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Authors

Deborah Blacker

Summary

In this month’s issue, the article by Hanson and colleagues makes a serious effort to understand whether dietary factors can affect the biology of Alzheimer disease (AD). Although their sample size is small and their analyses complex, the answer [...]]]> Deborah Blacker. Food for Thought. JAMA Neurol., 2013 DOI: 10.1001/jamaneurol.2013.3288

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Authors

Deborah Blacker

Summary

In this month’s issue, the article by Hanson and colleagues makes a serious effort to understand whether dietary factors can affect the biology of Alzheimer disease (AD). Although their sample size is small and their analyses complex, the answer is a very tentative “yes.” More interestingly, the authors also ask how this effect might occur, and their preliminary findings provide some tantalizing food for thought.

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Authors

Olumide A. Olulade, Eileen M. Napoliello, Guinevere F. Eden

Summary

Developmental dyslexia is a reading disorder, yet deficits also manifest in the magnocellular-dominated dorsal visual system. Uncertainty about whether [...]]]> Olumide A. Olulade, Eileen M. Napoliello, Guinevere F. Eden. Abnormal Visual Motion Processing Is Not a Cause of Dyslexia. Neuron, 2013; DOI: 10.1016/j.neuron.2013.05.002

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Authors

Olumide A. Olulade, Eileen M. Napoliello, Guinevere F. Eden

Summary

Developmental dyslexia is a reading disorder, yet deficits also manifest in the magnocellular-dominated dorsal visual system. Uncertainty about whether visual deficits are causal or consequential to reading disability encumbers accurate identification and appropriate treatment of this common learning disability. Using fMRI, we demonstrate in typical readers a relationship between reading ability and activity in area V5/MT during visual motion processing and, as expected, also found lower V5/MT activity for dyslexic children compared to age-matched controls. However, when dyslexics were matched to younger controls on reading ability, no differences emerged, suggesting that weakness in V5/MT may not be causal to dyslexia. To further test for causality, dyslexics underwent a phonological-based reading intervention. Surprisingly, V5/MT activity increased along with intervention-driven reading gains, demonstrating that activity here is mobilized through reading. Our results provide strong evidence that visual magnocellular dysfunction is not causal to dyslexia but may instead be consequential to impoverished reading.

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Authors

Gloria K. Mak, Michael C. Antle, Richard H. Dyck, Samuel Weiss

Abstract

Early life events can modulate brain development to produce persistent [...]]]> Mak GK, Antle MC, Dyck RH, Weiss S (2013) Bi-Parental Care Contributes to Sexually Dimorphic Neural Cell Genesis in the Adult Mammalian Brain. PLoS ONE 8(5): e62701. doi:10.1371/journal.pone.0062701

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Authors

Gloria K. Mak, Michael C. Antle, Richard H. Dyck, Samuel Weiss

Abstract

Early life events can modulate brain development to produce persistent physiological and behavioural phenotypes that are transmissible across generations. However, whether neural precursor cells are altered by early life events, to produce persistent and transmissible behavioural changes, is unknown. Here, we show that bi-parental care, in early life, increases neural cell genesis in the adult rodent brain in a sexually dimorphic manner. Bi-parentally raised male mice display enhanced adult dentate gyrus neurogenesis, which improves hippocampal neurogenesis-dependent learning and memory.
Female mice display enhanced adult white matter oligodendrocyte production, which increases proficiency in bilateral motor coordination and preference for social investigation. Surprisingly, single parent-raised male and female offspring, whose fathers and mothers received bi-parental care, respectively, display a similar enhancement in adult neural cell genesis and phenotypic behaviour. Therefore, neural plasticity and behavioural effects due to bi-parental care persist throughout life and are transmitted to the next generation.

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Authors

Evan L. Thacker, Barbara McKnight, Bruce M. Psaty, W.T. Longstreth Jr, Colleen [...]]]> Evan L. Thacker, Barbara McKnight, Bruce M. Psaty, W.T. Longstreth Jr, Colleen M. Sitlani, Sascha Dublin, Alice M. Arnold, Annette L. Fitzpatrick, Rebecca F. Gottesman, and Susan R. Heckbert. Atrial fibrillation and cognitive decline. Neurology, June 5, 2013, doi: 10.1212/WNL.0b013e31829a33d1

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Authors

Evan L. Thacker, Barbara McKnight, Bruce M. Psaty, W.T. Longstreth Jr, Colleen M. Sitlani, Sascha Dublin, Alice M. Arnold, Annette L. Fitzpatrick, Rebecca F. Gottesman, and Susan R. Heckbert

Abstract

Objective
We sought to determine whether in the absence of clinical stroke, people with atrial fibrillation experience faster cognitive decline than people without atrial fibrillation.

