Motor Coordination Research Articles

Neuroprotective effects of punicalagin and/or micronized zeolite clinoptilolite on manganese-induced Parkinson's disease in a rat model: Involvement of multiple pathways.

Manganism, a central nervous system dysfunction correlated with neurological deficits such as Parkinsonism, is caused by the substantial collection of manganese chloride (MnCl2) in the brain. To explore the neuroprotective effects of natural compounds, namely, micronized zeolite clinoptilolite (ZC) and punicalagin (PUN), either individually or in combination, against MnCl2-induced Parkinson's disease (PD). Fifty male albino rats were divided into 5 groups (Gps). Gp I was used as the control group, and the remaining animals received MnCl2 (Gp II-Gp V). Rats in Gps III and IV were treated with ZC and PUN, respectively. Gp V received both ZC and PUN as previously reported for the solo-treated plants. ZC and/or PUN reversed the depletion of monoamines in the brain and decreased acetyl choline esterase activity, which primarily adjusted the animals' behavior and motor coordination. ZC and PUN restored the balance between glutamate/γ-amino butyric acid content and markedly improved the brain levels of brain-derived neurotrophic factor and nuclear factor erythroid 2-related factor 2/heme oxygenase-1 and decreased glycogen synthase kinase-3 beta activity. ZC and PUN also inhibited inflammatory and oxidative markers, including nuclear factor kappa-light-chain-enhancer of activated B cells, Toll-like receptor 4, nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 and caspase-1. Bcl-2-associated X-protein and B-cell leukemia/lymphoma 2 protein (Bcl-2) can significantly modify caspase-3 expression. ZC and/or PUN ameliorated PD in rats by decreasing the levels of endoplasmic reticulum (ER) stress markers (p-protein kinase-like ER kinase (PERK), glucose-regulated protein 78, and C/EBP homologous protein (CHOP)) and enhancing the levels of an autophagy marker (Beclin-1). ZC and/or PUN mitigated the progression of PD through their potential neurotrophic, neurogenic, anti-inflammatory, antioxidant, and anti-apoptotic activities and by controlling ER stress through modulation of the PERK/CHOP/Bcl-2 pathway.

Deep brain stimulation mitigates memory deficits in a rodent model of traumatic brain injury

BackgroundTraumatic brain injury (TBI) is a major life-threatening event. In addition to neurological deficits, it can lead to long-term impairments in attention and memory. Deep brain stimulation (DBS) is an established therapy for movement disorders that has been recently investigated for memory improvement in various disorders. In models of TBI, stimulation delivered to different brain targets has been administered to rodents long after the injury with the objective of treating motor deficits, coordination and memory impairment. ObjectiveTo test the hypothesis that DBS administered soon after TBI may prevent the development of memory deficits and exert neuroprotective effects. MethodsMale rats were implanted with DBS electrodes in the anterior nucleus of the thalamus (ANT) one week prior to lateral fluid percussion injury (FPI). Immediately after TBI, animals received active or sham stimulation for 6 h. Four days later, they were assessed in a novel object/novel location recognition test (NOR/NLR) and a Barnes maze paradigm. After the experiments, hippocampal cells were counted. Separate groups of animals were sacrificed at different timepoints after TBI to measure cytokines and brain derived neurotrophic factor (BDNF). In a second set of experiments, TBI-exposed animals receiving active or sham stimulation were injected with the tropomyosin receptor kinase B (TrkB) antagonist ANA-12, followed by behavioural testing. ResultsRats exposed to TBI given DBS had an improvement in several variables of the Barnes maze, but no significant improvements in NOR/NLR compared to Sham DBS TBI animals or non-implanted controls. Animals receiving stimulation had a significant increase in BDNF levels, as well as in hippocampal cell counts in the hilus, CA3 and CA1 regions. DBS failed to normalize the increased levels of TNFα and the proinflammatory cytokine IL1β in the perilesional cortex and the hippocampus of the TBI-exposed animals. Pharmacological experiments revealed that ANA-12 administered alongside DBS did not counter the memory improvement observed in ANT stimulated animals. ConclusionsDBS delivered immediately after TBI mitigated memory deficits, increased the expression of BDNF and the number of hippocampal cells in rats. Mechanisms for these effects were not related to an anti-inflammatory effect or mediated via TrkB receptors.

