BACKGROUND: Type 2 diabetes is one of the most prevalent and preventable diseases worldwide and impulsivity, a psychological trait characterized by making quick decisions without forethought, has been suggested as a key feature for health-related conditions. However, there have been no studies examining the relationships between impulsivity and the incidence of type 2 diabetes and our aim was to assess the prospective association between trait impulsivity and the risk of developing type 2 diabetes.
METHODS: A prospective observational study design was conducted between May 2014 and February 2023 within the NutriNet-Santé cohort. A web-based platform was used to collect data from the French adult population, with voluntary enrollment and participation. Of the 157,591 adults (≥ 18 years old) participating in the NutriNet-Santé study when impulsivity was assessed, 109,214 participants were excluded due to prevalent type 1 or 2 diabetes or missing data for impulsivity or follow-up data for type 2 diabetes. Trait impulsivity, and the attention, motor, and non-planning subfactors, were assessed at baseline using the Barratt Impulsiveness Scale 11. Incident type 2 diabetes was ascertained through follow-up. Medical information was reviewed by NutriNet-Santé physician experts to ascertain incident diabetes cases based on the ICD-10. Cox regression models, using hazard ratios and 95% confidence intervals (HR [95% CI]), were performed to evaluate associations between impulsivity per 1 standard deviation increment and type 2 diabetes risk, adjusting by recognized confounders.
RESULTS: Of the 48,377 individuals studied (women 77.6%; age at baseline = 50.6 year ± 14.5 years), 556 individuals developed type 2 diabetes over a median follow-up of 7.78 (IQR: 3.97-8.49) years. Baseline impulsivity was associated with an increased risk of type 2 diabetes incidence (HR = 1.10 [1.02, 1.20]). The motor impulsivity subfactor was positively associated with type 2 diabetes risk (HR = 1.14 [1.04, 1.24]), whereas no associations were found for attention and non-planning impulsivity subfactors.
CONCLUSIONS: Trait impulsivity was associated with an increased type 2 diabetes risk, mainly driven by the motor impulsivity subfactor. If these results are replicated in other populations and settings, trait impulsivity may become an important psychological risk factor to be considered in the prevention of type 2 diabetes.
UNASSIGNED: Name of registry: The NutriNet-Santé Study. A Web-based Prospective Cohort Study of the Relationship Between Nutrition and Health and of Dietary Patterns and Nutritional Status Predictors. Cohort registration number: NCT03335644. Date of registration: October 11, 2017. URL: https://clinicaltrials.gov/ct2/show/NCT03335644.

Developmental co-ordination disorder (DCD) is characterised by difficulties in motor control and coordination from early childhood. While problems processing facial identity are often associated with neurodevelopmental conditions, such issues have never been directly tested in adults with DCD. We tested this possibility through a range of tasks, and assessed the prevalence of developmental prosopagnosia (i.e., lifelong difficulties with faces), in a group comprising individuals who self-reported a diagnosis of, or suspected that they had, DCD. Strikingly, we found 53% of this probable DCD group met recently recommended criteria for a diagnosis of prosopagnosia, with 22% acquiring a diagnosis using traditional cognitive task-based methods. Moreover, their problems with faces were apparent on both unfamiliar and familiar face memory tests, as well as on a facial perception task (i.e., could they tell faces apart). Positive correlations were found between self-report measures assessing movement and coordination problems, and objective difficulties on experimental face identity processing tasks, suggesting widespread neurocognitive disruption in DCD. Importantly, issues in identity processing in our probable DCD group remained even after excluding participants with comorbid conditions traditionally associated with difficulties in face recognition, i.e., autism and dyslexia. We recommend that any diagnostic test for DCD should include an assessment for prosopagnosia. Given the high prevalence of prosopagnosia in our probable DCD group, and the positive correlations between DCD and prosopagnosia symptoms, there may be a stronger link between movement and facial identity abilities than previously thought.