Methods
We conducted a longitudinal analysis in the Cardiovascular Health Study, a community-based study of 5,888 men and women aged 65 years and older, enrolled in 1989/1990 or 1992/1993. Participants did not have atrial fibrillation or a history of stroke at baseline. Participants were censored when they experienced incident clinical stroke. Incident atrial fibrillation was identified by hospital discharge diagnosis codes and annual study ECGs. The main outcome was rate of decline in mean scores on the 100-point Modified Mini-Mental State Examination (3MSE), administered annually up to 9 times.

Results
Analyses included 5,150 participants, of whom 552 (10.7%) developed incident atrial fibrillation during a mean of 7 years of follow-up. Mean 3MSE scores declined faster after incident atrial fibrillation compared with no prior atrial fibrillation. For example, the predicted 5-year decline in mean 3MSE score from age 80 to age 85 was −6.4 points (95% confidence interval [CI]: −7.0, −5.9) for participants without a history of atrial fibrillation, but was −10.3 points (95% CI: −11.8, −8.9) for participants experiencing incident atrial fibrillation at age 80, a 5-year difference of −3.9 points (95% CI: −5.3, −2.5).

Conclusions
In the absence of clinical stroke, people with incident atrial fibrillation are likely to reach thresholds of cognitive impairment or dementia at earlier ages than people with no history of atrial fibrillation.

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Authors

Robert A. Bartona and Chris Venditti

Abstract

One of the most pervasive assumptions about human brain evolution is that it involved relative enlargement of the frontal lobes. We show that this assumption is [...]]]> Robert A. Barton and Chris Venditti. Human frontal lobes are not relatively large. PNAS, May 13, 2013 DOI: 10.1073/pnas.1215723110

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Authors

Robert A. Bartona and Chris Venditti

Abstract

One of the most pervasive assumptions about human brain evolution is that it involved relative enlargement of the frontal lobes. We show that this assumption is without foundation. Analysis of five independent data sets using correctly scaled measures and phylogenetic methods reveals that the size of human frontal lobes, and of specific frontal regions, is as expected relative to the size of other brain structures. Recent claims for relative enlargement of human frontal white matter volume, and for relative enlargement shared by all great apes, seem to be mistaken. Furthermore, using a recently developed method for detecting shifts in evolutionary rates, we find that the rate of change in relative frontal cortex volume along the phylogenetic branch leading to humans was unremarkable and that other branches showed significantly faster rates of change. Although absolute and proportional frontal region size increased rapidly in humans, this change was tightly correlated with corresponding size increases in other areas and whole brain size, and with decreases in frontal neuron densities. The search for the neural basis of human cognitive uniqueness should therefore focus less on the frontal lobes in isolation and more on distributed neural networks.

Tazu Aoki, Masae Kinoshita, Ryo Aoki, Masakazu Agetsuma, Hidenori Aizawa, Masako Yamazaki, Mikako Takahoko, Ryunosuke Amo, Akiko Arata, Shin-ichi Higashijima, Takashi Tsuboi, Hitoshi Okamoto. Imaging of [...]]]> Researchers from the RIKEN Brain Science Institute have visualized for the first time how information stored as long-term memory in the cerebral cortex is processed to guide behavioral choices.

Tazu Aoki, Masae Kinoshita, Ryo Aoki, Masakazu Agetsuma, Hidenori Aizawa, Masako Yamazaki, Mikako Takahoko, Ryunosuke Amo, Akiko Arata, Shin-ichi Higashijima, Takashi Tsuboi, Hitoshi Okamoto. Imaging of Neural Ensemble for the Retrieval of a Learned Behavioral Program. Neuron, 2013; DOI: 10.1016/j.neuron.2013.04.009

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Authors

Tazu Aoki, Masae Kinoshita, Ryo Aoki, Masakazu Agetsuma, Hidenori Aizawa, Masako Yamazaki, Mikako Takahoko, Ryunosuke Amo, Akiko Arata, Shin-ichi Higashijima, Takashi Tsuboi, Hitoshi Okamoto

