We consider three issues concerning unexpected difficulty in the acquisition of motor skills: terminology, diagnosis, and intervention. Our preference for the label Developmental Coordination Disorder (DCD) receives justification. Problems in diagnosis are discussed, especially in relation to the aetiology-dominated medical model. The high degree of overlap between DCD and other childhood disorders appears to militate against its acceptance as a distinct syndrome. In this context, we emphasize the need to determine whether incoordination takes different forms when it occurs alone is combined with general developmental delay or with other specific disorders in children of normal intelligence. Studies of intervention have mostly shown positive effects but do not, as yet, allow adjudication between different sorts of content. We suggest that the study of DCD and its remediation would benefit greatly from the employment of the simple but rich paradigms developed for the experimental analysis of fully formed adult movement skills.
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http://dx.doi.org/10.1123/apaq.19.1.11 | DOI Listing |
Curr Biol
December 2024
Department of Pharmacology, Vanderbilt Brain Institute, Vanderbilt Center for Addiction Research, Vanderbilt University, Nashville, TN 37232, USA; Department of Anatomy, Cell Biology, & Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA. Electronic address:
Human and non-human primate studies clearly implicate the dorsolateral prefrontal cortex (dlPFC) as critical for advanced cognitive functions. It is thought that intracortical synaptic architectures within the dlPFC are the integral neurobiological substrate that gives rise to these processes. In the prevailing model, each cortical column makes up one fundamental processing unit composed of dense intrinsic connectivity, conceptualized as the "canonical" cortical microcircuit.
View Article and Find Full Text PDFMouse embryonic stem cells (mESCs) and other naïve pluripotent stem cells can reverse typical developmental trajectories and, at low frequency, de-differentiate into 2-cell-like cells (2CLCs) that resemble the mammalian embryo during zygotic genome activation (ZGA). This affords the opportunity to reveal molecular principles that govern the pre-implantation stages of mammalian development. We leveraged a multipurpose allele for acute protein depletion and efficient immunoprecipitation to dissect the molecular functions of the chromatin repressor EHMT2, a candidate antagonist of the mESC-to-2CLC transition.
View Article and Find Full Text PDFDiagn Pathol
January 2025
Cell Culture Laboratory, School of Dentistry, Federal University of Para, Rua Augusto Correa, 01 Guama, Belem, PA, 66075110, Brazil.
Background: Considering the significant participation of the microenvironment in the local aggressiveness of odontogenic keratocysts, this study aims to evaluate the expression of ADAMTS-1 and its substrates, versican, aggrecan and brevican in this locally invasive odontogenic cyst.
Methods: Immunohistochemistry and polymerase chain reaction (PCR) were conducted on 30 cases of odontogenic keratocysts (OKCs) and 20 dental follicles (DFs).
Results: The immunohistochemical expression of these proteins was predominantly cytoplasmic and granular across all samples.
Physiol Behav
January 2025
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address:
C1q/TNF-related protein 14 (CTRP14), also known as C1q-like 1 (C1QL1), is a synaptic protein predominantly expressed in the brain. It plays a critical role in the formation and maintenance of the climbing fiber-Purkinje cell synapses, ensuring that only one single winning climbing fiber from the inferior olivary neuron synapses with the proximal dendrites of Purkinje cells during the early postnatal period. Loss of CTRP14/C1QL1 results in incomplete elimination of supernumerary climbing fibers, leading to multiple persistent climbing fibers synapsing with the Purkinje cells.
View Article and Find Full Text PDFiScience
December 2024
Department of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Different neuron types develop characteristic axonal and dendritic arborizations that determine their inputs, outputs, and functions. Expression of fate-determinant transcription factors is essential for specification of their distinct identities. However, the mechanisms downstream of fate-determinant factors coordinating different aspects of neuron identity are not understood.
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