The Mental Health Social Worker

A new poll finds the majority of college students are stressed and a significant number are at risk of depression. The Associated Press-mtvU poll found eighty-five percent of the students reported feeling stress in their daily lives in recent months, with worries about grades, school work, money and relationships the major reason. Forty-two percent said they had felt down, depressed or hopeless several days during the past two weeks, and 13 percent showed signs of being at risk for at least mild depression, based on the students’ answers to a series of questions that medical practitioners use to diagnose depressive illness. (Associated Press, 5/22/09)

WASHINGTON–Helping middle school students with their homework may not be the best way to get them on the honor roll. But telling them how important academic performance is to their future job prospects and providing specific strategies to study and learn might clinch the grades, according to a research review.

“Instilling the value of education and linking school work to future goals is what this age group needs to excel in school, more than parents’ helping with homework or showing up at school,” said lead researcher Nancy E. Hill, PhD, of Harvard University. She examined 50 studies with more than 50,000 students over a 26-year period looking at what kinds of parent involvement helped children’s academic achievement.

These findings are reported in the May issue of Developmental Psychology, published by the American Psychological Association.

“Middle school is the time when grades and interest in school decline,” said Hill. “Entering puberty, hanging out with friends, wanting distance from parents and longing to make one’s own decisions win over listening to parents and studying.”

But adolescence is also a time when analytic thinking, problem-solving, planning and decision-making skills start to increase, Hill said. At this age, “teens are starting to internalize goals, beliefs and motivations and use these to make decisions. Although they may want to make their own decisions, they need guidance from parents to help provide the link between school and their aspirations for future work.”

This type of parental involvement works for middle school students because it is not dependent on teacher relationships, like in elementary school. Middle school students have different teachers for each subject so it is much more difficult for parents to develop relationships with teachers and to influence their teenagers through their teachers, Hill said.

Parents’ involvement in school events still had a positive effect on adolescents’ achievement, Hill said, but not as much as parents’ conveying the importance of academic performance, relating educational goals to occupational aspirations and discussing learning strategies.

Helping with homework had mixed results. Some students felt that parents were interfering with their independence or putting too much pressure on them. Some found that their parents’ help was confusing because they didn’t use the same strategies as their teachers. Still others felt that parents helped them complete or understand their homework, said Hill and co-author Diana F. Tyson, PhD, of Duke University.

Another possible explanation for the negative return on homework, said Hill, “was that those students who needed help with their homework were already doing poorly in school and this showed up as being associated with lower levels of achievement.”

The review did not rule out ethnic and socioeconomic influences. Findings showed no difference between whites and blacks in which types of parental involvements influenced achievement but the same interventions did not necessarily produce the same results for Hispanics and Asian-Americans. Some of the studies showed that parental involvement had different meanings across different ethnic groups, which could be the result of differences in economic resources.

“Lack of guidance is the chief reason that academically able students do not go to college,” said Hill. “So communicating the value of education and offering curriculum advice about what to focus on helps these students plan their long-term goals.”

Article: “Parental Involvement in Middle School: A Meta-Analytic Assessment of the Strategies That Promote Achievement,” Nancy E. Hill, PhD, Graduate School of Education, Harvard University, and Diana F. Tyson, PhD, Duke University; Developmental Psychology, Vol. 45, No. 3.

(Full text of the article is available from the APA Public Affairs Office and at http://www.apa.org/journals/releases/dev453740.pdf)

Contact Nancy E. Hill by e-mail and by phone at 617-496-1182

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Washington—Significant and widespread cognitive problems appear to exist in schizophrenia in its earliest phase, making it very hard for people with the disorder to work, study or be social, according to a new study published by the American Psychological Association.

Understanding the early and central role of cognitive problems may help clinicians to more accurately diagnose incipient schizophrenia by telling it apart from other neuropsychiatric disorders that also have cognitive problems, such as attention-deficit hyperactivity disorder (ADHD). It could also allow them to provide more appropriate treatment. Combining schizophrenia’s cognitive warning signs with family history and signs of worsening daily functioning may also aid early diagnosis. Should improved early treatments become available, early diagnosis could make it possible to ease or even prevent these problems.

