Fragile X

Older news items (pre-2010) brought over from the old website

New method of scoring IQ tests for fragile X children

IQ tests can tell us little about the learning abilities of children with intellectual disabilities, as parents of such children know only too well. So it’s exciting to learn that a new system of scoring IQ tests has been devised for children with fragile X syndrome. This new test reflects the variability evident among learning disabled children, and tells parents, teachers and doctors how a child with fragile x syndrome deviates from the normal population in every sub-test area. The researchers also found a significant correlation between the scores and the level of FMR1 protein in the blood (the protein expressed by the normal variant of the so-called fragile X gene), and between the IQ test scores and scores on the Vineland Adaptive Behavior Composite, which measures personal and social skills used in everyday living.

[886] Reiss, A. L., Hall S., Hessl D., Nguyen D. V., Green C., Chavez A., et al.
(2009).  A solution to limitations of cognitive testing in children with intellectual disabilities: the case of fragile X syndrome.
Journal of Neurodevelopmental Disorders. 1(1), 33 - 45.

Acne drug may help those with Fragile X syndrome

A new mouse study has found that a readily available drug called minocycline, used widely to treat acne and skin infections, helps Fragile X syndrome. Human trials have already been approved. The study has revealed that dendritic spine development is impaired in mice with Fragile X, and that this drug reduces levels of the enzymes interfering with their healthy development. The mice showed healthier dendritic spines, reduced anxiety, and improved cognition.

[863] Bilousova, T. V., Dansie L., Ngo M., Aye J., Charles J. R., Ethell D. W., et al.
(2009).  Minocycline promotes dendritic spine maturation and improves behavioural performance in the fragile X mouse model.
Journal of Medical Genetics. 46(2), 94 - 102.

Fragile X retardation syndrome corrected in mice

In another study targeting the glutamate receptor mGluR5, researchers have fixed multiple defects in fragile X mice by reducing these receptors by 50%. They achieved this through genetic engineering, but drugs blocking mGluR5 receptors are now entering human clinical trials. Fragile X is the most common form of inherited mental retardation and a leading identified genetic cause of autism.

[1306] Dölen, Gül, Osterweil E., Rao S. B. S., Smith G. B., Auerbach B. D., Chattarji S., et al.
(2007).  Correction of Fragile X Syndrome in Mice.
Neuron. 56(6), 955 - 962.

Mouse study points to new therapy for Fragile X sufferers

A mouse study has found evidence that fragile X mutation produces a highly selective impairment to long-term potentiation in hippocampal cells, and that adding brain-derived neurotrophic factor (BNDF) proteins to the hippocampus restored it.

[1064] Lauterborn, J. C., Rex C. S., Kramar E., Chen L. Y., Pandyarajan V., Lynch G., et al.
(2007).  Brain-Derived Neurotrophic Factor Rescues Synaptic Plasticity in a Mouse Model of Fragile X Syndrome.
J. Neurosci.. 27(40), 10685 - 10694.

Fundamental defect in fragile X syndrome identified and corrected

In an exciting new cell study, scientists have not only discovered the fundamental defect that causes fragile X syndrome (the most common inherited form of mental retardation), but also how to correct the problem. It is hoped that this will eventually lead to the development of human therapies for this previously untreatable condition.

[647] Nakamoto, M., Nalavadi V., Epstein M. P., Narayanan U., Bassell G. J., & Warren S. T.
(2007).  Fragile X mental retardation protein deficiency leads to excessive mGluR5-dependent internalization of AMPA receptors.
Proceedings of the National Academy of Sciences. 104(39), 15537 - 15542.

Fragile X syndrome -- A stimulating environment restores neuronal function in mice

Mice in which the gene that causes Fragile X syndrome —- the most common form of inherited mental retardation — in humans had been knocked out, showed reduced long-term potentiation in neurons due to abnormalities in the channels that regulate the flow of calcium into neurons. Excitingly, exposure to an enriched environment restored normal neuronal plasticity, suggesting that mechanisms for synaptic plasticity are in place, they just require stronger neuronal activity to be triggered.

[638] Meredith, R. M., Holmgren C. D., Weidum M., Burnashev N., & Mansvelder H. D.
(2007).  Increased Threshold for Spike-Timing-Dependent Plasticity Is Caused by Unreliable Calcium Signaling in Mice Lacking Fragile X Gene Fmr1.
Neuron. 54(4), 627 - 638.

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Dyslexia Therapy

Older news items (pre-2010) brought over from the old website

Remedial reading program improves brain wiring in children

An imaging study involving 72 children aged 8 to 10 has provided the first evidence that intensive instruction to improve reading skills in young children causes the brain to physically rewire itself. The study found that the ability of white matter tracts to transmit signals efficiently improved substantially after the children received six months (100 hours) of remedial training. Moreover, those who showed the most white matter change also showed the most improvement in reading ability. Previous research has found that both children and adults with reading difficulty display areas of compromised white matter.

