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Peiffer, A.

Publications and source records attributed to Peiffer, A..

4 recordsLinked to original sources

Theta-band brain synchronization supports the immediate and post-sleep dynamics of memory recall in children

Memory engrams emerge from dynamic, coordinated interactions among synchronized functional brain networks. Yet, how these networks are selectively reactivated upon cued recall and gradually (re)organized over time, especially through sleep, remains poorly understood. Using magnetoencephalography (MEG), sleep electroencephalography (EEG) and behavioral measures, we investigated the spatiotemporal neural dynamics of cued recall memory during immediate and post-sleep (i.e., 90-minute post-learning nap) recall sessions in school-aged children. Results showed that immediate recall engaged a temporally ordered sequence of theta-band phase synchronization across two transiently synchronized networks: an early (150-350 ms) network involving the ventral visual pathway and left medial temporal lobe (MTL), followed by a later (550-750 ms) network encompassing the bilateral MTL and widespread neocortical associative regions. Post-sleep recall was associated, relative to wakefulness, with strengthened theta-band phase synchronization between the left MTL and widespread bilateral neocortical regions in a similar late window (450-650 ms). Post-sleep theta-band synchronization and memory gains in performance positively correlated with slow oscillation-spindle coupling during the post-learning nap. Altogether, these findings highlight oscillatory and spatiotemporal dynamics of memory recall networks and suggest that sleep, possibly driven by slow-oscillation-spindle coupling mechanisms, supports the efficient reinstatement of memory traces in the developing brain.

neuroscience↗

Association between theta-band resting-state functional connectivity and declarative memory abilities in children

Declarative memory formation critically relies on the synchronization of brain oscillations in the theta (4-8 Hz) frequency band within specific brain networks. The development of this capacity is closely linked to the functional organization of these networks already at rest. However, the relationship between theta-band resting-state functional connectivity and declarative memory abilities remains unexplored in children. Here, using magnetoencephalography, we examined the association between declarative memory performance and pre-learning resting-state functional connectivity across frequency bands in 32 school-aged children. Declarative memory was assessed as the percentage of correct retrieval of 50 new associations between non-objects and magical functions, while resting-state functional connectivity was measured through power envelope correlation of the theta, alpha, low and high beta frequency bands. We found that stronger theta-band resting-state functional connectivity within occipito-temporo-frontal networks correlated with better declarative memory retrieval, while no correlation was observed in the alpha and beta frequency bands. These findings suggest that the functional brain architecture at rest, specifically involving theta-band oscillations, supports declarative memory in children. This mechanism may facilitate the subsequent rapid transformation of sensory input into visuo-semantic representations, highlighting the critical role of theta-band connectivity in early cognitive development.

neuroscience↗

Norstictic acid is a selective allosteric transcriptional regulator

Inhibitors of transcriptional protein-protein interactions (PPIs) have high value both as tools and for therapeutic applications. The PPI network mediated by the transcriptional coactivator Med25, for example, regulates stress-response and motility pathways and dysregulation of the PPI networks contributes to oncogenesis and metastasis. The canonical transcription factor binding sites within Med25 are large (~900 [A]2) and have little topology, and thus do not present an array of attractive small-molecule binding sites for inhibitor discovery. Here we demonstrate that the depsidone natural product norstictic acid functions through an alternative binding site to block Med25-transcriptional activator PPIs in vitro and in cell culture. Norstictic acid targets a binding site comprised of a highly dynamic loop flanking one canonical binding surface and in doing so, it both orthosterically and allosterically alters Med25-driven transcription in a patient-derived model of triple negative breast cancer. These results highlight the potential of Med25 as a therapeutic target as well as the inhibitor discovery opportunities presented by structurally dynamic loops within otherwise challenging proteins.

biochemistry↗

Analytical and Clinical Validity Study of FirstStepDx PLUS: A Chromosomal Microarray Optimized for Patients with Neurodevelopmental Conditions

