The narrative coherence of witness transcripts in children on the autism spectrum

Background and Aims. Autistic children often recall fewer details about witnessed events than typically developing children (of comparable age and ability), although the information they recall is generally no less accurate. Previous research has not examined the narrative coherence of such accounts, despite higher quality narratives potentially being perceived more favourably by criminal justice professionals and juries. This study compared the narrative coherence of witness transcripts produced by autistic and typically developing (TD) children (ages 6-11 years, IQs 70+). Methods and Procedures. Secondary analysis was carried out on interview transcripts from a subset of 104 participants (autism=52, TD=52) who had taken part in a larger study of eyewitness skills in autistic and TD children. Groups were matched on chronological age, IQ and receptive language ability. Coding frameworks were adopted from existing narrative research, featuring elements of ‘story grammar’. Outcomes and Results. Whilst fewer event details were reported by autistic children, there were no group differences in narrative coherence (number and diversity of ‘story grammar’ elements used), narrative length or semantic diversity. Conclusions and Implications. These findings suggest that the narrative coherence of autistic children’s witness accounts is equivalent to TD peers of comparable age and ability

The performance of eyewitnesses with intellectual disabilities on identification lineups

Despite the large number of people with intellectual disabilities (ID) and the fact they are more likely to be victims and witnesses of crime, only two published studies have investigated their performance on identification line-up parades. In the present study we examined the identification performance of adults with and without ID on both a perpetrator-present and a perpetrator-absent photographic line-up. In addition, we investigated factors that could explain any potential difficulties with identification performance, such as face recognition performance (as measured by a standardised test), eyewitness confidence, understanding of the purpose of a line-up, and memory for non-biased line-up instructions. In comparison with typical adults, participants with ID demonstrated poorer performance across both perpetrator-present and perpetrator-absent photographic line-ups, yet were more confident in the accuracy of their responses. In addition they had poorer face recognition performance, were less likely to understand the purpose of the line-up, and were less likely to remember the non-biased line-up instructions. This pattern of difficulties is discussed in relation to the development of future research and interventions

Utility of accelerometers to measure physical activity in children attending an obesity treatment intervention

Objectives. To investigate the use of accelerometers to monitor change in physical activity in a childhood obesity treatment intervention. Methods. 28 children aged 7–13 taking part in “Families for Health” were asked to wear an accelerometer (Actigraph) for 7-days, and complete an accompanying activity diary, at baseline, 3-months and 9-months. Interviews with 12 parents asked about research measurements. Results. Over 90% of children provided 4 days of accelerometer data, and around half of children provided 7 days. Adequately completed diaries were collected from 60% of children. Children partake in a wide range of physical activity which uniaxial monitors may undermonitor (cycling, nonmotorised scootering) or overmonitor (trampolining). Two different cutoffs (4 METS or 3200 counts⋅min-1) for minutes spent in moderate and vigorous physical activity (MVPA) yielded very different results, although reached the same conclusion regarding a lack of change in MVPA after the intervention. Some children were unwilling to wear accelerometers at school and during sport because they felt they put them at risk of stigma and bullying. Conclusion. Accelerometers are acceptable to a majority of children, although their use at school is problematic for some, but they may underestimate children's physical activity

Dysregulation of Na+/K+ ATPase by amyloid in APP+PS1 transgenic mice

BACKGROUND: The pathology of Alzheimer's disease (AD) is comprised of extracellular amyloid plaques, intracellular tau tangles, dystrophic neurites and neurodegeneration. The mechanisms by which these various pathological features arise are under intense investigation. Here, expanding upon pilot gene expression studies, we have further analyzed the relationship between Na+/K+ ATPase and amyloid using APP+PS1 transgenic mice, a model that develops amyloid plaques and memory deficits in the absence of tangle formation and neuronal or synaptic loss. RESULTS: We report that in addition to decreased mRNA expression, there was decreased overall Na+/K+ ATPase enzyme activity in the amyloid-containing hippocampi of the APP+PS1 mice (although not in the amyloid-free cerebellum). In addition, dual immunolabeling revealed an absence of Na+/K+ ATPase staining in a zone surrounding congophilic plaques that was occupied by dystrophic neurites. We also demonstrate that cerebral Na+/K+ ATPase activity can be directly inhibited by high concentrations of soluble Aβ. CONCLUSIONS: The data suggest that the reductions in Na+/K+ ATPase activity in Alzheimer tissue may not be purely secondary to neuronal loss, but may results from direct effects of amyloid on this enzyme. This disruption of ion homeostasis and osmotic balance may interfere with normal electrotonic properties of dendrites, blocking intraneuronal signal processing, and contribute to neuritic dystrophia. These results suggest that therapies aimed at enhancing Na+/K+ ATPase activity in AD may improve symptoms and/or delay disease progression