GSK-3β inhibitor amplifies autophagy-lysosomal pathways by regulating TFEB in Parkinson's disease models

Parkinson's disease (PD), a common neurodegenerative disorder characterized by degeneration of the substantia nigra and a marked increase in Lewy bodies in the brain, primarily manifests as motor dysfunction. Glycogen synthase kinase-3 beta (GSK-3β) is known to play a critical role in various pathological processes of neurodegenerative diseases. However, the impact of GSK-3β inhibitors on PD progression and the underlying molecular mechanisms responsible for the effects have not been fully elucidated. Using in vitro and mouse models of 1-methyl-4-phenylpyridine (MPP+)-or methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD, we found that inhibition of GSK-3β activity alleviated mitochondrial damage, cell apoptosis, and neuronal cell loss by promoting the nuclear translocation of transcription factor EB (TFEB), thereby amplifying the autophagy-lysosomal pathway (ALP). Importantly, siRNA silencing of the TFEB gene impaired the GSK-3β inhibitor-mediated activation of the ALP pathway, thus negating the metabolic support required for neuronal functional improvement. Short-term treatment with the GSK-3β inhibitor significantly ameliorated motor dysfunction and improved motor coordination in model mice with MPTP-induced PD. GSK-3β inhibition increased the ALP and TFEB activities in the mice, thereby reducing α-synuclein aggregation and neuronal damage. In conclusion, our study demonstrates that inhibition of GSK-3β activity can delay the pathological processes of PD via promotion of the TFEB–ALP pathway, potentially providing a novel therapeutic target for this neurodegenerative disorder.

The Relationship Between Family Income And Motor Coordination Function In Children With Autism And Typically Developing Peers

The Relationship Between Family Income And Motor Coordination Function In Children With Autism And Typically Developing Peers

Knockout of neutrophil cytosolic factor 1 ameliorates neuroinflammation and motor deficit after traumatic brain injury

Traumatic brain injury (TBI) is a predominant cause of long-term disability in adults, yet the molecular mechanisms underpinning the neuropathological processes associated with it remain inadequately understood. Neutrophil cytosolic factor 1 (NCF1, also known as p47phox) is one of the cytosolic components of NADPH oxidase NOX2. In this study, we observed a reduction in the volume of TBI-induced brain lesions in NCF1-knockout mice compared to controls. Correspondingly, the neuronal loss induced by TBI was mitigated in the NCF1-knockout mice. Behavioral analysis also demonstrated that the motor coordination deficit following TBI was mitigated by the depletion of NCF1. Mechanistically, our findings revealed that NCF1 deficiency attenuated TBI-induced inflammatory responses by inhibiting the release of proinflammatory factors and reducing neutrophil infiltration into the brain parenchyma. Additionally, our results indicated that NCF1 deficiency significantly decreased the levels of reactive oxygen species in neutrophils. Taken together, our findings indicate that NCF1 plays a crucial role in the regulation of brain injury and secondary inflammation post-TBI.

Difficulties in perceptual–motor coordination of reaching behavior in children with autism spectrum disorder

Increased risk of injury from collisions with objects is an important issue in children with autism spectrum disorder (ASD). The purpose of the present study was to examine whether impaired perceptual–motor coordination may underlie the high frequency of collisions. Specifically, we hypothesized that collisions are likely to occur frequently in children with ASD due to their difficulty with body-related spatial perception and their inadequate motor planning, due to their detail-focused processing style, i.e., a tendency to focus attention on specific details rather than on the overall context. To evaluate impairment of perceptual–motor coordination in children with ASD, an original action selection task was developed to assess (a) body-related spatial perception and (b) predictive attentional properties for planning the subsequent movements based on the measures of hand movement and gaze behavior. Twenty-six children (13 diagnosed as ASD and 13 with typical development [TD]) completed the task, and their parents completed a questionnaire regarding their child's susceptibility to injury. Results showed that children with ASD displayed inaccurate body-related spatial perception and inadequate motor planning under conditions that induced their detail-focused processing style. In addition, analyses of gaze behavior reflected the characteristics of a detail-focused processing in children with ASD. This was correlated with the severity of ASD and the measure of motor planning. The present findings suggest that difficulty with perceptual–motor coordination, resulting in part from the detail-focused processing style, might contribute to susceptibility to injury in children with ASD. We consider that our evaluation of the difficulty with perceptual–motor of individuals with ASD provides a framework for understanding their high rate of collision-related injuries and could inform strategies for preventing these injuries.