These were among the conclusions of a meta-analysis conducted by researchers at Harvard Medical School and SUNY Upstate Medical University in Syracuse, N.Y. The researchers examined 47 previously published, peer-reviewed studies of first-episode schizophrenia that involved 43 separate samples comprising 2,204 patients and 2,775 largely age- and gender-matched control participants. Results of this new analysis appear in the May issue of Neuropsychology, which is published by the American Psychological Association.

The psychologists sorted the studies’ collective findings into10 areas of neurocognition, including general cognitive ability, attention, memory, and various verbal, motor and visuospatial skills. Among their main findings:

• In the very first episode of schizophrenia, cognitive problems were already broad and serious. Early impairment approached or matched the severity of problems seen in patients who had been sick for a while.
• People experiencing their first episode of schizophrenia had significantly worse performance on all cognitive measures than healthy controls who were largely matched for gender and age.
• Patients struggled the most with processing speed and with verbal learning and memory, especially when encoding information. Although many psychiatric and neurological illnesses, such as bipolar disorder, affect processing speed, schizophrenia seems to disrupt it more profoundly.
• Measured IQ and other cognitive abilities dropped the most between the high-risk period just before symptoms appear and the first acute phases. After that, these cognitive abilities were stable. This cognitive pattern, when combined with other signs such as clinical symptoms and family history, could suggest a diagnosis of schizophrenia.

The first episode of schizophrenia, which is typically in the late teens or early 20s, brings “a sense of tremendous terror, trauma and shock, along with prominent cognitive disorganization, increasingly compelling unusual and/or paranoid thoughts, altered perceptions, and loss of insight,” according to lead co-authors Raquelle Mesholam-Gately, PhD, and Anthony Giuliano, PhD. Popular images of schizophrenia focus on its auditory and visual hallucinations, and strange or distressing behaviors.

However, as the authors noted, people with schizophrenia have experienced a high-risk period for a few months to two years before illness sets in, showing increased problems with daily living that foreshadow full-blown illness. Early intervention for cognitive problems might lessen their intensity and duration, allowing for a better prognosis, lower relapse rates, and better preservation of cognitive and social skills, and of family and social supports, according to the authors. The high-risk, or “prodromal,” period is now a focal point for prevention, diagnosis and treatment.

Cognitive testing could also be useful for older children who have a family history of schizophrenia and emerging clinical symptoms. Doctors viewing cognitive impairments in a vacuum might think of something like ADHD, but the researchers said the new findings play up the importance of family history (schizophrenia has a genetic component) and better characterization of clinical or behavioral symptoms, especially around the age of peak risk.

At this time, there are no effective treatments for cognitive problems in schizophrenia. In the United States, the National Institute of Mental Health recently sponsored two nationwide initiatives to develop assessment standards for cognition in schizophrenia and to evaluate medicines that may potentially treat its cognitive problems. They are called Measurement and Treatment Research to Improve Cognition in Schizophrenia, or MATRICS, and Treatment Units for Research on Neurocognition and Schizophrenia, or TURNS.

Article: “Neurocognition in First-Episode Schizophrenia: A Meta-Analytic Review,” Raquelle I. Mesholam-Gately, PhD, and Anthony J. Giuliano, PhD; Kirsten P. Goff, PhD, Harvard Medical School and Private Practice, Kentfield, California; Stephen V. Faraone, PhD, SUNY Upstate Medical University; Larry J. Seidman, PhD, Harvard Medical School; Neuropsychology, Vol. 23, No. 3.

(Full text of the article is available from the APA Public Affairs Office and at http://www.apa.org/journals/releases/neu233315.pdf)

Raquelle Mesholam-Gately can be reached via e-mail or by phone at (617) 626-9409 or (617) 998-5042. Anthony Giuliano can be reached at via e-mail or by phone at (617) 998-5018.

WASHINGTON—Children who suffer traumatic brain injuries can experience lasting or late-appearing neuropsychological problems, highlighting the need for careful watching over time, according to two studies published by the American Psychological Association.

In one study, a team of psychologists used a longitudinal approach to gain a better idea of what to expect after traumatic brain injury (TBI). The researchers found that severe TBI can cause many lasting problems with day-to-day functioning. Some children may recover academically but then start acting up; other children do surprisingly well for unknown reasons.