[963] Keller, T. A., & Just M A.
(2009).  Altering Cortical Connectivity: Remediation-Induced Changes in the White Matter of Poor Readers.
Neuron. 64(5), 624 - 631.

Pre-school exercises can prevent dyslexia

A study comparing 107 children with either parent dyslexic and a control group of children without a hereditary predisposition to dyslexia has found that half the children with a dyslexic parent found learning to read more challenging than children in the control group. The predictors of reading and writing difficulties were evident primarily in two contexts: as a delayed ability to perceive and mentally process the subtleties of speech sound, and as a sluggishness in naming familiar, visually presented objects. The difficulties children experience when learning to read can be significantly reduced through training, and the CoE in Learning and Motivation Research has developed computer game-like learning environments to aid preventive training, and made them available on the internet free of charge. It’s recommended that the child start these exercises before school, if possible.  The exercises and tools are all available at

The results were presented at the Academy of Finland's science breakfast on 21 August.

Remedial instruction can close gap between good, poor readers

A brain imaging study of poor readers has found that 100 hours of remedial instruction not only improved the skills of struggling readers, but also changed the way their brains activated when they comprehended written sentences. 25 fifth-graders who were poor readers worked in groups of three for an hour a day with a reading "personal trainer," a teacher specialized in administering a remedial reading program. The training included both word decoding exercises in which students were asked to recognize the word in its written form and tasks in using reading comprehension strategies. Brain scans while the children were reading revealed that the parietotemporal region — responsible for decoding the sounds of written language and assembling them into words and phrases that make up a sentence — was significantly less activated among the poor readers than in the control group. The increases in activation seen as a result of training were still evident, and even greater, a year later.
Although dyslexia is generally thought of as caused by difficulties in the visual perception of letters, leading to confusions between letters like "p" and "d", such difficulties occur in only about 10% of the cases. Most commonly, the problem lies in relating the visual form of a letter to its sound.

[702] Meyler, A., Keller T. A., Cherkassky V. L., Gabrieli J. D. E., & Just M A.
(2008).  Modifying the brain activation of poor readers during sentence comprehension with extended remedial instruction: A longitudinal study of neuroplasticity.
Neuropsychologia. 46(10), 2580 - 2592.

Having right timing 'connections' in brain is key to overcoming dyslexia

New research has found that key areas for language and working memory involved in reading are connected differently in dyslexics than in children who are good readers and spellers. But, after the children with dyslexia went through a three-week instructional program, their patterns of functional brain connectivity normalized and were similar to those of good readers. The study looked specifically at activity in the left and right inferior front gyrus. The left inferior front gyrus may control the communication between the different areas involved in language, especially spoken language, while the right is thought to be involved in controlling the processing of letters in written words. Prior to the treatment these two areas were overconnected in the dyslexics, and the left inferior frontal gyrus also was overconnected to the middle frontal gyrus, which is involved in working memory that requires temporal coordination. It is not yet known how long the improvement in connectivity is maintained.

[844] Richards, T. L., & Berninger V. W.
(2008).  Abnormal fMRI Connectivity in Children with Dyslexia During a Phoneme Task: Before But Not After Treatment.
Journal of neurolinguistics. 21(4), 294 - 304.

New insight into brain and speech promises help for learning disabilities

Following a new understanding of the nature of certain language dysfunctions, researchers have devised a new non-invasive diagnostic tool called BioMAP that can quickly identify children with a subset of learning disabilities that results from a dysfunction in the way the brainstem encodes certain basic sounds of speech. Such children accounted for nearly a third of the language-disordered children the researchers studied. BioMAP measures whether a child's nervous system can accurately translate a sound wave into a brain wave. If it cannot, the affected individual demonstrates problems in discriminating speech sounds that interfere with normal learning. Once identified, children with these problems will be able to improve their speech discrimination skills through auditory training.

[789] Kraus, N., & Nicol T.
(2005).  Brainstem origins for cortical 'what' and 'where' pathways in the auditory system.
Trends in Neurosciences. 28(4), 176 - 181.

Promise for helping adults with dyslexia

Recent studies have demonstrated that children with dyslexia can benefit from programs aimed at “retraining” the brain. Now a new study shows that adults with dyslexia can also benefit from tutoring in processing words, and their brains show changes that indicate neural modifications due to the training.

[454] Eden, G. F., Jones K. M., Cappell K., Gareau L., Wood F. B., Zeffiro T. A., et al.
(2004).  Neural Changes following Remediation in Adult Developmental Dyslexia.
Neuron. 44(3), 411 - 422.