Boosting Serotonin Synthesis Is Not Sufficient to Improve Motor Coordination of Mecp2 Heterozygous Mouse Model of Rett Syndrome.

Motor deficit is a core symptom of Rett syndrome, a rare neurological disease caused in most cases by mutations of the methyl-CpG-binding protein2 (MECP2) gene. Serotonin reuptake inhibitors improve motor coordination in Mecp2 heterozygous (Het) mice and serotonin depletion prevented this effect. Here, we assess alterations in indole levels in various brain regions and whether boosting brain serotonin synthesis with the serotonin precursors tryptophan, 5-hydroxytryptophan and α-lactalbumin rescued motor coordination deficit of Mecp2 Het mice. Motor coordination was assessed in the accelerated rotarod during and after systemic administration of serotonin precursors for 2-3 weeks. Since no data are available, the effect of α-lactalbumin on tryptophan, serotonin and 5-hydroxyindoleacetic acid levels was evaluated in various brain regions in order to identify the dose of ALAC to evaluate on motor coordination. As compared to WT, Mecp2 Het mice show reduced levels of serotonin in the whole brain, hippocampus, brainstem and cerebral cortex, but not the striatum. Reduced levels of 5-hydroxyindoleacetic acid were observed in the hippocampus and brainstem. Doses of serotonin precursors increasing brain tryptophan and/or serotonin production and metabolism had no effect on motor coordination. The results indicate that boosting serotonin synthesis is not sufficient to improve motor coordination of Mecp2 Het mice.

Lamotrigine for cognitive deficits associated with neurofibromatosis type 1: A phase II randomized placebo-controlled trial.

To find proof-of-principle evidence for short-term treatment with lamotrigine to improve cognitive functioning of adolescents with neurofibromatosis type 1 (NF1). This was a double-blind, parallel-group, randomized, placebo-controlled clinical trial (the NF1-EXCEL trial: Examining the Cognitive and Electrophysiological benefit of Lamotrigine in Neurofibromatosis type 1; Clinicaltrials.gov identifier NCT02256124), with the aim of enrolling 60 adolescents with NF1 aged 12 to 17 years 6 months. The short-term study intervention was 200 mg of lamotrigine taken orally for 26 weeks. The primary outcome was performance IQ tested with the Wechsler Intelligence Scale for Children, Third Edition, complemented with secondary outcomes for visuospatial learning efficacy, visual perception, visual sustained attention, fine motor coordination, attention-deficit/hyperactivity problems, and executive functioning. We screened 402 adolescents with NF1, of whom 31 (eight females) entered the study. Complete-case analysis showed no effect of lamotrigine on either performance IQ (-0.23, 95% CI -6.90 to 6.44) or most secondary outcomes. Visual sustained attention showed a trend towards better performance in the lamotrigine group (-0.81, 95% CI -1.67 to 0.04). Lamotrigine did not improve cognitive functioning in adolescents with NF1. The small treatment effects make it unlikely that a larger sample size could have changed this conclusion.

Prospective Interrelation Between Sensory Sensitivity and Fine Motor Skills During the First 18 Months Predicts Later Autistic Features.