In the second study, the first systematic meta-analysis summarizing the collective results of many single studies, the researchers found that problems lasted over time and, in some cases, worsened with more serious injury. Some children with severe TBI started to fall even further behind their peers than one would normally expect, in a snowball effect that requires further study.

The results of both studies were reported in the May issue of Neuropsychology, published by the American Psychological Association.

The Centers for Disease Control in 2000 cited traumatic brain injury as the single most common cause of death and disability in children and adolescents.

Long-Term Study Digs Out Individual Differences

In the first study, researchers at The Ohio State University, Case Western Reserve University, and hospitals in Columbus and Cleveland followed 37 children after severe TBI, 40 children after moderate TBI, and 44 children after musculoskeletal injury (a common way to control for trauma and the hospital experience). All of the children were injured between the ages of 6 and 12, and assessed six months, 12 months, and three to five years following their injuries.

As expected, the children with severe brain injuries showed greater problems than children with other injuries in the areas of mental processing, learning and memory, behavior, adaptation and academics. Children whose comas were longer and more severe had more, and more serious, problems.

Some children seemed at first to be doing all right on cognitive tests and in the classroom, but then developed significant behavioral problems. Parents and doctors should watch children who’ve had traumatic brain injury closely because something may come up later – perhaps, the authors suggested, as a secondary reaction to the disruption caused by the injury, or because the family has not functioned very well, especially in response to the injury.

Generally, one year after injury, nearly 60 percent of the severe TBI group had problems in at least one area, compared with 25 percent of the controls. Four years after injury, 40 percent of children suffering severe TBI and 20 percent of the controls showed deficits. At both intervals, the share of brain-injured children with cognitive problems was at least twice that of the control group members with problems.

Even so, the researchers were intrigued that many children with moderate to severe TBI showed no significant weaknesses from six months to four years after the injury, in one or more of the areas measured.

Perhaps, they speculated, that was because in previous long-term studies, group averages may have hidden the fact that some individual children can do well over time. This team, by tracking individuals, revealed that some children are more mentally resilient. If researchers can learn why, they may be able to help more children to recover more fully from this type of injury.

“It’s probably a complex interplay of child, family and broader environmental/cultural factors. The care and treatment children receive may make a difference, such as whether they have access to rehabilitation and special-education services,” said co-author Keith Yeates, PhD, who also mentioned genetic differences in the brain’s ability to heal itself.

Meta-Analysis Shows Problems Grow Over Time

In the second study, conducted by Talin Babikian, PhD, and Robert Asarnow, PhD, at the University of California-Los Angeles, the authors analyzed 28 carefully selected articles published between 1988 and 2007. The children were sorted by TBI severity and time since injury. Severity levels were mild, moderate or severe TBI, and follow-ups were on average 0-5 months, 6-23 months, or 24+ months, for 14 key aspects of neurocognition.

According to their analysis:

• The worse the injury, the worse the neurocognitive outcome, especially on measures of general intellectual functioning and processing speed.

• Time didn’t heal all. The moderate and severe groups were even more similar by the third time band, especially on general intellectual functioning and attention/executive skills.

• Most problems stick. Despite modest recovery in intellectual functioning and attention, weaknesses in many children with moderate TBI persist even two years after the injury, compared to the children in control groups.

• Memory and visual-spatial skills seemed more or less normal by two-plus years, with even the moderately injured performing in the same range as controls.

• Children with severe TBI needed more help, showing robust and significant problems within months on IQ, executive functioning (processing speed, attention), and verbal memory (both immediate and delayed). After two or more years, all areas studied were impaired.

“It appears that there are significant, persistent neurocognitive impairments in a subset of children with severe TBI,” the authors concluded. Despite some recovery during the first two years, children in this group not only failed to catch up to peers, but appeared to fall further behind over time. Thus, severe traumatic brain injury may throw off children’s normal developmental timetable. The authors noted that well-controlled longitudinal studies evaluating the same children over time are necessary to confirm these findings.

That makes severe brain injuries at younger ages a “double hazard,” the authors noted. Because younger children have more development ahead of them, the same injury can affect a 4-year-old and a 12-year-old very differently. This finding highlights the importance of targeted treatment developed specifically for children with severe TBI.