Immature motion pathways in the brain associated with poor reading skills

An interactive computer game called MovingToRead (MTR) has significantly improved reading skills in poor second-grade readers within three months by practicing left-right movement discrimination for 5 to 10 minutes once or twice a week. It has been suggested that immature motion pathways — the circuit of neurons that helps readers determine the location of letters of a word and words on a page — may be related to reading problems in children. The therapy appears to be most effective with second-graders (age 7).

Short-term dyslexia treatment strengthens key brain regions

A group of dyslexic children and a group of good readers of the same age underwent functional magnetic resonance imaging (fMRI) to map their brain activation patterns during two types of reading tests. Both groups of children were found to use the same specific parts of their brains to perform the reading tasks, however, the activation of these regions was much weaker in the dyslexic children. The children with dyslexia then received a three-week training program based on principles outlined by the National Reading Panel ( After this program the levels of brain activation were found to be essentially the same in the two groups.

[261] Aylward, E. H., Richards T. L., Berninger V. W., Nagy W. E., Field K. M., Grimme A. C., et al.
(2003).  Instructional treatment associated with changes in brain activation in children with dyslexia.
Neurology. 61(2), 212 - 219.
More background on dyslexia including initial steps toward identifying it in a child, how it may be treated, and additional resources can be found in Neurology's "Patient Page" at

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Older news items (pre-2010) brought over from the old website

Pollutants affect babies' brains

It appears that exposure to polychlorinated biphenyls (PCBs) in a mother's blood and breast milk can hinder the development of a baby's brain before and after birth. Although PCBs are now banned, these chemicals were once widely used in industry as coolants and lubricants and are still being leaked into the environment from old electrical equipment.

[591] Walkowiak, J., Wiener J. A., Fastabend A., Heinzow B., Krämer U., Schmidt E., et al.
(2001).  Environmental exposure to polychlorinated biphenyls and quality of the home environment: effects on psychodevelopment in early childhood.
Lancet. 358(9293), 1602 - 1607.

PCB-laden fish may affect adult verbal memory

The dangers of PCBs (once widely used as electrical insulators and lubricants and in paints and varnishes) have long been known, and assumed to apply chiefly to children and developing fetuses. A long-term study of those who eat the PCB-laden fish from Lake Michigan suggests for the first time that high levels of PCB may cause problems learning and remembering new verbal information in adults. In particular, those with high blood PCB levels had difficulties recalling a story told just 30 minutes earlier, and were less likely than their less-exposed peers to cluster words given orally into categories based on their meaning to boost recall.

Schantz, S.L., Gasior, D.M., Polverejan, E., McCaffrey, R.J., Sweeney, A.M., Humphrey, H.E.B. & Gardiner, J.C. 2001. Impairments of Memory and Learning in Older Adults Exposed to Polychlorinated Biphenyls via Consumption of Great Lakes Fish. Environmental Health Perspectives, 109 (6), 605.

How chronic exposure to solvents can impair the brain

Chronic occupational exposure to organic solvents, found in materials such as paints, printing and dry cleaning agents, has been linked to long-term cognitive impairment, but chronic solvent-induced encephalopathy (CSE) is still a controversial diagnosis. An imaging study of 10 CSE patients who had been exposed to solvents and had mild to severe cognitive impairment, 10 participants who had been exposed to solvents but had no CSE symptoms, and 11 participants who were not exposed to solvents and had no symptoms, has now found impairment in the frontal-striatal-thalamic (FST) circuitry of CSE patients. The disturbances are predictive of the clinical findings — impaired psychomotor speed and attention — and were also linked to exposure severity.

[989] van Dijk, F. J. H., Schene A. H., Heeten G D. J., Visser I., Lavini C., Booij J., et al.
(2008).  Cerebral impairment in chronic solvent-induced encephalopathy.
Annals of Neurology. 63(5), 572 - 580.

Chemical in clear plastics can impair learning

A rat study has found that low doses of the environmental contaminant bisphenol–A (BPA), widely used to make many plastics found in food storage containers (including feeding bottles for infants), inhibit estrogen–induction of synaptic connections in the hippocampus, suggesting implications for children's learning ability. Also, when the ability to make estrogen is impaired, as in old age, exposure to BPA could adversely affect hippocampal function and contribute to age–related neurodegenerative diseases such as Alzheimer's disease, in which hippocampal function is impaired. The doses were below the current U.S. Environmental Protection Agency reference daily limit for human exposure.

[740] MacLusky, N. J., Hajszan T., & Leranth C.
(2005).  The Environmental Estrogen Bisphenol A Inhibits Estradiol-Induced Hippocampal Synaptogenesis.
Environmental Health Perspectives. 113(6), 675 - 679.