It is a paradox of neurological rehabilitation that, in an era in which preclinical models have produced significant advances in our mechanistic understanding of neural plasticity, there is inadequate support for many therapies recommended for use in clinical practice. When the goal is to estimate the probability that a specific form of therapy will have a positive clinical effect, the integration of mechanistic knowledge (concerning \'the structure or way of working of the parts in a natural system\') may improve the quality of inference. This is illustrated by analysis of three contemporary approaches to the rehabilitation of lateralized dysfunction affecting people living with stroke: constraint-induced movement therapy; mental practice; and mirror therapy. Damage to \'cross-road\' regions of the structural (white matter) brain connectome generates deficits that span multiple domains (motor, language, attention and verbal/spatial memory). The structural integrity of these regions determines not only the initial functional status, but also the response to therapy. As structural disconnection constrains the recovery of functional capability, \'disconnectome\' modelling provides a basis for personalized prognosis and precision rehabilitation. It is now feasible to refer a lesion delineated using a standard clinical scan to a (dis)connectivity atlas derived from the brains of other stroke survivors. As the individual disconnection pattern thus obtained suggests the functional domains most likely be compromised, a therapeutic regimen can be tailored accordingly. Stroke is a complex disorder that burdens individuals with distinct constellations of brain damage. Mechanistic knowledge is indispensable when seeking to ameliorate the behavioural impairments to which such damage gives rise.

Background Nerve conduction studies ease the understanding of the various pathologies of the peripheral nervous system. It helps physicians to delineate between the two principal types of peripheral etiologies: axonal degeneration and demyelination. An increase in weight in the form of excessive fat deposition or obesity could have a worrisome effect on nerve conduction. So, to find the association of various anthropometric parameters (age, gender, height, weight, waist-hip ratio and body mass index) with motor and sensory median nerve conduction parameters (latency, amplitude and velocity) this cross-sectional study was conducted. Materials and method A total of 87 subjects were taken and their height, weight, waist-hip ratio and body mass index were measured using standard techniques. Motor and sensory nerve conduction parameters were measured on an electromyography machine. Data was stored, tabulated and analyzed. Results The average height of male and female subjects ± SD was 1.699 ± 0.072 m and 1.589 ± 0.067 m respectively. The average weight of male and female subjects ± SD was 64.089 ± 11.497 kg and 52.949 ± 8.404 kg, respectively. The average BMI of normal, underweight and overweight subjects ± SD was 21.668 ± 2.048 kg/m2, 17.074 ± 0.794 kg/m2 and 26.595 ± 0.915 kg/m2 respectively. Weight showed a significant (p = 0.0025) correlation with the latency of motor median nerve conduction. Waist-hip ratio showed a significant (p = 0.042 and p = 0.036) correlation with motor median nerve conduction velocity in both male and female subjects, respectively. BMI in the overweight category showed a significant (p = 0.0156 and p = 0.0290) correlation with latency and amplitude of motor median nerve conduction study, respectively. Conclusions This study exemplifies that an increase in BMI of our body can affect nerve conduction. This could serve as a preliminary study to assess the effect of obesity on peripheral nerve conduction, especially in the Indian population.

CTNNB1 syndrome is a rare monogenetic disorder caused by CTNNB1 de novo pathogenic heterozygous loss-of-function variants that result in cognitive and motor disabilities. Treatment is currently lacking; our study addresses this critical need. CTNNB1 encodes β-catenin which is essential for normal brain function via its dual roles in cadherin-based synaptic adhesion complexes and canonical Wnt signal transduction. We have generated a Ctnnb1 germline heterozygous mouse line that displays cognitive and motor deficits, resembling key features of CTNNB1 syndrome in humans. Compared with wild-type littermates, Ctnnb1 heterozygous mice also exhibit decreases in brain β-catenin, β-catenin association with N-cadherin, Wnt target gene expression, and Na/K ATPases, key regulators of changes in ion gradients during high activity. Consistently, hippocampal neuron functional properties and excitability are altered. Most important, we identify a highly selective inhibitor of glycogen synthase kinase (GSK)3α,β that significantly normalizes the phenotypes to closely meet wild-type littermate levels. Our data provide new insights into brain molecular and functional changes, and the first evidence for an efficacious treatment with therapeutic potential for individuals with CTNNB1 syndrome.