IntroductionChromosomal microarray analysis (CMA) is recognized as the first-tier test in the genetic evaluation of children with developmental delays, intellectual disabilities, congenital anomalies and autism spectrum disorders of unknown etiology.\n\nArray DesignTo optimize detection of clinically relevant copy number variants associated with these conditions, we designed a whole-genome microarray, FirstStepDx PLUS (FSDX). A set of 88,435 custom probes was added to the Affymetrix CytoScanHD platform targeting genomic regions strongly associated with these conditions. This combination of 2,784,985 total probes results in the highest probe coverage and clinical yield for these disorders.\n\nResults and DiscussionClinical testing of this patient population is validated on DNA from either non-invasive buccal swabs or traditional blood samples. In this report we provide data demonstrating the analytic and clinical validity of FSDX and provide an overview of results from the first 7,570 consecutive patients tested clinically. We further demonstrate that buccal sampling is an effective method of obtaining DNA samples, which may provide improved results compared to traditional blood sampling for patients with neurodevelopmental disorders who exhibit somatic mosaicism.\n\nClinical scenarioNeurodevelopmental disabilities, including developmental delays (DD), intellectual disabilities (ID), and autism spectrum disorders (ASD), affect up to 15% of children (1). In the majority of cases, a childs clinical presentation does not allow for a definitive etiological diagnosis. In such cases, CMA is recommended as the first-tier test that should be used to evaluate for a potential genetic etiology (2-7). A definitive genetic diagnosis allows patients to more often receive appropriate medical care tailored to their condition, as reflected by medical management changes and improved access to necessary support and educational services (8-13).\n\nTest descriptionFirstStepDx PLUS (FSDX) is an optimized clinical microarray test provided in the context of a comprehensive clinical service. Testing starts with either a non-invasive buccal swab sample or traditional blood sample from which DNA extraction using a Gentra Puregene(R) kit specific to the sample type (Qiagen, Inc., Valencia, CA) is performed in one of several contracted CLIA/CAP credentialed laboratories according to manufacturers protocols. High quality genomic DNA is fragmented, labeled and hybridized to FSDX arrays using reagents, equipment and methodology as specified by by the manufacturer (Affymetrix, Inc., Santa Clara, CA)(14). Washed arrays are scanned and raw data files are processed to CYCHP files using a reference file comprising at least 100 samples with normal array findings. Data analysis is performed using Chromosome Analysis Suite software version 2.0.1 (Affymetrix). Hybridization of patient DNA to oligonucleotide and SNP probes is independently compared against a previously analyzed cohort of normal samples to call CNVs and allele genotypes. The percentage mosaicism of whole-chromosome aneuploidies is determined using the average log2 ratio of the entire chromosome (14).\n\nMicroarray designFSDX was optimized by the addition of 88,435 custom probes targeting genomic regions strongly associated with ID/DD/ASD (15-24). This was effected, under GMP by Affymetrix, to the CytoScanHD platform using their microarray design process specifications which have been previously described (14). This is consistent with the ACMG recommendation of \"enrichment of probes targeting dosage-sensitive genes known to result in phenotypes consistent with common indications for a genomic screen\" (25). Critical regions that did not meet a desired probe density [≥]1 probe/1000 bp on the CytoScanHD were supplemented with additional probe content to allow for improved detection of smaller deletions and duplications in these critical regions. Finally, additional probes were added to improve detection of CNVs encompassing genes involved in other well-characterized neurodevelopmental disorders, for example GAMT (26) and GATM (27). All incremental probes were added in substitution for probes deemed sub-optimal by Affymetrix and previously masked, bringing FSDX to a grand total of 2,784,985 probes. Custom SNP probes (n =416) on FSDX are targeted by 12 oligonucleotides, three for each strand of each allele, which is approximately double the typical probe coverage for SNPs.\n\nTest interpretationCYCHP files are evaluated by ABMG certified cytogeneticists. Determination of CNVs is consistent with established cytogenetic standards. A minimum of 25-consecutive impacted probes is the baseline determinant for deletions and 50 probes for duplications independent of variant size. Rare CNVs are determined to be \"pathogenic\" if there is sufficient evidence published (at least two independent publications) to indicate that haploinsufficiency or triplosensitivity of the region or gene(s) involved is causative of clinical features or of sufficient overall size (28). If however, there is insufficient but at least preliminary evidence for a causative role for the region or gene(s) therein they are classified as variants of unknown significance (VOUS) independent of CNV size. Areas of absence of heterozygosity (AOH) are also classed as VOUS if of sufficient size and location to increase the risk for conditions with autosomal recessive inheritance or conditions with parent-of-origin/imprinting effects. Other CNVs are typically not reported after determination that they most likely represent normal common population variants and are contained in databases documenting presumptively benign CNVs, e.g., the Database of Genomic Variants (DGV) (29). These parameters were standard independent of the microarray used for analysis in comparative studies.\n\nPublic health importanceA definitive genetic diagnosis facilitates patient access to appropriate and necessary medical and support services. Defining the underlying genetic cause of DD/ID/ASD and/or multiple congenital anomalies (MCA) in each unique patient is vital to understanding etiology, prognosis, and course. It informs physicians of potential comorbid conditions for which a patient should be evaluated and treated proactively and optimally. Improved understandings of the appropriate therapeutic and behavioral approaches to that patient are also enabled. Genetic testing is best provided in the context of an integrated service (30), so FSDX provides comprehensive, clear, readable, and personalized reports for the healthcare provider and a family-friendly section to facilitate understanding of the often-complex results. The report is complemented by availability of pre- and post-test genetic counseling and technical support to providers. Moreover, FSDX includes personalized insurance pre-authorization and appeals assistance to overcome barriers encountered by both providers and families that, in many circumstances, prevent access to crucial genetic testing services (10-11).\n\nPublished reviews, recommendations and guidelinesThe American College of Medical Genetics (ACMG) (2,3), the American Academy of Child and Adolescent Psychiatry (4,7), the American Academy of Pediatrics (5), and the American Academy of Neurology/Child Neurology Society (6) recommend CMA as the first-tier test in the genetic evaluation of children with unexplained DD, ID, or ASD. Considerable data supporting these guidelines are documented in numerous reviews and publications (31-36). The ACMG has also published guidelines on both array design (25) and the validation of arrays, including validation of a new version of a platform in use by the laboratory from the same manufacturer, and of additional sample types (28).

genomics↗