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Inflammation in Alzheimer's

Older news items (pre-2010) brought over from the old website

Evidence challenges inflammation theory for Alzheimer's

Although it has long been theorized that inflammation plays a role in the development of Alzheimer’s, repeated studies have failed to find consistent evidence that anti-inflammatory drugs are helpful. Now a brain tissue study reveals that supporting brain cells called microglia are not activated in the presence of tau tangles in the brains of Alzheimer’s patients, as has been predicted, and as would be the case if there were inflammation. Instead, microglia are degenerating. It’s suggested that it is this loss of microglia that contributes to the loss of neurons, and thus to the development of dementia. The next step is to find out why the microglia are dying.

Streit, W.J. et al. 2009. Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in Alzheimer’s disease. Acta Neuropathologica, Published online ahead of print.

Blood inflammation plays role in Alzheimer's disease

Data from the Framingham Heart Study has found that those with the highest amount of cytokines (protein messengers that trigger inflammation) in their blood were more than twice as likely to develop Alzheimer's disease as those with the lowest amount of cytokines, providing further evidence that inflammation plays a role in the development of Alzheimer's disease.

Tan, Z.S. et al. 2007. Inflammatory markers and the risk of Alzheimer disease: The Framingham Study. Neurology, 68, 1902-1908.

Alzheimer's disease linked to early inflammation

A new study of dementia in identical twins suggests that exposure to inflammation early in life quadruples one's risk of developing Alzheimer's disease. The study involved sifting the 20,000 participants in the Swedish Twin Registry for the 109 "discordant" pairs where only one twin had been diagnosed with dementia. Answers to health questions in the survey enabled the researchers to build a crude indicator of periodontal disease, measured indirectly by teeth lost or loose. Because this is not a direct measure of inflammation, the results need to be confirmed, but they do suggest that an inflammatory burden early in life, as represented by chronic gum disease, may have severe consequences later. The study also found that mental activities at age 40 did not seem to lower the risk of developing Alzheimer's, and the level of education was not a large factor once genes were taken into account (nevertheless, those with less high school and college education had 1.6 times the risk of dementia). Previous studies have shown that Alzheimer's is strongly genetic: If one twin has the disease, his or her identical twin has a 60% chance of developing it.

The study was presented at the first Alzheimer's Association International Conference on Prevention of Dementia, to be held June 18-21 in Washington, D.C.

Antibody detection in Alzheimer's may improve diagnosis, treatment

A study has found that people with Alzheimer’s disease have three to four times more antibodies to RAGE (receptor for advanced glycation end products) and beta amyloid — both major players in Alzheimer’s — than their healthy counterparts. The ability to measure these specific antibody levels could lead to a method for very early diagnosis. The finding may also point to a new treatment approach. The study supports the theory that autoimmunity and resulting inflammation play a big role in Alzheimer’s.

Mruthinti, S., Buccafusco, J.J., Hill, W.D., Waller, J.L., Jackson, T.W., Zamrini, E.Y. & Schade, R.F. 2004. Autoimmunity in Alzheimer’s disease: increased levels of circulating IgGs binding Ab and RAGE peptides. Neurobiology of Aging, 25 (8), 1023-1032.

A new hypothesis about Alzheimer's

A new theory about the cause of Alzheimer's disease has been proposed. According to this theory, Alzheimer’s arises as a consequence of inflammation, which creates abnormal metabolites out of normal brain molecules. These abnormal metabolites then modify "amyloid beta" proteins in the brain and cause them to misfold, thus accumulating into the fibrils and plaques characteristic of the disease. The inflammation process that creates these metabolites can be triggered by numerous stimuli, including infections that precede the onset of Alzheimer's disease by a significant amount of time — perhaps years. Traumatic head injuries, for example, are a major risk factor for later developing Alzheimer's disease. Inflammation is increasingly seen as playing a role in neurodegenerative diseases.

Zhang, Q., Powers, E.T., Nieva, J., Huff, M.E., Dendle, M.A., Bieschke, J., Glabe, C.G., Eschenmoser, A., Wentworth, P.Jr., Lerner, R.A. & Kelly, J.W. 2004. Metabolite-initiated protein misfolding may trigger Alzheimer's disease. Proceedings of the National Academy of Sciences, 101 (14), 4752-7.

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Some interesting articles on the topic:

Crux of Schizophrenia’s Emotional and Social Deficits May Be Cognitive

Good article on the experience of schizophrenia

Our understanding of schizophrenia

Article in the journal Nature

News in brief

Schizophrenia patients' ability to monitor reality may be helped by computerized training

Schizophrenia patients who received 80 hours of computerized training over the course of 16 weeks became better at performing complex tasks that required them to distinguish their internal thoughts from reality.. This improvement coincided with increased activation in a key part of the brain: the medial prefrontal cortex.