Early motor skills may be important early markers of neurodevelopmental conditions or predictors of their later onset. To explore this, we conducted a systematic review and meta-analysis of infant motor skill assessments in those who go on to gain a clinical diagnosis of autism, attention deficit hyperactivity disorder (ADHD), schizophrenia, language conditions, tic disorders, or developmental coordination disorder (DCD). In total, 65 articles met inclusion criteria. Three three-level meta-analyses were run. Meta-analysis of milestone achievement in N=21354 individuals revealed gross motor milestones were significantly delayed compared to controls (g= 0.53, p< 0.001). Subgroup analyses revealed autism (g= 0.63) and DCD (g= 0.53) had the highest magnitude delays. Specific delays were revealed for holding the head up (g= 0.21), sitting (g= 0.28), standing (g= 0.35), crawling (g=0.19), and walking (g= 0.71). Meta-analyses of standardised motor skill measurements in N=1976 individuals revealed reduced performance compared to controls in autism and language conditions (g= -0.54, p< 0.001). Together, these findings demonstrate delayed milestone attainment and motor impairments in early childhood in neurodevelopmental conditions.

Neurodevelopmental outcomes for preschool-age children in the United States with in utero Zika virus (ZIKV) exposure have not yet been reported. We performed a case-control study to assess whether children exposed in utero to ZIKV have abnormal neurodevelopment at age 4-5 years compared to unexposed controls. Thirteen ZIKV-exposed cases that did not have microcephaly or other specific features of congenital Zika syndrome and 12 controls were evaluated between ages 4-5 years. Child neurodevelopment was assessed using the Pediatric Evaluation of Disability Inventory, Behavior Rating Inventory of Executive Function, Peabody Picture Vocabulary Test, Bracken School Readiness Assessment (BSRA), and Movement Assessment Battery for Children (MABC). Caregivers answered questions on the child\'s medical history and family demographics. Cases and controls were evaluated at mean (SD) ages 4.9 (0.3) and 4.8 (0.4) years, respectively. Caregivers reported more behavior and mood problems in cases than controls. MABC scores showed more gross and fine motor coordination difficulties among cases than controls. Controls trended towards higher performance on concepts underlying school readiness on BSRA. Three cases had a diagnosis of autism spectrum disorder or global developmental delay. Continued follow-up through school age for children with prenatal ZIKV exposure is needed to understand the impact of in utero ZIKV exposure on motor coordination, cognition, executive function, and academic achievement.

BACKGROUND: Amyloid-beta (Aβ) plaque is a neuropathological hallmark of Alzheimer\'s disease (AD). As anti-amyloid monoclonal antibodies enter the market, predicting brain amyloid status is critical to determine treatment eligibility.
OBJECTIVE: To predict brain amyloid status utilizing machine learning approaches in the Advancing Reliable Measurement in Alzheimer\'s Disease and Cognitive Aging (ARMADA) study.
METHODS: ARMADA is a multisite study that implemented the National Institute of Health Toolbox for Assessment of Neurological and Behavioral Function (NIHTB) in older adults with different cognitive ability levels (normal, mild cognitive impairment, early-stage dementia of the AD type).
METHODS: Participants across various sites were involved in the ARMADA study for validating the NIHTB.
METHODS: 199 ARMADA participants had either PET or CSF information (mean age 76.3 ± 7.7, 51.3% women, 42.3% some or complete college education, 50.3% graduate education, 88.9% White, 33.2% with positive AD biomarkers).
METHODS: We used cognition, emotion, motor, sensation scores from NIHTB, and demographics to predict amyloid status measured by PET or CSF. We applied LASSO and random forest models and used the area under the receiver operating curve (AUROC) to evaluate the ability to identify amyloid positivity.
RESULTS: The random forest model reached AUROC of 0.74 with higher specificity than sensitivity (AUROC 95% CI:0.73 - 0.76, Sensitivity 0.50, Specificity 0.88) on the held-out test set; higher than the LASSO model (0.68 (95% CI:0.68 - 0.69)). The 10 features with the highest importance from the random forest model are: picture sequence memory, cognition total composite, cognition fluid composite, list sorting working memory, words-in-noise test (hearing), pattern comparison processing speed, odor identification, 2-minutes-walk endurance, 4-meter walk gait speed, and picture vocabulary. Overall, our model revealed the validity of measurements in cognition, motor, and sensation domains, in associating with AD biomarkers.
CONCLUSIONS: Our results support the utilization of the NIH toolbox as an efficient and standardizable AD biomarker measurement that is better at identifying amyloid negative (i.e., high specificity) than positive cases (i.e., low sensitivity).

