to our knowledge a totally unique finding,” said Lynn Hasher, senior scientist on the study and a leading authority in attention and inhibitory functioning in younger and older adults. “Poor regulation of attention by older adults may actually have some benefits for memory.”

The findings, published online in Psychological Science, ahead of print publication, have intriguing implications for designing learning strategies for the mature, older student and equipping senior-housing with relevant visual distraction cues throughout the living environment that would serve as rehearsal opportunities to remember things like an upcoming appointment or medications to take, even if the cues aren’t consciously paid attention to.

Memory appears susceptible to eradication of fear responses

Fear responses can only be erased when people learn something new while retrieving the fear memory. This is the conclusion of a study conducted by scientists from the University of Amsterdam (UvA) and published in the leading journal Science.

Researchers Dieuwke Sevenster MSc, Dr Tom Beckers and Prof. Merel Kindt have developed a method to determine whether an acquired fear response is susceptible to modification. By doing so, they have revealed the circumstances under which an acquired fear response can be eradicated. In order to measure whether a person actually learnt something new, the researchers used a measure for Prediction Error – in other words, the discrepancy between a person’s anticipation of what is going to happen and what actually happens.

No fear response

Cognitive Behavioural Therapy is currently the most common and effective type of treatment for people suffering from anxiety disorders. However, the effects are often short-lived and the fear returns in many patients. One major finding of Van Kindt’s research lab is that when participants were given propranolol, a beta blocker, while retrieving a specific fear memory, the acquired fear response was shown to be totally erased a day or month later. The researchers repeatedly found that the fear did not come back, despite the use of techniques specifically aimed to make it return. This indicates that the fear memory was either fully eradicated, or could no longer be accessed. One crucial finding was that while participants could still remember the association with the fear, that particular memory no longer triggered the former fear response.

Fear conditioning

For their study the researchers used a fear conditioning procedure in which a specific picture was followed by a nasty painful stimulus. While the participants viewed the pictures, the researchers measured the anticipation of the painful stimulus as well as the more autonomous fear response on the basis of the startle reflex.

The current findings will contribute to the further development of more effective and efficient therapies for patients suffering from excessive anxiety disorders, such as trauma victims. There was no independent measure to indicate whether the memory is susceptible to modification up until now. The researchers have shown that the fear response can be eradicated completely, provided that the person concerned actually learns something new while retrieving the fear memory.

(Image: iStock)

Chimpanzees have faster working memory than humans

Chimpanzees have a faster working memory than humans according to a remarkable study showing that it takes them a fraction of a second to remember something that it would take several seconds for humans to memorise.

A Japanese scientist has demonstrated the prowess of chimps in remembering in less than half a second the precise position and correct sequence of up to nine numbers on a computer screen.

The numbers are shown together randomly distributed on a computer screen and as soon as the chimps press the number “one” the rest of the numerals are masked. However, they can almost invariably remember where each number was.

It is impossible for people to do the same cognitive task that quickly, said Tetsuro Matsuzawa, a primatologist at Kyoto University. “They have a better working memory than us,” he told the American Association for the Advancment of Science meeting in Boston.

Professor Matsuzawa had carried out the memory experiments on a female chimp called Ai, which means “love” in Japanese, and Ayumu, her son who was born in 2000 and has shown even better memory skills, he said.

Professor Matsuzawa suggested that chimps have developed this part of their memory because they live in the “here and now” whereas humans are thinking more about the past and planning for the future.

Researchers identify potential target for age-related cognitive decline

Cognitive decline in old age is linked to decreasing production of new neurons. Scientists from the German Cancer Research Center have discovered in mice that significantly more neurons are generated in the brains of older animals if a signaling molecule called Dickkopf-1 is turned off. In tests for spatial orientation and memory, mice in advanced adult age whose Dickkopf gene had been silenced reached an equal mental performance as young animals.

The hippocampus – a structure of the brain whose shape resembles that of a seahorse – is also called the “gateway” to memory. This is where information is stored and retrieved. Its performance relies on new neurons being continually formed in the hippocampus over the entire lifetime. “However, in old age, production of new neurons dramatically decreases. This is considered to be among the causes of declining memory and learning ability”, Prof. Dr. Ana Martin-Villalba, a neuroscientist, explains.