Greater activation within the medial prefrontal cortex was also linked with better social functioning six months after training.

31 patients with schizophrenia and 15 healthy controls were involved in the study.

Brain activity linked to delusion-like experience

Support for a theory that the overactive firing of dopamine neurons in specific brain regions is involved in converting neutral, external information into personally relevant information among people with schizophrenia, comes from a brain scan study.

The study involved 14 people with a schizophrenia diagnosis and 15 controls.

Those with schizophrenia were significantly more likely to say that generic statements referred to them. Brain activity suggested they had greater difficulty in distinguishing what was self-relevant to what was not.

Once these processes are better understood, approaches such as attentional retraining therapy may be explored as possible treatments of delusions.

More clues in the genetics of schizophrenia

Two of the largest studies yet carried out on the genetics of schizophrenia in Chinese populations have turned up three genetic loci, or chromosomal regions, previously not known to be related to the disease.

Mutations not inherited from parents cause more than half the cases of schizophrenia

Following on from earlier studies showing that a rare de novo mutation accounts for 1-2% of sporadic (non-hereditary) cases of schizophrenia, study of the human genome has found 40 new (not inherited) mutations, all from different genes and most of them protein-altering, involved in more than half the cases of sporadic schizophrenia.

The potentially large number of mutations makes a gene-therapy approach to treating schizophrenia unlikely. Researchers suspect, however, that all of the mutations affect the same neural circuitry mechanisms.

The study's results also help to explain two puzzles: the persistence of schizophrenia, despite the fact that those with the disease do not tend to pass down their mutations through children; and the high global incidence of the disease, despite large environmental variations.

Brain development goes off track as vulnerable individuals develop schizophrenia

Two new research studies point to progressive abnormalities in brain development that emerge during adolescence as at-risk individuals develop schizophrenia.

Role of DISC1 gene in schizophrenia clarified

The Disrupted In Schizophrenia gene (DISC1) and its protein product plays many distinct roles in the development and functioning of the brain, including regulation of new neuron production in the cerebral cortex, and the programmed migration of these neurons.

New research has found a molecular switch that regulates this protein. If it malfunctions, the brain may not develop properly.

It’s suggested that perhaps 10% of psychiatric illness is primarily driven by defects in this switch system.

Communication Breakdown in Brain Caused by a Gene Defect May Contribute to Schizophrenia

Nearly a third (30%) of those with a specific deletion on chromosome 22 develop schizophrenia, making it one of the largest genetic risk factors for the disorder. Mouse research now suggests that the gene defect produces a faulty connection between the hippocampus and the prefrontal cortex.

Cognition already seriously impaired in first episode of schizophrenia

A meta-analysis of 47 studies of first-episode schizophrenia suggest that 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.

Patients struggled the most with processing speed and with verbal learning and memory, especially when encoding information. Measured IQ and other cognitive abilities dropped the most between the high-risk period just before symptoms appear and the first acute phases.

Schizophrenia and Manic-depressive Disorder: Genetic Variant Impairs Communication Within Brain

A genetic variant that increases risk of schizophrenia, and also manic-depressive disorder, has been found to be associated with impaired communication between the two hemispheres of the dorsolateral prefrontal cortex.

In contrast, the link between the DLPFC and the hippocampus was improved, as were the connections between the amygdala and a number of other regions.

Autism and schizophrenia may reflect different variations in the same genes

Copy number variations in the same genes may determine whether individuals suffer from autism or schizophrenia, according to a review. The review identified seven genetic regions linked to both disorders, of which five were deleted in one disease and duplicated in the other.

Is schizophrenia our price for having a large brain?

Comparison of the brains of healthy and schizophrenic humans with chimpanzee and rhesus macaque brains indicates that expression levels of many genes and metabolites that are altered in schizophrenia, especially those related to energy metabolism, also changed rapidly during evolution.

It’s suggested that the human brain, which uses 20% of the body's total energy supply compared with about 13% for nonhuman primates, runs so close to the limit of its metabolic capabilities, that small changes in energy-related genes can cause mental problems.

The finding also confirms previous evidence that brain metabolism is substantially altered in schizophrenia.

Different use of brain areas may explain memory problems in schizophrenics

New research indicates that schizophrenics’ memory problems may be related to differences in how their brains process information. While both schizophrenic patients and healthy individuals used their frontal cortex while remembering and forgetting, healthy subjects used the right side when asked to remember spatial locations and schizophrenics used a wider network in both hemispheres. When healthy people were correct in their remembering, there was an increased activation of the right frontal cortex, an increase that didn’t occur when they couldn’t remember, and this was associated with a lack of confidence in their memory. However, schizophrenic patients showed an activation pattern on error trials indicating that they were remembering something, albeit incorrect. This was associated with a feeling of confidence about their memory.