Sensory features are included in the diagnostic criteria of autism and atypical sensory responsiveness may produce "cascading effects" on later development. Similarly, autistic individuals often struggle with motor coordination and early delays in the motor domain appear to be linked to later development. However, the longitudinal interrelation between early sensory profiles and motor features on later socio-communicative skills remains to be defined. This study aimed to investigate whether sensory sensitivity impacts fine motor abilities and vice versa from 12 to 18 months of age and to examine how sensory-motor interplay would be associated with later autistic traits at 24-36 months of age. The sample included 118 infant siblings of autistic children recruited at 12 months of age. Sensory sensitivity and eye-hand coordination were assessed at 12 and 18 months of age and autistic traits were evaluated at 24-36 months of age. Cross-lagged panel analysis revealed significant within-domain effects for sensory sensitivity and eye-hand coordination from 12 to 18 months. Furthermore, a significant association between these two domains on later autistic traits was found. In analyzing the longitudinal bidirectional relationship, we found that lower eye-hand coordination skills at 12 months predicted later sensory sensitivity at 18 months, and in turn, social communication skills at 24-36 months. The present study offers new empirical evidence supporting the potential clinical value of including sensory and motor measures besides social communication skills within early autism surveillance programs.

Effects of chronic ankle instability after grade I ankle sprain on the post-traumatic osteoarthritis

BackgroundUntreated acute ankle sprains often result in chronic ankle instability (CAI) and can ultimately lead to the development of post-traumatic osteoarthritis (PTOA). At present, a typical animal model of ankle instability in mice is established by transecting the ligaments around the ankle joint. This study aimed to establish a grade I acute ankle sprain animal model by rapid stretching of peri-ankle joint ligaments. Furthermore, we tried to explore the pathophysiological mechanism of ankle osteoarthritis.MethodsIn all, 18 male C57BL/6 J mice (7 weeks) were randomly divided into three groups: calcaneofibular ligament (CFL) laxity group, deltoid ligament (DL) laxity group, and SHAM group. One week after the surgical procedure, all mice were trained to run in the mouse rotation fatigue machine daily. The mice were tested on the balance beam before surgery and three days, 4 weeks, 8 weeks, and 12 weeks after surgery. Footprint analyses were performed on each mouse before surgery and 12 weeks after surgery. Micro-CT scanning was then performed to evaluate the degeneration of ankle joints and histological staining was performed to analyze and evaluate PTOA caused by ankle joint instability.ResultsAfter surgery, the mice in the CFL and DL laxity groups took longer to cross the balance beam and slipped more often than those in the SHAM group (p < 0.05). The step length and width in the CFL and DL laxity groups were significantly shorter and smaller than those in the SHAM group 12 weeks after surgery (p < 0.05). There was a significant increase in the bone volume fraction (BV/TV) in the CFL and DL laxity groups compared with the SHAM group (p < 0.05). Histological staining results suggested obvious signs of PTOA in the CFL and DL laxity groups.ConclusionsBased on CFL and DL laxity in a mouse ankle instability model, this study suggests that grade I ankle sprain can contribute to chronic ankle instability, impair motor coordination and balance, and eventually lead to PTOA of ankle with significant degeneration of its adjacent joints.

Aberrant copper metabolism and hepatic inflammation cause neurological manifestations in a mouse model of Wilson’s disease

Pathogenic germline mutations in the P-type copper-transporting ATPase (ATP7B) gene cause Wilson’s disease (WD), a hereditary disorder characterized by disrupted copper metabolism. The Arg778Leu (R778L) mutation in exon 8 is prevalent among individuals with WD in East Asia and is associated with more severe phenotypes. In this study, we generated a WD mouse model harboring R778L mutation (R778L mice) using CRISPR/Cas9. R778L mice exhibit a range of pathological characteristics resembling those of patients with WD and the same point mutations, including aberrant copper metabolism, pathological cellular injury, inflammation, and severe hepatic fibrosis. At 3–5 months of age, these mice started to display neurological deficits in motor coordination and cognitive dysfunction, accompanied by increased expression of inflammatory cytokines in the central nervous system. Microglia in the striatum and cortex exhibit significant activation, shorter processes, and decreased branch points. However, the Cu2+ levels in the brain tissue of R778L mice did not differ significantly from those of wild-type mice. Notably, inhibition of hepatic inflammation with PJ34 or siNfkb markedly alleviated the deficiencies in cognitive performance and improved locomotor activity in R778L mice. Thus, this study establishes a novel murine model to investigate the pathophysiology of WD, highlights the liver-brain crosstalk responsible for neurological manifestations in individuals with WD caused by the R778L point mutation, and demonstrates the potential of modulating liver inflammation as a therapeutic strategy for alleviating the neurological manifestations of WD.

