Coping patterns associations with cognitive function in older adults.

Objective: Cognitive function may contribute to variability in older adults' ability to cope with chronic stress; however, limited research has evaluated this relationship. This study investigated the relationship between theoretically derived coping domains and cognitive function in 165 middle-to-older adults during the Omicron stage of COVID-19.

Method: Participants completed a clinical interview and self-report measures of health.

The development and validation of an Army team resilience measure.

Given the demanding nature of its mission, the collective units of the Army, not just individual Soldiers, need to be able to withstand and adapt to a wide range of challenges. Therefore, it is important to be able to effectively assess resilience at the team-level and to understand the factors that can enable or diminish it. This article describes the development of a construct valid and psychometrically-sound measure of team resilience - the Team Resilience Scale (TRS).

Out of Line or Altered States? Neural Progenitors as a Target in a Polygenic Neurodevelopmental Disorder.

The genesis of a mature complement of neurons is thought to require, at least in part, precursor cell lineages in which neural progenitors have distinct identities recognized by exclusive expression of one or a few molecular markers. Nevertheless, limited progenitor types distinguished by specific markers and lineal progression through such subclasses cannot easily yield the magnitude of neuronal diversity in most regions of the nervous system. The late Verne Caviness, to whom this edition of Developmental Neuroscience is dedicated, recognized this mismatch.

Sex-specific differences in neuropsychological profiles of mild cognitive impairment in a hospital-based clinical sample.

Objective: Mild cognitive impairment (MCI) is an etiologically nonspecific diagnosis including a broad spectrum of cognitive decline between normal aging and dementia. Several large-scale cohort studies have found sex effects on neuropsychological test performance in MCI. The primary aim of the current project was to examine sex differences in neuropsychological profiles in a clinically diagnosed MCI sample using clinical and research diagnostic criteria.

Ranbp1 modulates morphogenesis of the craniofacial midline in mouse models of 22q11.2 deletion syndrome.

Facial dysmorphology is a hallmark of 22q11.2 deletion syndrome (22q11DS). Nearly all affected individuals have facial features characteristic of the syndrome: a vertically long face with broad nasal bridge, narrow palpebral fissures and mild micrognathia, sometimes accompanied by facial skeletal and oropharyngeal anomalies.

Identity, lineage and fates of a temporally distinct progenitor population in the embryonic olfactory epithelium.

We defined a temporally and transcriptionally divergent precursor cohort in the medial olfactory epithelium (OE) shortly after it differentiates as a distinct tissue at mid-gestation in the mouse. This temporally distinct population of Ascl1+ cells in the dorsomedial OE is segregated from Meis1+/Pax7+ progenitors in the lateral OE, and does not appear to be generated by Pax7+ lateral OE precursors. The medial Ascl1+ precursors do not yield a substantial number of early-generated ORNs.

DNA Methylation "GrimAge" Acceleration Mediates Sex/Gender Differences in Verbal Memory and Processing Speed: Findings From the Health and Retirement Study.

Whether sex/gender differences in rates of biological aging mediate sex/gender differences in cognition in older adults has not been fully examined. The aim of the current study was to investigate this association. Data from up to 1 928 participants (mean age = 75, standard deviation = 7.

Development and implementation of a scalable and versatile test for COVID-19 diagnostics in rural communities.

Rapid and widespread testing of severe acute respiratory coronavirus 2 (SARS-CoV-2) is essential for an effective public health response aimed at containing and mitigating the coronavirus disease 2019 (COVID-19) pandemic. Successful health policy implementation relies on early identification of infected individuals and extensive contact tracing. However, rural communities, where resources for testing are sparse or simply absent, face distinctive challenges to achieving this success.

Personality in Autism Spectrum Disorder: Associations With Face Memory Deficit and Theory of Mind.

Objective: To examine the personality profiles of adults with autism spectrum disorder (ASD) using a standard personality assessment and to investigate the association between personality, ASD-related face memory deficit (FMD), and theory of mind (ToM). In a broader context, to examine whether there are distinct clinical phenotypes in the ASD population that have implications for personality development and treatment.

Method: Fifty-five adults with ASD and 22 neurotypical (NT) adults underwent a battery of neuropsychological tests, including measures of personality, face memory, and ToM.

Selective disruption of trigeminal sensory neurogenesis and differentiation in a mouse model of 22q11.2 deletion syndrome.

22q11.2 Deletion Syndrome (22q11DS) is a neurodevelopmental disorder associated with cranial nerve anomalies and disordered oropharyngeal function, including pediatric dysphagia. Using the LgDel 22q11DS mouse model, we investigated whether sensory neuron differentiation in the trigeminal ganglion (CNgV), which is essential for normal orofacial function, is disrupted.

Aberrant early growth of individual trigeminal sensory and motor axons in a series of mouse genetic models of 22q11.2 deletion syndrome.

We identified divergent modes of initial axon growth that prefigure disrupted differentiation of the trigeminal nerve (CN V), a cranial nerve essential for suckling, feeding and swallowing (S/F/S), a key innate behavior compromised in multiple genetic developmental disorders including DiGeorge/22q11.2 Deletion Syndrome (22q11.2 DS).

Variations in maternal vitamin A intake modifies phenotypes in a mouse model of 22q11.2 deletion syndrome.

Background: Vitamin A regulates patterning of the pharyngeal arches, cranial nerves, and hindbrain that are essential for feeding and swallowing. In the LgDel mouse model of 22q11.2 deletion syndrome (22q11DS), morphogenesis of multiple structures involved in feeding and swallowing are dysmorphic.