Lee, J. et al. 2008. Origins of Spatial Working Memory Deficits in Schizophrenia: An Event-Related fMRI and Near-Infrared Spectroscopy Study. PLoS ONE, 3(3), e1760.

Full text at

Schizophrenia candidate genes affect even healthy individuals

A study of over 2000 healthy young men has found that those with several of the genetic variants linked to schizophrenia had small reductions in cognitive ability such as decreased attentional capacity and worse performance on memory tasks, as well as atypical experiences that might be associated with schizophrenia.

Brain function in schizophrenia can improve with support, holds promise for cognitive rehabilitation

A study shows how people with schizophrenia can be helped to remember information just as well as their healthy counterparts, as long as they are given proper cues and memory aids.

The study involved 17 schizophrenia patients and 26 healthy controls. Participants performed incidental encoding tasks of words and faces in response to instructions to make either deep (abstract/concrete) or shallow (alphabetization) judgments for words and deep (gender) judgments for faces, followed by subsequent recognition tests.

Both groups recognized significantly more words encoded deeply than shallowly, activated regions in the inferior frontal cortex, and showed greater left frontal activation for the processing of words compared with faces. However, during deep encoding and material-specific processing (words vs. faces), participants with schizophrenia activated regions not activated by controls, including several in prefrontal cortex.

The findings suggest that an important reason for cognitive deficits in those with schizophrenia is their failure to use everyday memory strategies.

Bonner-Jackson, A., Haut, K., Csernansky, J.G. & Barch, D.M. 2005. The Influence of Encoding Strategy on Episodic Memory and Cortical Activity in Schizophrenia. Biological Psychiatry, 58 (1), 47-55.

Scans link 2 key pieces of schizophrenia puzzle

Brain scans have linked two key, but until now unconnected, brain abnormalities in schizophrenia. They have shown that the less patients' frontal lobes activate during a working memory task, the more the chemical messenger dopamine, thought to underlie the delusions and hallucinations of schizophrenia, rises abnormally in the striatum. Given that dopamine activity in the striatum is under the control of the prefrontal cortex, this suggests that the excess dopamine activity that antipsychotic drugs quell may be driven by a defect in the prefrontal cortex.

Even tiny interruptions can double or treble work errors

January, 2013

A new study quantifies the degree to which tasks that involve actions in a precise sequence are vulnerable to interruptions.

In my book on remembering intentions, I spoke of how quickly and easily your thoughts can be derailed, leading to ‘action slips’ and, in the wrong circumstances, catastrophic mistakes. A new study shows how a 3-second interruption while doing a task doubled the rate of sequence errors, while a 4s one tripled it.

The study involved 300 people, who were asked to perform a series of ordered steps on the computer. The steps had to be performed in a specific sequence, mnemonically encapsulated by UNRAVEL, with each letter identifying the step. The task rules for each step differed, requiring the participant to mentally shift gears each time. Moreover, task elements could have multiple elements — for example, the letter U could signal the step, one of two possible responses for that step, or be a stimulus requiring a specific response when the step was N. Each step required the participant to choose between two possible responses based on one stimulus feature — features included whether it was a letter or a digit, whether it was underlined or italic, whether it was red or yellow, whether the character outside the outline box was above or below. There were also more cognitive features, such as whether the letter was near the beginning of the alphabet or not. The identifying mnemonic for the step was linked to the possible responses (e.g., N step – near or far; U step — underline or italic).

At various points, participants were very briefly interrupted. In the first experiment, they were asked to type four characters (letters or digits); in the second experiment, they were asked to type only two (a very brief interruption indeed!).

All of this was designed to set up a situation emulating “train of thought” operations, where correct performance depends on remembering where you are in the sequence, and on producing a situation where performance would have reasonably high proportion of errors — one of the problems with this type of research has been the use of routine tasks that are generally performed with a high degree of accuracy, thus generating only small amounts of error data for analysis.

In both experiments, interruptions significantly increased the rate of sequence errors on the first trial after the interruption (but not on subsequent ones). Nonsequence errors were not affected. In the first experiment (four-character interruption), the sequence error rate on the first trial after the interruption was 5.8%, compared to 1.8% on subsequent trials. In the second experiment (two-character interruption), it was 4.3%.

The four-character interruptions lasted an average of 4.36s, and the two-character interruptions lasted an average of 2.76s.