Martin-Villalba, who heads a research department at the German Cancer Research Center (DKFZ), and her team are trying to find the molecular causes for this decrease in new neuron production (neurogenesis). Neural stem cells in the hippocampus are responsible for continuous supply of new neurons. Specific molecules in the immediate environment of these stem cells determine their fate: They may remain dormant, renew themselves, or differentiate into one of two types of specialized brain cells, astrocytes or neurons. One of these factors is the Wnt signaling molecule, which promotes the formation of young neurons. However, its molecular counterpart, called Dickkopf-1, can prevent this.

"We find considerably more Dickkopf-1 protein in the brains of older mice than in those of young animals. We therefore suspected this signaling molecule to be responsible for the fact that hardly any young neurons are generated any more in old age." The scientists tested their assumption in mice whose Dickkopf-1 gene is permanently silenced. Professor Christof Niehrs had developed these animals at DKFZ. The term "Dickkopf" (from German "dick" = thick, "Kopf" = head) also goes back to Niehrs, who had found in 1998 that this signaling molecule regulates head development during embryogenesis.

Number of People with Alzheimer’s Disease May Triple by 2050

The number of people with Alzheimer’s disease is expected to triple in the next 40 years, according to a new study by researchers from Rush University Medical Center published in the February 6, 2013, online issue of Neurology, the medical journal of the American Academy of Neurology.

“This increase is due to an aging baby boom generation. It will place a huge burden on society, disabling more people who develop the disease, challenging their caregivers, and straining medical and social safety nets,” said co-author, Jennifer Weuve, MPH, ScD, assistant professor of medicine, Rush Institute for Healthy Aging at Rush University Medical Center in Chicago. “Our study draws attention to an urgent need for more research, treatments and preventive strategies to reduce the impact of this epidemic.”

For the study, researchers analyzed information from 10,802 African-American and Caucasian people living in Chicago, ages 65 and older between 1993 and 2011. Participants were interviewed and assessed for dementia every three years. Age, race and level of education were factored into the research.

The data was combined with U.S. death rates, education and current and future population estimates from the U.S. Census Bureau.

The study found that the total number of people with Alzheimer’s dementia in 2050 is projected to be 13.8 million, up from 4.7 million in 2010. About 7 million of those with the disease would be age 85 or older in 2050.

“Our projections use sophisticated methods and the most up-to-date data, but they echo projections made years and decades ago. All of these projections anticipate a future with a dramatic increase in the number of people with Alzheimer’s and should compel us to prepare for it,” said Weuve.

Human memory study adds to global debate

An international study involving researchers from the University of Adelaide has made a major contribution to the ongoing scientific debate about how processes in the human brain support memory and recognition.

The study used a rare technique in which data was obtained from within the brain itself, using electrodes placed inside the brains of surgery patients.

Obtained in Germany, the data was sent to the University of Adelaide’s School of Psychology for further analysis using new techniques developed there. The results are published today in the Proceedings of the National Academy of Sciences (PNAS).

"Being able to understand how human memory works is important because there is a range of conditions that affect memory, such as Alzheimer’s disease, head injury, and ageing," says Professor John Dunn, Head of the School of Psychology at the University of Adelaide and a co-author of the study, which was led by researchers at the universities of Cambridge, UK, and Bonn, Germany.

"Scientists know a lot about memory from years of study, but there is an ongoing debate about how certain mechanisms in the brain process memory, and how those mechanisms work together.

"What we’re looking at is how the human brain processes ‘recognition memory’, which is our ability to recognise people, objects or events that we’ve encountered in the past."

The debate has centered on two key regions in the brain:

• the hippocampus, which is very important to memory and is one of the first regions of the brain to suffer damage from Alzheimer’s disease; and
• the perirhinal cortex, which receives sensory information from all of the body’s sensory regions.

"The debate is whether or not these two regions work in the same or different ways to support memory and recognition Studies over the years have led to both conclusions," Professor Dunn says.

He says this new study, which uses data from inside the brain instead of from electrodes on the scalp, far from the critical regions, revealed that different processes are at work in the hippocampus and the perirhinal cortex.

"Our analysis shows that these regions are responding to and processing memory in two very different ways. The activity levels in those regions changed in different ways according to the amount of information that could be remembered," Professor Dunn says.

"This study won’t settle the debate once and for all, but it does add weight to those scientists who believe that these two distinct parts of the brain respond to memory in different ways," he says.