Harmaline attenuates chemotherapy-induced peripheral neuropathy: Modulation of Nrf-2 pathway and NK-1 receptor signaling

Peripheral neuropathy, resulting from damage to peripheral nerves, manifests as weakness, numbness, and pain, primarily affecting extremities and significantly impairing quality of life, especially in the elderly. Current treatments often entail severe side effects, necessitating the exploration of alternative therapies. Harmaline, a β-carboline alkaloid derived from Peganum harmala, exhibits promising antioxidant and anti-inflammatory properties. This study aimed to assess the efficacy of harmaline in a vincristine-induced mouse model of peripheral neuropathy. Swiss albino mice received vincristine (0.1 mg/kg, i.p.) for 10 days to induce neuropathy. Harmaline (5 and 10 mg/kg, i.p.) was administered 30 min before vincristine and continued until day 14 to evaluate its protective effects. Behavioral assessments were conducted on days 7 and 14. Vincristine treatment significantly heightened sensitivity to cold, measured by cold plate and acetone drop tests, and to heat, assessed via the hot plate test, while also impairing motor coordination. Biochemical analyses revealed decreased levels of GSH and Nrf-2, alongside elevated TBARS and IL-1β levels in sciatic nerve tissue. Harmaline administration markedly alleviated both behavioral and biochemical alterations induced by vincristine, with the 10 mg/kg dose exhibiting the most pronounced effects. Notably, harmaline treatment elevated GSH and Nrf-2 levels while reducing TBARS and IL-1β. Furthermore, substance-P treatment reversed the protective effects of harmaline, implicating the NK-1 receptor in its mechanism of action. In conclusion, harmaline demonstrates significant potential in mitigating vincristine-induced peripheral neuropathy by reducing oxidative stress through Nrf-2 activation and lowering IL-1β levels, likely via NK-1 receptor inhibition.

Hippotherapy Used in Medical Recovery

Hippotherapy, also known as equine-assisted therapy, falls into the category of alternative therapies that involve human-horse interaction for therapeutic purposes. Horse therapies are especially used for children with various physical, cognitive, and emotional disorders. They can also be successfully used with adults and the elderly. The horse's movement is what stimulates the development of motor skills, balance, and coordination. Direct interaction with the horse, including caring for it, riding, and other related activities, is effective in developing social, emotional, and cognitive skills in both children and adults, as well as in the elderly. Hippotherapy encourages self-confidence, concentration, and motor coordination, making it suitable for people who are anxious, antisocial, depressed, have language difficulties, or low self-esteem. Studies highlight that the presence of horses changes the frequency of the human brain, with subjects becoming more aware and focused when around horses. Horses help therapy beneficiaries stay connected to the present, becoming more aware of their experiences. Additionally, patients learn to pay more attention to the feelings and nonverbal language transmitted by the being they come into contact with. Numerous studies show that horseback riding improves balance, coordination, and reflexes, induces muscle relaxation, reduces spasticity, increases joint mobility, and improves respiratory function and blood circulation. The main objective of the paper is to identify therapies that use horses for patients diagnosed with various conditions, the benefits of these therapies on patients' motor skills, and their effects on patients' mental state. Additionally, we aim to identify horse-related activities that enhance concentration, help address behavioral issues, and facilitate patients' integration into social groups.

Specific and shared cognitive predictors of drawing and block building in typically developing children.