Whether the characters being typed were letters or digits made no difference, suggesting that the disruptive effects of interruptions are not overly sensitive to what’s being processed during the interruption (although of course these are not wildly different processes!).

The absence of effect on nonsequence errors shows that interruptions aren’t disrupting global attentional resources, but more specifically the placekeeping task.

As I discussed in my book, the step also made a significant difference — for sequence errors, middle steps showed higher error rates than end steps.

All of this confirms and quantifies how little it takes to derail us, and reminds us that, when engaged in tasks involving the precise sequence of sub-tasks (which so many tasks do), we need to be alert to the dangers of interruptions. This is, of course, particularly true for those working in life-critical areas, such as medicine.


[3207] Altmann, E. M., Gregory J., & Hambrick D. Z.
(2013).  Momentary Interruptions Can Derail the Train of Thought.
Journal of Experimental Psychology: General. No - Pagination Specified.



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Why acute stress makes it hard to think properly

October, 2012

A rat study indicates that acute stress disrupts feedback loops in the prefrontal cortex that may be keeping information alive in working memory.

Stress is a major cause of workplace accidents, and most of us are only too familiar with the effects of acute stress on our thinking. However, although the cognitive effects are only too clear, research has had little understanding of how stress has this effect. A new rat study sheds some light.

In the study, brain activity was monitored while five rats performed a working memory task during acute noise stress. Under these stressful conditions, the rats performed dramatically worse on their working memory task, with performance dropping from an average of 93% success to 65%.

The stress also significantly increased the discharge rate of a subset of neurons in the medial prefrontal cortex during two phases of the task: planning and assessment.

This brain region is vital for working memory and executive functions such as goal maintenance and emotion regulation. The results suggest that the firing and re-firing of these neurons keeps recent information ‘fresh’. When the re-firing is delayed, the information can be lost.

What seems to be happening is that the stress is causing these neurons to work even more furiously, but instead of performing their normal task — concentrating on keeping important information ‘alive’ during brief delays — they are reacting to all the other, distracting and less relevant, stimuli.

The findings contradict the view that stress simply suppresses prefrontal cortex activity, and suggests a different approach to treatment, one that emphasizes shutting out distractions.

The findings are also exciting from a theoretical viewpoint, suggesting as they do that this excitatory recursive activity of neurons within the prefrontal cortex provide the neural substrate for working memory. That is, that we ‘hold’ information in the front of our mind through reverberating feedback loops within this network of neurons, that keep information alive during the approximately 1.5 seconds of our working memory ‘span’.




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How stress affects your learning

October, 2012

A small study shows that stress makes it more likely for learning to use more complicated and subconscious processes that involve brain regions involved in habit and procedural learning.

We know that stress has a complicated relationship with learning, but in general its effect is negative, and part of that is due to stress producing anxious thoughts that clog up working memory. A new study adds another perspective to that.

The brain scanning study involved 60 young adults, of whom half were put under stress by having a hand immersed in ice-cold water for three minutes under the supervision of a somewhat unfriendly examiner, while the other group immersed their hand in warm water without such supervision (cortisol and blood pressure tests confirmed the stress difference).

About 25 minutes after this (cortisol reaches peak levels around 25 minutes after stress), participants’ brains were scanned while participants alternated between a classification task and a visual-motor control task. The classification task required them to look at cards with different symbols and learn to predict which combinations of cards announced rain and which sunshine. Afterward, they were given a short questionnaire to determine their knowledge of the task. The control task was similar but there were no learning demands (they looked at cards on the screen and made a simple perceptual decision).

In order to determine the strategy individuals used to do the classification task, ‘ideal’ performance was modeled for four possible strategies, of which two were ‘simple’ (based on single cues) and two ‘complex’ (based on multiple cues).

Here’s the interesting thing: while both groups were successful in learning the task, the two groups learned to do it in different ways. Far more of the non-stressed group activated the hippocampus to pursue a simple and deliberate strategy, focusing on individual symbols rather than combinations of symbols. The stressed group, on the other hand, were far more likely to use the striatum only, in a more complex and subconscious processing of symbol combinations.

The stressed group also remembered significantly fewer details of the classification task.

There was no difference between the groups on the (simple, perceptual) control task.

In other words, it seems that stress interferes with conscious, purposeful learning, causing the brain to fall back on more ‘primitive’ mechanisms that involve procedural learning. Striatum-based procedural learning is less flexible than hippocampus-based declarative learning.

Why should this happen? Well, the non-conscious procedural learning going on in the striatum is much less demanding of cognitive resources, freeing up your working memory to do something important — like worrying about the source of the stress.

Unfortunately, such learning will not become part of your more flexible declarative knowledge base.