Finding the way to memory

Our ability to learn and form new memories is fully dependent on the brain’s ability to be plastic – that is to change and adapt according to new experiences and environments. A new study from the Montreal Neurological Institute – The Neuro, McGill University, reveals that DCC, the receptor for a crucial protein in the nervous system known as netrin, plays a key role in regulating the plasticity of nerve cell connections in the brain. The absence of DCC leads to the type of memory loss experienced by Dr. Brenda Milner’s famous subject HM.  Although HM’s memory loss resulted from the removal of an entire brain structure, this study shows that just removing DCC causes the same type of memory deficit. The finding published in this week’s issue of Cell Reports, extends Dr. Milner’s seminal finding to another level, revealing a key part of the molecular basis for learning and memory.

Although both netrin and DCC are essential for normal development (in terms of guiding nerve cell growth) until now their function in the adult brain was not known. Dr. Tim Kennedy, lead researcher and neuroscientist at The Neuro, contributed to the discovery of netrins as a young post-doctoral fellow. This new study reveals the answer to the question that drove him to first start a lab. “I remember that exact moment when I knew I could run a research lab, it was 1993 and I was studying the developing nervous system and I was amazed to spot netrins in the adult brain - raising the important question, ‘what are they doing there?’ 20 years of dedicated research later the answer provides an important piece of the puzzle for understanding our nervous system and neurological disorders.

“The power of this study is that it looks at the animal on all levels, molecular, structural, and behavioural. We show that the netrin receptor DCC is a critical component of synapses between neurons in the adult brain, and is required for synapses to function properly. To demonstrate this, we selectively removed DCC from a specific subset of neurons in the adult mouse brain. This results in progressive degeneration of synapses, leading to defects in synaptic plasticity and memory. The synapses continue to function in that they still communicate but, the synapses cannot adjust or change in response to new experiences. Therefore, you can’t learn anymore.”

Furthermore, DCC deletion from mature neurons results in changes in the shape of specialized protrusions called dendritic spines, and alters the NMDA receptor, a critical trigger for mechanisms that make changes in synaptic strength. Therefore the study reveals that DCC is required to maintain proper synapse morphology or shape, and to regulate the ability of the NMDA receptor to switch on, which ensures activity-dependent synaptic plasticity.

Chemical reaction keeps stroke-damaged brain from repairing itself

Nitric oxide, a gaseous molecule produced in the brain, can damage neurons. When the brain produces too much nitric oxide, it contributes to the severity and progression of stroke and neurodegenerative diseases such as Alzheimer’s. Researchers at Sanford-Burnham Medical Research Institute recently discovered that nitric oxide not only damages neurons, it also shuts down the brain’s repair mechanisms. Their study was published by the Proceedings of the National Academy of Sciences the week of February 4.

“In this study, we’ve uncovered new clues as to how natural chemical reactions in the brain can contribute to brain damage—loss of memory and cognitive function—in a number of diseases,” said Stuart A. Lipton, M.D., Ph.D., director of Sanford-Burnham’s Del E. Webb Neuroscience, Aging, and Stem Cell Research Center and a clinical neurologist.

Lipton led the study, along with Sanford-Burnham’s Tomohiro Nakamura, Ph.D., who added that these new molecular clues are important because “we might be able to develop a new strategy for treating stroke and other disorders if we can find a way to reverse nitric oxide’s effect on a particular enzyme in nerve cells.”

Nitric oxide inhibits the neuroprotective ERK1/2 signaling pathway

Learning and memory are in part controlled by NMDA-type glutamate receptors in the brain. These receptors are linked to pores in the nerve cell membrane that regulate the flow of calcium and sodium in and out of the nerve cells. When these NMDA receptors get over-activated, they trigger the production of nitric oxide. In turn, nitric oxide attaches to other proteins via a reaction called S-nitrosylation, which was first discovered by Lipton and colleagues. When those S-nitrosylated proteins are involved in cell survival and lifespan, nitric oxide can cause brain cells to die prematurely—a hallmark of neurodegenerative disease.

In their latest study, Lipton, Nakamura and colleagues used cultured neurons as well as a living mouse model of stroke to explore nitric oxide’s relationship with proteins that help repair neuronal damage. They found that nitric oxide reacts with the enzyme SHP-2 to inhibit a protective cascade of molecular events known as the ERK1/2 signaling pathway. Thus, nitric oxide not only damages neurons, it also blocks the brain’s ability to self-repair.