Article 1: “Predicting Longitudinal Patterns of Functional Deficits in Children With Traumatic Brain Injury,” Taryn B. Fay, PhD, Ohio State University and Nationwide Children’s Hospital; Keith Owen Yeates, PhD, Nationwide Children’s Hospital; Shari L Wade, PhD, University of Cincinnati; Dennis Drotar, PhD, Case Western Reserve University and Rainbow Babies & Children’s Hospital; Terry Stancin, PhD, Case Western Reserve University and MetroHealth Medical Center; and H. Gerry Taylor, PhD, Case Western Reserve University and Rainbow Babies & Children’s Hospital; Neuropsychology, Vol. 23, No. 3.

(Full text of the article is available from the APA Public Affairs Office and at http://www.apa.org/journals/releases/neu233271.pdf)

Taryn Fay can be reached via e-mail or via e-mail, or by phone at her office (403) 955-7097, mobile (403) 797-4014, or home (403) 289-0983. Keith Owen Yeates, in Australia in mid-May; can be reached in that time zone via e-mail. His administrative assistant, Pat Davis, is at (614) 722-4673. Gerry Taylor can be reached via e-mail or at (216) 844-6227 or mobile (216) 338-5679.

Article 2: “Neurocognitive Outcomes and Recovery After Pediatric TBI: Meta-Analytic Review of the Literature,” Talin Babikian, PhD, and Robert Asarnow, PhD, David Geffen School of Medicine at UCLA; Neuropsychology, Vol. 23, No. 3.

(Full text of the article is available from the APA Public Affairs Office and at http://www.apa.org/journals/releases/neu233283.pdf)

Talin Babikian can be reached via e-mail or at (310) 267-2659.

In cases of familial depression, changes in tissue thickness in key brain structures in the right half of the brain may increase a person’s risk for developing depression, according to NIMH-funded researchers. Similar changes in the left half of the brain were linked to the severity of a person’s existing depression or anxiety symptoms. Based on their findings, the researchers proposed a possible mechanism for how these brain changes affect depression risk in the April 14, 2009, issue of the Proceedings of the National Academy of Sciences.

Background

Some types of depression run in families, and certain changes in brain structure and function have been observed in people with the disorder. However, until recently, scientists have been unclear on the exact relationship between these brain changes and depression.

Building on previous research with a three-generation study population, Myrna Weissman, Ph.D., and Bradley Peterson, M.D., both of Columbia University College of Physicians & Surgeons and New York State Psychiatric Institute, and colleagues used magnetic resonance imaging (MRI) to assess brain changes in 131 people, ages 6-54. Roughly half of these participants were considered at high risk for major depressive disorder (MDD), due to having at least one parent or grandparent in the study diagnosed with the illness. The other half, considered at low risk, had no family history of the illness.

Results of the Study

From pre-scanning interviews, the researchers found that people in the high-risk group were more likely than those in the low-risk group to report having MDD or an anxiety disorder at some point in their lives. MRI scans showed that, on average, those in the high-risk group had 28 percent thinner brain tissue across a broad range of brain structures in the right half of the brain. These changes were observed in young children in the high-risk group and in older high-risk individuals who had never suffered from MDD or an anxiety disorder themselves.

The brain areas most affected by this thinning govern attention and the ability to process emotional or social cues (such as faces or family pictures). In tests involving these right-brain tasks, the researchers found that thinner tissue in these areas was linked to greater inattention and poorer performance in immediate and delayed visual memory.

Similar patterns of tissue thinning in the left half of the brain appeared to be related to the severity of a person’s existing MDD or anxiety disorder symptoms in both the high- and low-risk groups. This thinning was not as pronounced as the thinning in the right half of the brain, and the difference in tissue thickness between the high- and low-risk groups was not statistically significant.

Significance

The findings strongly suggest that changes in tissue thickness in the right half of the brain directly affect a person’s inherited risk for developing MDD. The pattern of tissue thinning appears to be related to problems with attention and processing of emotional or social signals. Such problems may increase a person’s vulnerability to developing mood or anxiety disorders, according to the researchers.