The finding may have implications for stress disorders such as depression, addiction, and PTSD. It may also have relevance for a memory phenomenon known as “forgotten baby syndrome”, in which parents forget their babies in the car. This may be related to the use of non-declarative memory, because of the stress they are experiencing.


[3071] Schwabe, L., & Wolf O. T.
(2012).  Stress Modulates the Engagement of Multiple Memory Systems in Classification Learning.
The Journal of Neuroscience. 32(32), 11042 - 11049.



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Quick therapy may reduce post-traumatic stress when delivered immediately

July, 2012

A pilot study supports the value of brief cognitive therapy for victims of traumatic events, when delivered as soon as possible after the event. The benefit appears greatest for sexual assault victims.

A new study has found that, when delivered quickly, a modified form of prolonged exposure therapy reduces post-traumatic stress reactions and depression.

The study involved 137 patients being treated in the emergency room of a major trauma center in Atlanta. The patients were chosen from survivors of traumatic events such as rape, car or industrial accidents, and shooting or knife attacks. Participants were randomly assigned to either receive three sessions of therapy beginning in the emergency department (an average of 12 hours after the event), or assessment only. Stress reactions were assessed at 4 and 12 weeks, and depression at baseline and 4 weeks.

Those receiving the therapy reported significantly lower post-traumatic stress at 4 weeks and 12 weeks, and significantly lower depression at 4 weeks. Analysis of subgroups revealed that the therapy was most effective in rape victims. In the cases of transport accidents and physical (non-sexual) assault, the difference between therapy and assessment-only was only barely significant (for transport at 4 weeks) or non-significant. In both subgroups, the effect was decidedly less at 12 weeks than at 4 weeks.

The therapy, carried out by trained therapists, involved participants describing the trauma they had experienced while the therapist recorded the description. The bulk of the hour-long session was taken up with reliving and processing the experience. There were three sessions spaced a week apart. The patients were instructed to listen to their recordings every day, and 85% were compliant. The therapists also explained normal reactions to trauma, helped the patients look at obtrusive thoughts of guilt or responsibility, and taught them a brief breathing or relaxation technique and self care.

While this study doesn’t itself compare the effects of immediate vs delayed therapy, the assumption that delivering the therapy so soon after the trauma is a crucial factor in its success is in line with other research (mainly to do with fear-conditioning in rodent and human laboratory studies). Moreover, while brief cognitive-behavioral therapy has previously been shown to be effective with people diagnosed with acute stress disorder, such therapy is normally begun some 2-4 weeks after trauma, and a study of female assault survivors found that although such therapy did indeed accelerate recovery compared with supportive counseling, after 9 months, PTSD severity was similar in both groups.

Another, severe, limitation of this study is that the therapy involved multiple items. We cannot assume that it was the repeated re-experiencing of the event that is critical.

However, this study is only a pilot study, and its findings are instructive rather than decisive. But at the least it does support the idea that immediate therapy is likely to help victims of trauma recover more quickly.

One final, important, note: It should not, of course, be assumed that simply having the victim describe the events — say to police officers — is in itself therapeutic. Done badly, that experience may itself be traumatic.




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Older news items (pre-2010) brought over from the old website

Prenatal exposure to urban air pollutants affects cognitive development

A study of 183 three-year-old children of non-smoking African-American and Dominican women residing in New York City has found that exposure during pregnancy to combustion-related urban air pollutants (specifically, polycyclic aromatic hydrocarbons) was linked to significantly lower scores on mental development tests and more than double the risk of developmental delay at age three.

[1096] Camann, D., Kinney P., Perera F. P., Rauh V. A., Whyatt R. M., Tsai W-Y., et al.
(2006).  Effect of Prenatal Exposure to Airborne Polycyclic Aromatic Hydrocarbons on Neurodevelopment in the First 3 Years of Life among Inner-City Children.
Environmental Health Perspectives. 114(8), 1287 - 1292.

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Prenatal exposure to secondhand smoke increases risk of developmental delay

A new study funded by the National Institute of Environmental Health Sciences has found that children whose mothers are exposed during pregnancy to second-hand smoke have reduced scores on tests of cognitive development at age two, when compared to children from smoke-free homes. In addition, the children exposed to second-hand smoke during pregnancy are approximately twice as likely to have developmental scores below 80, which is indicative of developmental delay. These differences were magnified for children whose mothers lived in inadequate housing or had insufficient food or clothing during pregnancy. The combined effect results in a developmental deficit of about seven points in tests of cognitive performance.

Rauh, V.A., Whyatt, R.M., Garfinkel, R., Andrews, H., Hoepner, L., Reyes, A., Diaz, D., Camann, D. & Perera, F.P. 2004. Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children. Neurotoxicology and Teratology, 26 (3), 373-385.

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