OBJECTIVE: The relationship between somatosensory and motor components of urinary incontinence in individuals with MS has not been extensively addressed. The study was aimed at investigating the association of urinary incontinence severity with motor and sensory performance in women with multiple sclerosis (MS).
METHODS: A cross-sectional single-center prospective study was conducted in 337 women with MS. The severity of MS symptoms was assessed using the SymptoMScreen questionnaire. The urinary incontinence status of the participants was evaluated using the Urinary Incontinence Inventory (UDI-6) and the Incontinence Impact Questionnaire (IIQ-7). Physical performance was considered with the Timed Up and Go (TUG) test and the 5-Times Sit-to-Stand (5TSTS) test. In addition, the sensory performance of the individuals with MS was queried using the Somatosensory Amplification Scale (SSAS) and Sensory Sensitivity Scale (SeSS).
RESULTS: The UDI-6 (r=0.685, p<0.05) and IIQ-7 (r=0.759, p<0.05) correlated highly with SymptoMScreen. Among the physical performance measures, TUG (r=0.012, p<0.05) and 5TSTS (r=0.096, p<0.05) were weakly associated with UDI-6, but not statistically significantly. Similarly, there was a low correlation between IIQ-7 and TUG (r=-0.005, p<0.05) and 5TSTS (r=0.068, p<0.05). UDI-6 (0.360, p<0.05) and IIQ-7 (0.378, p<0.05) correlated moderately with SASS. On the other hand, SeSS had a low correlation coefficient with UDI-6 (0.305, p<0.05) and IIQ-7 (0.272, p<0.05).
CONCLUSIONS: The results revealed that sensory performance was more associated with urinary incontinence in women with MS than physical performance. The urinary incontinence severity was also related to MS symptoms (bladder control, walking, spasticity, stiffness cognitive function). Future studies should consider the potential impact of sensory performance on urinary incontinence and focus on explaining the mechanism behind this relationship.

OBJECTIVE: This study aimed to explore the relationships between potential neurophysiological biomarkers and upper limb motor function recovery in stroke patients, specifically focusing on combining two neurophysiological markers: electroencephalography (EEG) and transcranial magnetic stimulation (TMS).
METHODS: This cross-sectional study analyzed neurophysiological, clinical, and demographical data from 102 stroke patients from the DEFINE cohort. We searched for correlations of EEG and TMS measurements combined to build a prediction model for upper limb motor functionality, assessed by five outcomes, across five assessments: Fugl-Meyer Assessment (FMA), Handgrip Strength Test (HST), Finger Tapping Test (FTT), Nine-Hole Peg Test (9HPT), and Pinch Strength Test (PST).
RESULTS: Our multivariate models agreed on a specific neural signature: higher EEG Theta/Alpha ratio in the frontal region of the lesioned hemisphere is associated with poorer motor outcomes, while increased MEP amplitude in the non-lesioned hemisphere correlates with improved motor function. These relationships are held across all five motor assessments, suggesting the potential of these neurophysiological measures as recovery biomarkers.
CONCLUSIONS: Our findings indicate a potential neural signature of brain compensation in which lower frequencies of EEG power are increased in the lesioned hemisphere, and lower corticospinal excitability is also increased in the non-lesioned hemisphere. We discuss the meaning of these findings in the context of motor recovery in stroke.