Differences in Early Stages of Tactile ERP Temporal Sequence (P100) in Cortical Organization during Passive Tactile Stimulation in Children with Blindness and Controls.

Compared to their seeing counterparts, people with blindness have a greater tactile capacity. Differences in the physiology of object recognition between people with blindness and seeing people have been well documented, but not when tactile stimuli require semantic processing. We used a passive vibrotactile device to focus on the differences in spatial brain processing evaluated with event related potentials (ERP) in children with blindness (n = 12) vs. normally seeing children (n = 12), when learning a simple spatial task (lines with different orientations) or a task involving recognition of letters, to describe the early stages of its temporal sequence (from 80 to 220 msec) and to search for evidence of multi-modal cortical organization. We analysed the P100 of the ERP. Children with blindness showed earlier latencies for cognitive (perceptual) event related potentials, shorter reaction times, and (paradoxically) worse ability to identify the spatial direction of the stimulus. On the other hand, they are equally proficient in recognizing stimuli with semantic content (letters). The last observation is consistent with the role of P100 on somatosensory-based recognition of complex forms. The cortical differences between seeing control and blind groups, during spatial tactile discrimination, are associated with activation in visual pathway (occipital) and task-related association (temporal and frontal) areas. The present results show that early processing of tactile stimulation conveying cross modal information differs in children with blindness or with normal vision.

PGMRA: a web server for (phenotype x genotype) many-to-many relation analysis in GWAS.

It has been proposed that single nucleotide polymorphisms (SNPs) discovered by genome-wide association studies (GWAS) account for only a small fraction of the genetic variation of complex traits in human population. The remaining unexplained variance or missing heritability is thought to be due to marginal effects of many loci with small effects and has eluded attempts to identify its sources. Combination of different studies appears to resolve in part this problem. However, neither individual GWAS nor meta-analytic combinations thereof are helpful for disclosing which genetic variants contribute to explain a particular phenotype. Here, we propose that most of the missing heritability is latent in the GWAS data, which conceals intermediate phenotypes. To uncover such latent information, we propose the PGMRA server that introduces phenomics--the full set of phenotype features of an individual--to identify SNP-set structures in a broader sense, i.e. causally cohesive genotype-phenotype relations. These relations are agnostically identified (without considering disease status of the subjects) and organized in an interpretable fashion. Then, by incorporating a posteriori the subject status within each relation, we can establish the risk surface of a disease in an unbiased mode. This approach complements-instead of replaces-current analysis methods. The server is publically available at http://phop.ugr.es/fenogeno.

[Neurodevelopment and schizophrenia]. / Neurodesarrollo y Esquizofrenia. La paradoja de la teoría dopaminérgica. Vino nuevo en odres viejos.

The evidence of neuroleptics' antipsychotic action due to their antagonism of dopamine receptors led to the hyperdopaminergic theory of schizophrenia. But the functional disturbance of the dopamine neurons should explain the increase and the reduction of some symptoms at the same time through the D2 receptors blockade. The prodromical manifestations of schizophrenia include abnormal movements which precede and predict the beginning of the disease. They also suggest a dopamine deficit. An injury in the mesocortical dopamine projection during the neural development could result in a functional impairment of the prefrontal cortex which causes the cognitive deficit symptoms. It would result also in an excessive compensatory subcortical dopamine activity which would cause the psychotic symptoms. The evidence in behalf of this physiopathology is complex. The mechanism of the subcortical compensation of the prefrontal dopamine deficit remains unknown. It is necessary to find out which is the exact mechanism of the injury that causes the mesocortical projection loss in the schizophrenia. We have suggested that the injury would depend on the excitotoxicity induced by the perinatal hypoxia which would provoke the selective death of a dopamine neurons subset which are very sensitive during the critical period of the mesencephalic development.