That the thinning was present in people at high risk, but who had never had MDD or an anxiety disorder, as well as in high-risk children who had not been diagnosed with depression, shows that these brain changes likely come before illness onset and that they occur very early in life, possibly before birth, say the researchers. Furthermore, while thinning in the right half of the brain contributes to risk, thinning in the left half of the brain appears to be required in order for a person to show symptoms of these illnesses.

What’s Next

More research is needed to determine if the inherited risk for MDD is purely genetic, if there are specific environmental factors necessary for triggering genetic risk, or whether there is a combination of factors involved. Increased understanding of how risk translates into developing MDD or other mental disorders may lead to new methods of diagnosing, treating, or preventing these illnesses.

Top: Color coded MRI brain maps of differences in tissue thickness between study participants at high- vs. low-risk for familial depression. Left half of brain is shown on the left and right half on the right. Cool colors (blue and purple) denote thinner areas in the high-risk group; warm colors (yellow, orange, and red) are significantly thicker areas; green areas show little to no difference in tissue thickness.

Bottom: Flowchart represents a proposed model for how some MDD or anxiety disorders develop. Double-headed arrows indicate factors that may influence each other and jointly contribute to disease risk. Block arrows show the hypothetical progression from inherited risk to development of symptoms.

Source: Bradley Peterson, M.D., Columbia University College of Physicians & Surgeons and New York State Psychiatric Institute

Reference

Peterson BS, Warner V, Bansal R, Zhu H, Hao X, Liu J, Durkin K, Adams PB, Wickramaratne P, Weissman MM. Cortical thinning in persons at increased familial risk for major depression. Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6273-8. PMID: 19329490

WASHINGTON–Children who can stay focused and don’t sweat the small stuff have a better shot at good health in adulthood — and this is especially true for girls, according to a new study.

“Certain characteristics already evident early in life are likely to spark positive or negative emotions, and also influence biological and behavioral responses to stress,” said lead author Laura D. Kubzansky, PhD, of the Harvard School of Public Health. “Some traits may contribute to developing healthier behaviors and better social relationships, and ultimately more resilience in mid-life.

“Supporting this idea, we found that children who were able to stay focused on a task and react less negatively to situations at age 7 reported better general health and fewer illnesses 30 years later.”

These findings are reported in the May issue of Health Psychology, published by the American Psychological Association.

Kubzansky and co-authors tracked 569 individuals from the National Collaborative Perinatal Project from age 7 to their mid-30s to see if certain personality traits influenced later health. Trained observers rated the 7-year-olds on 15 different behaviors. These behaviors were then assigned to three different personality attributes: attention (the ability to stay focused on a task and persist in solving a problem), distress-proneness (the tendency to react negatively to situations), and behavior inhibition (the tendency toward shyness, acting withdrawn and having difficulty communicating).

To determine adult health, the participants rated their health and reported whether they had any of the following illnesses: heart disease, diabetes, cancer, asthma, arthritis, stroke, bleeding ulcer, tuberculosis or hepatitis.

For all the participants, superior attention spans and having a more positive outlook in youth affected health the most. These effects were greater for women, the researchers found. The authors suggest that women may be more sensitive to interactions among emotion, behavior and biology and, therefore, be more predisposed to certain health risks, such as heart disease, although additional research is needed to understand this more completely.

The authors found no differences in these effects across race or ethnicity; they also controlled for childhood health and socicoeconomic status.

The sample consisted of 60 percent men and 40 percent women; 80 percent of participants were white and 20 percent were black. Of the sample, 76 percent reported good or excellent health and 18 percent reported illnesses.

“This longitudinal study provides more evidence that behavior and emotions generally linked to certain temperaments play a crucial role in long-term health,” Kubzansky said. “Fortunately, early childhood characteristics can be shaped and guided by social, family and peer interactions. Interventions can focus on altering certain ways of responding and behaviors that frequently accompany particular traits to prevent certain diseases.”

Article: “Early Manifestations of Personality and Adult Health: A Life Course Perspective,” Laura D. Kubzansky, PhD, Harvard School of Public Health; Laurie T. Martin, PhD, Rand Corporation; Stephen L. Buka, PhD, Brown University; Health Psychology, Vol. 13, No. 1.

