ObjectiveTo determine the prevalence of reported ‘household stressor’ adverse childhood experiences (ACEs) in families of children presenting with neurodevelopmental, behavioural or emotional difficulties and to determine whether family vulnerabilities, individually or cumulatively, were associated with particular clinical symptomatology.DesignRetrospective chart review followed by statistical analysis of family stressors and clinical symptomatology.SettingA community paediatric clinic in Australia.ParticipantsAll 267 children who attended an initial paediatric appointment during 2018.Results162 (60.7%) children had been exposed to one or more household stressor ACEs, including 116 (43.4%) children exposed to parental mental illness. Behavioural disturbance occurred in 144 (53.9%) children and externalising behaviours (other than attention deficit hyperactivity disorder) were more frequent than internalising behaviours. Externalising and internalising behaviours were associated with individual and cumulative household stressor ACEs. Most other symptomatology apart from genetic/neurological conditions, autistic symptoms and some developmental delays appeared to be partially associated with ACEs.ConclusionHousehold stressor ACEs were common, frequently occurred concurrently, and were associated with much of the symptomatology, in this cohort. Parental mental illness was the most prevalent stressor and behavioural disturbance the most prevalent symptomatology. These findings may have implications for clinical practice and service provision.
Background: Individuals with mild cognitive impairment (MCI) are at high risk of progression to Alzheimer’s disease (AD) dementia, but some remain stable. There is a need to identify those at higher risk of progression to improve patient management and outcomes. Objective: To evaluate the trajectory of plasma neurofilament light chain (pNFL) prior to progression from MCI to AD dementia, the performance of pNFL, in combination with the Mini-Mental State Examination (MMSE), as a predictor of progression from MCI to AD dementia and to inform clinicians on the use of pNFL as a predictive biomarker. Methods: Participants (n = 440) with MCI and longitudinal follow-up (mean = 4.2 years) from the AD Neuroimaging Initiative dataset were included. pNFL as a marker for neurodegeneration and the MMSE as a cognitive measure were investigated as simple/practical predictors of progression. The risk of progressing from MCI to AD dementia associated with pNFL and MMSE scores was assessed using Cox and logistic regression models. Results: The current risk of progression to AD dementia was 37%higher in individuals with high pNFL (> 56 ng/L) compared to those with average pNFL (≤40 ng/L). A combination of baseline pNFL and MMSE could differentiate those who progressed within 5 years (AUC = 0.75) from stable individuals. Including change in MMSE over 6-12 months further improved the model (AUC = 0.84). Conclusion: Our findings reveal that combining pNFL with a simple dementia screener (MMSE) can reliably predict whether a person with MCI is likely to progress to AD dementia within 5 years.
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