Summary

The encoding of long-term associative memories for learned behaviors is a fundamental brain function. Yet, how behavior is stably consolidated and retrieved in the vertebrate cortex is poorly understood. We trained zebrafish in aversive reinforcement learning and measured calcium signals across their entire brain during retrieval of the learned response. A discrete area of dorsal telencephalon that was inactive immediately after training became active the next day. Analysis of the identified area indicated that it was specific and essential for long-term memory retrieval and contained electrophysiological responses entrained to the learning stimulus. When the behavioral rule changed, a rapid spatial shift in the functional map across the telencephalon was observed. These results demonstrate that the retrieval of long-term memories for learned behaviors can be studied at the whole-brain scale in behaving zebrafish in vivo. Moreover, the findings indicate that consolidated memory traces can be rapidly modified during reinforcement learning.

Kuhl PK, Coffey-Corina S, Padden D, Munson J, Estes A, et al. (2013) Brain Responses to Words in 2-Year-Olds with Autism Predict Developmental Outcomes at Age 6. PLoS ONE 8(5): e64967. doi:10.1371/journal.pone.0064967

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Patricia K. Kuhl, Sharon Coffey-Corina, [...]]]> Here’s the link to an article about predicting developmental outcomes in children with autism.

Kuhl PK, Coffey-Corina S, Padden D, Munson J, Estes A, et al. (2013) Brain Responses to Words in 2-Year-Olds with Autism Predict Developmental Outcomes at Age 6. PLoS ONE 8(5): e64967. doi:10.1371/journal.pone.0064967

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Authors

Patricia K. Kuhl, Sharon Coffey-Corina, Denise Padden, Jeffrey Munson, Annette Estes, Geraldine Dawson

Abstract

Autism Spectrum Disorder (ASD) is a developmental disability that affects social behavior and language acquisition. ASD exhibits great variability in outcomes, with some individuals remaining nonverbal and others exhibiting average or above average function. Cognitive ability contributes to heterogeneity in autism and serves as a modest predictor of later function.
We show that a brain measure (event-related potentials, ERPs) of word processing in children with ASD, assessed at the age of 2 years (N = 24), is a broad and robust predictor of receptive language, cognitive ability, and adaptive behavior at ages 4 and 6 years, regardless of the form of intensive clinical treatment during the intervening years. The predictive strength of this brain measure increases over time, and exceeds the predictive strength of a measure of cognitive ability, used here for comparison. These findings have theoretical implications and may eventually lead to neural measures that allow early prediction of developmental outcomes as well as more individually tailored clinical interventions, with the potential for greater effectiveness in treating children with ASD.

Jaekel J, Baumann N, Wolke D (2013) Effects of Gestational Age at Birth on Cognitive Performance: A Function of Cognitive Workload Demands. PLoS ONE 8(5): e65219. doi:10.1371/journal.pone.0065219

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Authors

Julia Jaekel, Nicole Baumann, Dieter Wolke

Abstract

Objective

Cognitive deficits have been inconsistently described for late or [...]]]> A very interesting publication about preterm children.

Jaekel J, Baumann N, Wolke D (2013) Effects of Gestational Age at Birth on Cognitive Performance: A Function of Cognitive Workload Demands. PLoS ONE 8(5): e65219. doi:10.1371/journal.pone.0065219

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Authors

Julia Jaekel, Nicole Baumann, Dieter Wolke

Abstract

Objective

Cognitive deficits have been inconsistently described for late or moderately preterm children but are consistently found in very preterm children. This study investigates the association between cognitive workload demands of tasks and cognitive performance in relation to gestational age at birth.

Methods

Data were collected as part of a prospective geographically defined whole-population study of neonatal at-risk children in Southern Bavaria. At 8;5 years, n = 1326 children (gestation range: 23–41 weeks) were assessed with the K-ABC and a Mathematics Test.

Results

Cognitive scores of preterm children decreased as cognitive workload demands of tasks increased. The relationship between gestation and task workload was curvilinear and more pronounced the higher the cognitive workload: GA2 (quadratic term) on low cognitive workload: R2 = .02, p<0.001; moderate cognitive workload: R2 = .09, p<0.001; and high cognitive workload tasks: R2 = .14, p

Conclusions

The cognitive workload model may help to explain variations of findings on the relationship of gestational age with cognitive performance in the literature. The findings have implications for routine cognitive follow-up, educational intervention, and basic research into neuro-plasticity and brain reorganization after preterm birth.