Spatial construction is a complex ability involving attention, global/local visual processing, mental representation, visuo-motor coordination and, to varying extent, working memory and executive functions, and verbal abilities. In developmental neuropsychology, little attention has been paid to comprehend whether and to what extent the above cognitive processes are involved in two main spatial construction tasks, that is drawing and block building. We used path analysis to test shared and specific effects of verbal and spatial working memory, spatial attention, inhibition, verbal abilities (vocabulary and naming), figure disembedding, mental rotation, and visual-motor coordination, as well as of demographics (sex, age and socio-economic status), on two classical drawing (Rey-Osterrieth Complex Figure; ROCF) and block building (Block design; BD) tasks in a sample of 195 typically developing children (age range: 7-11 years). Figure disembedding and visuo-motor coordination were the only shared predictors of both spatial construction tasks. Moreover, ROCF score was directly related with spatial attention and inhibition, while BD score was directly related with sex, vocabulary, mental rotation and backward spatial working memory. These findings distinguish between abilities involved in spatial construction regardless of the type of task and those specifically related to ROCF or Block Design, thus providing clues relevant to neuropsychological assessment and intervention in children with spatial construction disorders.

Factors influencing sedentary behavior and its impact on early childhood psychomotor skills

Sedentary behavior can negatively impact motor and cognitive coordination in early childhood. This study explores the factors that influence sedentary behavior on early childhood psychomotor development. This research method uses a quantitative approach with a survey design and involves a sample of 400 early childhood education teachers. Data were collected through questionnaires distributed using Google Forms. Data analysis was carried out using descriptive and inferential statistics with the Partial Least Square (PLS) approach. The results of the analysis show that the factors of physical activity (β = -0.222), parental digital understanding (β = -0.109), physical activity support facilities (β = -0.080), parental involvement (β = -0.094), teacher competence (β = -0.128), and teacher digital competence (β = -0.235) have a negative correlation with sedentary behavior of early childhood, which means that the higher the factor, the lower the sedentary behavior. Sedentary behavior negatively affects motor coordination (β = -0.552) and child psychology (β = -0.545) increasing the risk of psychological problems such as anxiety and depression. Meanwhile, early childhood characteristics and technology did not have a major influence on early childhood sedentary behavior. The importance of awareness of sedentary behavior requires the creation of a physical activity program for children that involves parents. Keywords: sedentary behavior, psychomotor development, early childhood, early childhood education.

Deliberate synchronization of speech and gesture: effects of neurodiversity and development

Abstract The production of speech and gesture is exquisitely temporally coordinated. In autistic individuals, speech-gesture synchrony during spontaneous discourse is disrupted. To evaluate whether this asynchrony reflects motor coordination versus language production processes, the current study examined deliberately performed hand movements during speech in youth with autism spectrum disorder (ASD) compared to neurotypical youth. Neurotypical adult performance provided a mature baseline. Participants read aloud rhythmic nursery rhymes, while producing a beat-like hand movement. An automated pixel-change video measure identified kinematic peaks; using smoothed acoustic envelope analyses, we identified peaks in speech. Results indicated few diagnostic group differences in explicit speech-movement coordination, although adolescent performance differed from adults. Adults demonstrated higher tempo and greater rhythmicity in their coordination; this group difference suggests that the method is sufficiently subtle to reveal individual differences and that this form of complex coordination undergoes ongoing maturation beyond adolescence. The sample is small, and thus results are necessarily preliminary. In the context of prior speech-gesture coordination studies, these findings of intact synchrony are consistent with the hypothesis that it is the demands of discourse planning, rather than motor coordination, that have led to prior findings of asynchrony during spontaneous speech; this possibility awaits future research.

Precision in Progress: Unraveling the Clinimetric Properties of Beery-Buktenica Developmental Test of Visual-Motor Integration in Children With Cerebral Palsy Across Diverse Motor Severities