Intracranial Injection of Gammagard, a Human IVIg, Modulates the Inflammatory Response of the Brain and Lowers A\u3cem\u3eβ\u3c/em\u3e in APP/PS1 Mice Along a Different Time Course than Anti-A\u3cem\u3eβ\u3c/em\u3e Antibodies

Gammagard IVIg is a therapeutic approach to treat Alzheimer\u27s disease currently in phase 3 clinical trials. Despite the reported efficacy of the approach the mechanism of action is poorly understood. We have previously shown that intracranial injection of anti-Aβ antibodies into the frontal cortex and hippocampus reveals important information regarding the time course of events once the agent is in the brain. In the current study we compared IVIg, mouse-pooled IgG, and the anti-Aβ antibody 6E10 injected intracranially into the frontal cortex and hippocampus of 7-month-old APP/PS1 mice. We established a time course of events ranging from 1 to 21 d postinjection. IVIg and pooled mouse IgG both significantly reduced Aβ deposition to the same degree as the 6E10 anti-Aβ antibody; however, the clearance was much slower to occur, happening between the 3 and 7 d time points. In contrast, as we have previously shown, Aβ reductions were apparent with the 6E10 anti-Aβ group at the 1 d time point. Also, neuroinflammatory profiles were significantly altered by the antibody treatments. APP/PS1 transgenic mice at 7 months of age typically exhibit an M2a inflammatory phenotype. All antibody treatments stimulated an M2b response, yet anti-Aβ antibody was a more rapid change. Because the neuroinflammatory switch occurs before the detectable reductions in amyloid deposition, we hypothesize that the IVIg and pooled mouse IgG act as immune modulators and this immune modulation is responsible for the reductions in amyloid pathology

Explaining the effects of symptom attribution by carers on help-seeking for individuals living with dementia

This study investigated the effects of carer attributions on help-seeking behaviour for people with dementia using interviews with 84 carers recruited through general practice. Memory loss was the most commonly reported first symptom but psychological and behavioural symptoms were also common at onset. In over a third of individuals help-seeking was delayed for a mean of 25 months (range 6-69, SD 19.3). Help-seeking between those who attributed symptoms to dementia, or to unknown causes, and those who attributed symptoms to personality, ageing, life events or other illnesses was statistically significant ( p < 0.001). No statistically significant associations between help-seeking and patient or carer characteristics were found. There is a need to raise public awareness about the range of symptoms suggestive of dementia. Assumptions that age and other conditions may be the likely cause of an individual's cognitive decline needs to be challenged by practitioners. Attribution of symptoms to characteristics other than dementia delays help-seeking

Using participatory and creative methods to facilitate emancipatory research with people facing multiple disadvantage: a role for health and care professionals

Participatory and creative research methods are a powerful tool for enabling active engagement in the research process of marginalised people. It can be particularly hard for people living with multiple disadvantage, such as disabled people from ethnic minority backgrounds, to access research projects that are relevant to their lived experience. This article argues that creative and participatory methods facilitate the co-researchers’ engagement in the research process, which thus becomes more empowering. Exploring the congruence of these methods with their professional ethos, health and care professionals can use their skills to develop them further. Both theory and practice examples are presented

Hyperhomocysteinemia-Induced Gene Expression Changes in the Cell Types of the Brain

High plasma levels of homocysteine, termed hyperhomocysteinemia, are a risk factor for vascular cognitive impairment and dementia, which is the second leading cause of dementia. While hyperhomocysteinemia induces microhemorrhages and cognitive decline in mice, the specific effect of hyperhomocysteinemia on each cell type remains unknown. We took separate cultures of astrocytes, microglia, endothelial cells, and neuronal cells and treated each with moderate levels of homocysteine for 24, 48, 72, and 96 hr. We then determined the gene expression changes for cell-specific markers and neuroinflammatory markers including the matrix metalloproteinase 9 system. Astrocytes had decreased levels of several astrocytic end feet genes, such as aquaporin 4 and an adenosine triphosphate (ATP)-sensitive inward rectifier potassium channel at 72 hr, as well as an increase in matrix metalloproteinase 9 at 48 hr. Gene changes in microglia indicated a peak in proinflammatory markers at 48 hr followed by a peak in the anti-inflammatory marker, interleukin 1 receptor antagonist, at 72 hr. Endothelial cells had reduced occludin expression at 72 hr, while kinases and phosphatases known to alter tau phosphorylation states were increased in neuronal cells. This suggests that hyperhomocysteinemia induces early proinflammatory changes in microglia and astrocytic changes relevant to their interaction with the vasculature. Overall, the data show how hyperhomocysteinemia could impact Alzheimer’s disease and vascular cognitive impairment and dementia