(Full text of the article is available from the APA Public Affairs Office and at http://www.apa.org/journals/releases/hea283364.pdf)

Contact Todd R. Datz via e-mail and by phone at 617.432.3952

Blocking Errant Protein Could Stem Runaway Brain Activity in Psychosis

A study on schizophrenia has implicated machinery that maintains the flow of potassium in cells and revealed a potential molecular target for new treatments. Expression of a previously unknown form of a key such potassium channel was found to be 2.5 fold higher than normal in the brain memory hub of people with the chronic mental illness and linked to a hotspot of genetic variation.

An extensive series of experiments suggest that selectively inhibiting this suspect form could help correct disorganized brain activity in schizophrenia — without risk of cardiac side effects associated with some existing antipsychotic medications. Scientists at the National Institutes of Health and European colleagues report on threads of converging evidence in the May, 2009 issue of the journal Nature Medicine.

“The end game in linking genes with complex disorders like schizophrenia requires that we not only demonstrate statistical association, but also show how a gene version acts biologically to confer risk,” explained Daniel Weinberger, M.D., director of National Institute of Mental Health’s (NIMH) Genes Cognition and Psychosis Program, who led the research. “We found schizophrenia-like effects in brain circuitry and mental processing in perfectly healthy people who carry the risk-associated version of this potassium channel gene, even though they don’t show any psychotic behavior.”

Evidence suggests that schizophrenia stems from complex interactions between multiple genes and environmental factors. Several candidate genes have recently been statistically linked to the illness in large genome-wide association studies.

“Our study goes further, spanning discovery of a new gene variant, confirmation of its association with the illness, and multi-level probes into how it works — in human post mortem brain tissue, the living human brain, and neurons,” added Weinberger.

By regulating the flow of potassium ions into the cell, potassium channels control when neurons fire — electrically discharge and release a chemical messenger that signals neighboring neurons in a circuit. This flow is regulated, in part, by activity of the chemical messenger dopamine, the main target of antipsychotic medications used to treat schizophrenia.

One type of potassium channel, called KCNH2, attracted the researchers’ interest for its potential role in sustaining the type of neuronal firing that supports the higher mental functions disturbed in schizophrenia. Spurred by hints from postmortem studies of genetic variation linked to schizophrenia in the genomic neighborhood of KCNH2, the researchers analyzed the gene’s association with the illness in 5 independent samples comprising hundreds of families. This pinpointed 4 variations associated with schizophrenia within a small region of the KCNH2 gene.

“Yet this statistical association didn’t imply a mechanism,” said Weinberger. “It didn’t explain how KCNH2 might increase risk for schizophrenia. So we went back to the post-mortem brain tissue in search of an answer.”

It was only then that the researchers discovered a previously unknown version of KCNH2, called Isoform 3.1, that soared to levels 2.5 times higher-than-normal in the hippocampus (memory hub) of people who had schizophrenia — especially those with the risk-associated variations. Isoform 3.1 was also higher-than-normal in healthy individuals who carried the risk-associated variations. This signaled the existence of a risk-associated version of the KCNH2 gene.

Healthy controls carrying the risk gene version also:

• Performed significantly worse-than-normal on measures of IQ and mental processing speed. Previous studies have linked similar performance with genetic risk for schizophrenia.
• Inefficiently processed memory in the hippocampus and working memory in the prefrontal cortex, as revealed by functional MRI (magnetic resonance imaging) scans. Although they performed similarly to controls on these tasks, their brains had to work harder to compensate for disordered tuning of circuitry — a phenomenon previously implicated in schizophrenia.
• Showed significantly decreased volume in the hippocampus — a heritable trait — in anatomical MRI scans.

In addition, Isoform 3.1:

• Showed levels 1,000 times lower in the heart than the other main form of KCNH2 and does not exist in lower animals, suggesting that it has evolved a unique role in the primate brain. Mutant forms of KCNH2 in the heart can lead to arrhythmias and even sudden death — a rare risk of taking antipsychotic medications, many of which interact with KCNH2. So targeting this brain-specific form potentially opens the way to development of new treatments free of such cardiac side-effects.
• Dramatically changed activity in rodent brains toward a neuronal firing pattern that may be important for thinking and memory tasks unique to primates.
• Is expressed much more prior to birth, compared to the other main form of KCNH2, suggesting that it plays a prominent role in the early stages of brain development.
• Is associated with a hotspot of variation in an area that controls gene expression, hinting that the suspect variations may contribute to schizophrenia risk by over-expressing Isoform 3.1.

