Biomedical subjects

Gerd Schulte-Körne

Publications and source records attributed to Gerd Schulte-Körne.

7 recordsLinked to original sources

PubMed2006

[Genetics of dyslexia].

Dyslexia is a very common developmental disorder. The aetiology of this complex disorder must in large part still be clarified. Dyslexia segregates in families and the risk for a sibling to become dyslexic is 3.5-fold increased. Different phenotypic dimensions are correlated with dyslexia. These are mainly phonological awareness, phonological decoding, orthographic coding, auditory short-term memory, and rapid naming. The correlated dimensions segregate in families and were found to be heritable. The heritability of word reading lies between 50% and 60%, and that of spelling between 50% and 70%. Based on genome wide linkage analyses, nine candidate gene regions (DYX1-DYX9) could be identified. Recently, four candidate genes, DCDC2, KIAA0319, ROBO1 and DYX1C1 were identified by systematic association analyses. All these genes play a function role in neuronal migration, making them promising candidate genes for dyslexia. However, a functionally relevant mutation has not yet been identified. The comorbidity between dyslexia and ADHD and between dyslexia and SLI could be explained, at least in part, by genetic factors. For future research, all relevant factors playing a functional role in dyslexia should be investigated in sufficiently large samples. This research should integrate genetic, neurobiological, and environmental factors. For an understanding of causes, it is very helpful to understand the interaction between different factors, namely gene-environmental and gene-gene interaction. In a recent project funded by the EU in the Sixth Framework (www.neurodys.com), the worldwide largest sample of children with dyslexia will be sampled and investigated. The goal of this project is to investigate the biological basis of dyslexia in order to improve the basis for the development of successful diagnostics and therapies.

Adolescent↗

PubMed2006

[Influencing factors on the course of supervised visitations in a parental counselling office].

We report about a youth welfare service tool called supervised visitation (SV). SVs are intended to maintain contact and emotional relationship between child and absent parent. In the present study, we assessed a number of supposed influencing factors on course and result of SV. 55 % of the SV cases could eventually be transferred to regular contact without supervision. The majority of SV cases could be finished after a couple of months. The number of accompanying counselling sessions was often higher than the number of SVs themselves, a result stressing the significance of counselling. Younger as well as older children did benefit from SV. Opposed to some of the literature, in our study the success of SV did not depend on kind of referral or custody, specific indications, or the length of contact interruptions. We found a tendency though that a high number of risk factors is a potential risk for SV success.

Adolescent↗

PubMed2005

Strong genetic evidence of DCDC2 as a susceptibility gene for dyslexia.

We searched for linkage disequilibrium (LD) in 137 triads with dyslexia, using markers that span the most-replicated dyslexia susceptibility region on 6p21-p22, and found association between the disease and markers within the VMP/DCDC2/KAAG1 locus. Detailed refinement of the LD region, involving sequencing and genotyping of additional markers, showed significant association within DCDC2 in single-marker and haplotype analyses. The association appeared to be strongest in severely affected patients. In a second step, the study was extended to include an independent sample of 239 triads with dyslexia, in which the association--in particular, with the severe phenotype of dyslexia--was confirmed. Our expression data showed that DCDC2, which contains a doublecortin homology domain that is possibly involved in cortical neuron migration, is expressed in the fetal and adult CNS, which--together with the hypothesized protein function--is in accordance with findings in dyslexic patients with abnormal neuronal migration and maturation.

Base Sequence↗

PubMed2005

Developmental dyslexia--recurrence risk estimates from a german bi-center study using the single proband sib pair design.

OBJECTIVE: Several studies have demonstrated a genetic component for dyslexia. However, both segregation and linkage analyses show contradictory results pointing at the necessity of an optimal ascertainment scheme for molecular genetic studies. Previously, we have argued that the single proband sib pair design (SPSP) would be optimal. The aims of this paper therefore are to demonstrate the practicability of the SPSP design and the estimation of recurrence risks for reading and writing. METHODS: We assessed spelling and reading in a family sample ascertained through the SPSP design. 287 families with at least two siblings and their parents were recruited. At least one child was affected with spelling disorder according to a one standard deviation (1SD) discrepancy criterion. RESULTS: Mean values for probands and their siblings were different for both the spelling and the reading phenotype. For the probands, variances of the phenotype spelling were smaller. These effects became stronger with more extreme selection criteria. Both siblings fulfilled the 1SD criterion for spelling and reading in 60.3 and 28.9% of the families, respectively, indicating a low cost efficiency of the double proband sib pair approach. A recurrence risk of 4.52 (CI: 4.07-4.93) was obtained for spelling when the 1SD criterion was applied to both siblings. Recurrence risk estimates were similar for reading. CONCLUSION: The study demonstrates the suitability of the SPSP design for genetic analysis of dyslexia. The recurrence risk estimates may be used for determining sample sizes in gene mapping studies.

Child↗

PubMed2004

Motion-onset VEPs in dyslexia. Evidence for visual perceptual deficit.

The magnocellular deficit theory is one of the prominent theories in dyslexia. However, recent studies have produced conflicting results. In order to assess the validity of this theory, 8 dyslexic children and 14 controls were examined with a motion-onset visual evoked potential (VEP) paradigm at three different velocities (2, 8, and 16 deg/s). VEP elicited by stationary gratings served as a control condition. Amplitudes of motion-onset VEP components (P100, P200) but not of the stationary VEP are significantly attenuated in dyslexic children. Further, there is an interaction of group and velocity for the P200 in the way that group differences are more pronounced for higher velocities than for lower velocities. These results support the hypothesis of an impairment of a specific magnocellular function in dyslexia.

Adolescent↗

PubMed2004

Visual evoked potential elicited by coherenty moving dots in dyslexic children.

The magnocellular deficit theory is one of the prominent hypotheses in dyslexia research. However, recent studies have produced conflicting results. Ten dyslexic children and 12 controls were examined with visual evoked potentials elicited by random dot kinematogram. The experiment comprises two sequences, one with randomly moving dots (control condition) and a second sequence where a fraction of the dots were moved coherently at the left or right side (depending on the level of coherence, 10%, 20%, and 40% of the dots). Randomly moving dots elicited two components, a P100 and P200, which were not different between the groups. Coherently moving dots elicited a late positivity between 300 and 800 ms, which was significantly attenuated in dyslexic children. The area of this component becomes larger at a higher level of coherence. This study supports the hypothesis of an impairment of a specific magnocellular function in dyslexia.

Adolescent↗

PubMed2003

Developmental dyslexia in different languages: language-specific or universal?

Most of the research on developmental dyslexia comes from English-speaking countries. However, there is accumulating evidence that learning to read English is harder than learning to read other European orthographies (Seymour, Aro, & Erskine, 2003). These findings therefore suggest the need to determine whether the main English findings concerning dyslexia can be generalized to other European orthographies, all of which have less irregular spelling-to-sound correspondences than English. To do this, we conducted a study with German- and English-speaking children (n=149) in which we investigated a number of theoretically important marker effects of the reading process. The results clearly show that the similarities between dyslexic readers using different orthographies are far bigger than their differences. That is, dyslexics in both countries exhibit a reading speed deficit, a nonword reading deficit that is greater than their word reading deficit, and an extremely slow and serial phonological decoding mechanism. These problems were of similar size across orthographies and persisted even with respect to younger readers that were at the same reading level. Both groups showed that they could process larger orthographic units. However, the use of this information to supplement grapheme-phoneme decoding was not fully efficient for the English dyslexics.

Adolescent↗