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Cognitive defi cits are prevalent at the acute stage of stroke (Jaillard, Naegele, TrabuccoMiguel, LeBas, & Hommel, 2009). They interfere with the potential benefi ts of rehabilitation and affect recovery (Ballard et al., 2003; Barker-Collo & Feigin, 2006; de Haan, Nys, & van Zandvoort, 2006; Donovan et al., 2008; Edwards et al., 2006; Fure, Bruun Wyller, Engedal, & Thommessen, 2006; Narasimhalu et al., 2009; Nys et al., 2006; Pohjasvaara et al., 2000; Stephens et al., 2005; van Zandvoort, Kessels, Nys, de Haan, & Kappelle, 2005; Zinn et al., 2004). Moreover, cognitive defi cits are associated with a poorer quality of life (Moon, Kim, Kim, Won, & Kim, 2004; Nichols-Larsen, Clark, Zeringue, Greenspan, & Blanton, 2005; Paul et al., 2005) and depression (Kauhanen et al., 1999; Nys et al., 2006).
Bayesian mapping of the striatal microcircuit reveals robust asymmetries in the probabilities and distances of connections
ABSTRACTThe striatum’s complex microcircuit is made by connections within and between its D1- and D2-receptor expressing projection neurons and at least five species of interneuron. Precise knowledge of this circuit is likely essential to understanding striatum’s functional roles and its dysfunction in a wide range of movement and cognitive disorders. We introduce here a Bayesian approach to mapping neuron connectivity using intracellular recording data, which lets us simultaneously evaluate the probability of connection between neuron types, the strength of evidence for it, and its dependence on distance. Using it to synthesise a complete map of the rodent striatum, we find strong evidence for two asymmetries: a selective asymmetry of projection neuron connections, with D2 neurons connecting twice as densely to other projection neurons than do D1 neurons, but neither subtype preferentially connecting to another; and a length-scale asymmetry, with interneuron connection probabilities remaining non-negligible at more than twice the distance of projection neuron connections. We further show our Bayesian approach can evaluate evidence for wiring changes, using data from the developing striatum and a mouse model of Huntington’s disease. By quantifying the uncertainty in our knowledge of the microcircuit, our approach reveals a wide range of potential striatal wiring diagrams consistent with current data.
Visual motion and decision-making in dyslexia: Evidence of reduced accumulation of sensory evidence and related neural dynamics
AbstractChildren with and without dyslexia differ in their behavioural responses to visual information, particularly when required to pool dynamic signals over space and time. Importantly, multiple processes contribute to behavioural responses. Here we investigated which processing stages are affected in children with dyslexia when performing visual motion processing tasks, by combining two methods that are sensitive to the dynamic processes leading to responses. We used a diffusion model which decomposes response time and accuracy into distinct cognitive constructs, and high-density EEG. 50 children with dyslexia and 50 typically developing children aged 6 to 14 years judged the direction of motion as quickly and accurately as possible in two global motion tasks, which varied in their requirements for segregating signal-from-noise. Following our pre-registered analyses, we fitted hierarchical Bayesian diffusion models to the data, blinded to group membership. Unblinding revealed reduced evidence accumulation in children with dyslexia compared to typical children for both tasks. We also identified a response-locked EEG component which was maximal over centro-parietal electrodes which indicated a neural correlate of reduced drift-rate in dyslexia, thereby linking brain and behaviour. We suggest that children with dyslexia are slower to extract sensory evidence from global motion displays, regardless of whether they are required to segregate signal-from-noise, thus furthering our understanding of atypical perceptual decision-making processes in dyslexia.
Stage 2 Registered Report: Variation in neurodevelopmental outcomes in children with sex chromosome trisomies: testing the double hit hypothesis
Background: The presence of an extra sex chromosome is associated with an increased rate of neurodevelopmental difficulties involving language. The 'double hit' hypothesis proposes that the adverse impact of the extra sex chromosome is amplified when genes that are expressed from the sex chromosomes interact with autosomal variants that usually have only mild effects. We predicted that the impact of an additional sex chromosome on neurodevelopment would depend on common autosomal variants involved in synaptic functions. Methods: We analysed data from 130 children with sex chromosome trisomies (SCTs: 42 girls with trisomy X, 43 boys with Klinefelter syndrome, and 45 boys with XYY). Two comparison groups were formed from 370 children from a twin study. Three indicators of phenotype were: (i) Standard score on a test of nonword repetition; (ii). A language factor score derived from a test battery; (iii) A general scale of neurodevelopmental challenges based on all available information. Preselected regions of two genes, CNTNAP2 and NRXN1, were tested for association with neurodevelopmental outcomes using Generalised Structural Component Analysis. Results: There was wide phenotypic variation in the SCT group, as well as overall impairment on all three phenotypic measures. There was no association of phenotype with CNTNAP2 or NRXN1 variants in either the SCT group or the comparison groups. Supplementary analyses found no indication of any impact of trisomy type on the results, and exploratory analyses of individual SNPs confirmed the lack of association. Conclusions: We cannot rule out that a double hit may be implicated in the phenotypic variability in children with SCTs, but our analysis does not find any support for the idea that common variants in CNTNAP2 or NRXN1 are associated with the severity of language and neurodevelopmental impairments that often accompany an extra X or Y chromosome. Stage 1 report: http://dx.doi.org/10.12688/wellcomeopenres.13828.2