Even though it is normally important for our higher order executive functioning, such over expression of Isoform 3.1 in schizophrenia could result in “abnormally increased neuronal excitability, runaway circuit activity and inefficient information processing,” suggested Stephen Huffaker, Ph.D., the article’s lead author, now a medical student at Harvard. The researchers propose that a treatment designed to inhibit just Isoform 3.1, might spare any heart-related side effects while improving the disorganized neural firing characteristic of the brain in schizophrenia.

In addition to the NIMH, researchers from the NIH’s National Institute on Child Health and Human Development (NICHD) also participated in the research.

Reference:

A primate-specific, brain isoform of KCNH2 affects cortical physiology, cognition, neuronal repolarization and risk of schizophrenia. Huffaker SJ, Chen J, Nicodemus KK, Sambataro F, Yang F, Mattay V, Lipska BK, Hyde TM, Song J, Rujescu D, Giegling I, Mayilyan K, Proust MJ, Soghoyan A, Caforio G, Callicott JH, Bertolino A, Meyer-Lindenberg A, Chang J, Ji Y, Egan MF, Goldberg TE, Kleinman JE, Lu B, Weinberger DR.Nat Med. 2009 May 3.

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MEMORY GROWS LESS EFFICIENT VERY EARLY IN ALZHEIMER’S DISEASE

When learning new things, people with emerging symptoms find it harder to separate what’s important from what’s not

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WASHINGTON—Even very early in Alzheimer’s disease, people become less efficient at separating important from less important information, a new study has found.

Knowing this, clinicians may be able to train people in the early stages of Alzheimer’s to remember high-value information better, according to a report in the May issue of Neuropsychology, published by the American Psychological Association.

Remembering what’s most important is central to daily life. For example, if you went to the grocery store but left your shopping list at home, you’d at least want to remember the milk and bread, if not the jam. Or, when packing for a trip, you’d want to remember your wallet and tickets more than your slippers or belt.

Participants in the study were recruited from the Washington University in St. Louis Alzheimer’s Disease Research Center. They included 109 healthy older adults (average age of almost 75), 41 people with very mild (very early) Alzheimer’s disease (average age of almost 76), 13 people with mild (early) Alzheimer’s (average age of almost 77), and 35 younger adults (all 25 or under, average age of almost 20).

The researchers asked participants to study and learn neutral words that were randomly assigned different point values. When asked to recall the items, participants were asked to maximize the total value. All participants, even those with Alzheimer’s, recalled more high-value than low-value items. However, the Alzheimer’s groups were significantly less efficient than their healthy age peers at remembering items according to their value. It meant they no longer maximized learning and memory, which in healthy people are fairly efficient processes.

The authors speculated that Alzheimer’s disease makes it harder for people to encode what they learn in a strategic way. Because encoding is the first step in long-term memory, this affects their ability to remember things according to their value.

The findings also demonstrate that value-directed learning stays intact in healthy aging. Older adults might not remember as much as younger adults, but when healthy, they remain able to distinguish what’s important.

This research suggests the potential for improved memory training. People with early-stage Alzheimer’s might remember important information better by learning to be more strategic and selective when encoding high-value information, even though it comes at the expense of neglecting less-important information, the authors said.

Article: “Memory Efficiency and the Strategic Control of Attention at Encoding: Impairments of Value-Directed Remembering in Alzheimer’s Disease,” Alan D. Castel, PhD, University of California, Los Angeles; David A. Balota, PhD, Washington University in St. Louis; and David P. McCabe, PhD, Colorado State University; Neuropsychology, Vol. 23, No. 3.

(Full text of the article is available from the APA Public Affairs Office and at http://www.apa.org/journals/releases/neu233297.pdf)

Alan Castel can be reached by by e-mail or by phone at (310) 206-9262 or cell (310) 254-6555.