Suckling, Feeding, and Swallowing: Behaviors, Circuits, and Targets for Neurodevelopmental Pathology.

All mammals must suckle and swallow at birth, and subsequently chew and swallow solid foods, for optimal growth and health. These initially innate behaviors depend critically upon coordinated development of the mouth, tongue, pharynx, and larynx as well as the cranial nerves that control these structures. Disrupted suckling, feeding, and swallowing from birth onward-perinatal dysphagia-is often associated with several neurodevelopmental disorders that subsequently alter complex behaviors.

Persistent Feeding and Swallowing Deficits in a Mouse Model of 22q11.2 Deletion Syndrome.

Disrupted development of oropharyngeal structures as well as cranial nerve and brainstem circuits may lead to feeding and swallowing difficulties in children with 22q11. 2 deletion syndrome (22q11DS). We previously demonstrated aspiration-based dysphagia during early postnatal life in the mouse model of 22q11DS along with disrupted oropharyngeal morphogenesis and divergent differentiation and function of cranial motor and sensory nerves.

Transcriptional dysregulation in developing trigeminal sensory neurons in the LgDel mouse model of DiGeorge 22q11.2 deletion syndrome.

LgDel mice, which model the heterozygous deletion of genes at human chromosome 22q11.2 associated with DiGeorge/22q11.2 deletion syndrome (22q11DS), have cranial nerve and craniofacial dysfunction as well as disrupted suckling, feeding and swallowing, similar to key 22q11DS phenotypes.

Genetically Encoded Inverse Bolaamphiphiles.

Developing new protein-based materials with a programmable assembly is of great scientific interest and technological importance. Inspired by nature's use of post-translational modifications (PTMs) to control the function and location of proteins, we have leveraged lipidation-the PTM of proteins with lipids-to synthesize genetically encoded lipidated proteins with controllable hierarchical assembly. Specifically, we envisioned the combination of two orthogonal lipidation pathways with different regioselectivity and substrate preferences inside to produce recombinant nanomaterials with distinct lipidation domains at each terminus of proteins.

In the line-up: deleted genes associated with DiGeorge/22q11.2 deletion syndrome: are they all suspects?

Background: 22q11.2 deletion syndrome (22q11DS), a copy number variation (CNV) disorder, occurs in approximately 1:4000 live births due to a heterozygous microdeletion at position 11.2 (proximal) on the q arm of human chromosome 22 (hChr22) (McDonald-McGinn and Sullivan, Medicine 90:1-18, 2011).

Mitochondrial Dysfunction Leads to Cortical Under-Connectivity and Cognitive Impairment.

Under-connectivity between cerebral cortical association areas may underlie cognitive deficits in neurodevelopmental disorders, including the 22q11.2 deletion syndrome (22q11DS). Using the LgDel 22q11DS mouse model, we assessed cellular, molecular, and developmental origins of under-connectivity and its consequences for cognitive function.

Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia.

Parvalbumin inhibitory interneurons (PVIs) are crucial for maintaining proper excitatory/inhibitory balance and high-frequency neuronal synchronization. Their activity supports critical developmental trajectories, sensory and cognitive processing, and social behavior. Despite heterogeneity in the etiology across schizophrenia and autism spectrum disorder, PVI circuits are altered in these psychiatric disorders.

Foxd4 is essential for establishing neural cell fate and for neuronal differentiation.

Many molecular factors required for later stages of neuronal differentiation have been identified; however, much less is known about the early events that regulate the initial establishment of the neuroectoderm. We have used an in vitro embryonic stem cell (ESC) differentiation model to investigate early events of neuronal differentiation and to define the role of mouse Foxd4, an ortholog of a forkhead-family transcription factor central to Xenopus neural plate/neuroectodermal precursor development. We found that Foxd4 is a necessary regulator of the transition from pluripotent ESC to neuroectodermal stem cell, and its expression is necessary for neuronal differentiation.

Balancing Act: Maintaining Amino Acid Levels in the Autistic Brain.

The ever-expanding number of genes that are mutated in autism is showing us how imbalances in fundamental cellular processes can lead to disease. A recent study by Tărlungeanu et al. (2016) identifies a form of ASD resulting from a failure of the brain to properly import amino acids.

Neural transcription factors bias cleavage stage blastomeres to give rise to neural ectoderm.

The decision by embryonic ectoderm to give rise to epidermal versus neural derivatives is the result of signaling events during blastula and gastrula stages. However, there also is evidence in Xenopus that cleavage stage blastomeres contain maternally derived molecules that bias them toward a neural fate. We used a blastomere explant culture assay to test whether maternally deposited transcription factors bias 16-cell blastomere precursors of epidermal or neural ectoderm to express early zygotic neural genes in the absence of gastrulation interactions or exogenously supplied signaling factors.

Functional Divergence of the Nuclear Receptor NR2C1 as a Modulator of Pluripotentiality During Hominid Evolution.

Genes encoding nuclear receptors (NRs) are attractive as candidates for investigating the evolution of gene regulation because they (1) have a direct effect on gene expression and (2) modulate many cellular processes that underlie development. We employed a three-phase investigation linking NR molecular evolution among primates with direct experimental assessment of NR function. Phase 1 was an analysis of NR domain evolution and the results were used to guide the design of phase 2, a codon-model-based survey for alterations of natural selection within the hominids.