BackgroundIn the realm of pediatric cerebral palsy (CP), visual motor challenges often overshadow a child's developmental journey. This study delves into the responsiveness and crucial benchmarks, specifically the minimal clinically important difference (MCID), of the Beery-Buktenica Developmental Test of Visual-Motor Integration (Beery VMI) among children with varying motor severities. MethodEighty-eight children with CP (50 males, 38 females; aged three to 12 years) with Gross Motor Function Classification System (GMFCS) levels I to III were recruited from the rehabilitation department of Chang Gung Memorial Hospital in Taiwan. Each participant received the Beery VMI tests at baseline and at one-year follow-up. The standardized response mean (SRM) was calculated to determine the responsiveness of Beery VMI, and a distribution-based approach was used to estimate MCID. ResultsThe Beery VMI exhibited remarkable responsiveness across GMFCS levels I to III (SRM = 0.98-2.36). MCIDs for Beery VMI varied across severities, with ranges of 2.93 to 4.41 (0.2 S.D.), 7.31 to 11.49 (0.5 S.D.), and 11.70 to 18.38 (0.8 S.D.). Notably, in the visual perception subset, MCIDs were 3.93 to 4.03 (0.2 S.D.), 9.83 to 10.07 (0.5 S.D.), and 15.73 to 16.11 (0.8 S.D.). In the supplemental motor coordination subtest, MCIDs spanned 1.67 to 4.87 (0.2 S.D.), 4.18 to 12.17 (0.5 S.D.), and 6.68 to 19.47 (0.8 S.D.). ConclusionsBeery VMI demonstrates robust responsiveness in children with CP. Motor-severity-tailored MCIDs offer a guide for clinicians and researchers, hinting at treatment efficacy. Particularly, lower change scores in VMI and motor coordination subtests may signal effective interventions for moderate motor disability over mild cases.

The association between infant non-nutritive suck and oral motor development

This study investigated if non-nutritive suck (NNS) at 3 months is related to subsequent oral motor and motor skills using caregiver-reported scores on the Child Oral and Motor Proficiency Scale (ChOMPS) at 12 months in a cohort of 69 full-term infants and their caregivers. Longer NNS burst durations were associated with lower oral motor coordination and total ChOMPS scores. More NNS cycles per minute was associated with lower complex motor movement scores. More NNS bursts, cycles per burst, and cycles per minute were related with lower total ChOMPS scores. Early NNS outcomes can provide valuable insight in future neuromotor development.

Cognitive behavioral phenotyping of DSCAM heterozygosity as a model for autism spectrum disorder.

It is estimated that 1 in 36 children are affected by autism spectrum disorder (ASD) in the United States, which is nearly a twofold increase from a decade ago. Recent genetic studies have identified de novo loss-of-function (dnLoF) mutations in the Down Syndrome Cell Adhesion Molecule (DSCAM) as a strong risk factor for ASD. Previous research has shown that DSCAM ablation confers social interaction deficits and perseverative behaviors in mouse models. However, it remains unknown to what extent DSCAM underexpression captures the full range of behaviors, specifically cognitive phenotypes, presented in ASD. Here, we conducted a comprehensive cognitive behavioral phenotyping which revealed that loss of one copy of DSCAM, as in the DSCAM2J+/-, that is, DSCAM heterozygous mice, displayed hyperactivity, increased anxiety-like behavior, and motor coordination deficits. Additionally, hippocampal-dependent learning and memory was affected, including impairments in working memory, long-term memory, and contextual fear learning. Interestingly, implicit learning processes remained intact. Therefore, DSCAM LoF produces autistic-like behaviors that are similar to those observed in human cases of ASD. These findings further support a role for DSCAM dnLoF mutations in ASD and suggest DSCAM2J+/- as a suitable model for ASD research.

Behavioral laterality in Greater Flamingo (Phoenicopterus roseus)

Abstract From a behavioral adaptation perspective, lateralization in gregarious species likely evolved to maintain cohesiveness among individuals, particularly in behaviors related to social life that require higher levels of cognitive capabilities. Thus, we hypothesized that motor coordination (lateralization) would be observed at the population level rather than at the individual level. To test this hypothesis, we studied population-level laterality in a wild population of Greater Flamingos (Phoenicopterus roseus) during the winter in Eilat, Israel. In November and December 2019, we recorded 176 behaviors in 220 flamingos, observing four behaviors: ‘At rest,’ ‘Vigilant,’ ‘Scratching,’ and ‘Preening’. The laterality indices for ‘At rest’ and ‘Vigilant’ were similar to those of ambidextrous simulated populations, indicating that these behaviors were not lateralized. However, ‘Preening’ and ‘Scratching’ were significantly left-lateralized. We conclude that at the population level, the symmetry of these behaviors results from flock pressure to coordinate population-level behaviors. Furthermore, the mechanism of lateralization is characteristic not only of the local population but of the entire species sensu stricto.