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Fetal Alcohol Spectrum Disorder (FASD) is one of the leading causes of intellectual disability and learning difficulties around the world. Children with FASD often have extremely low adaptive behavior due to the severity of brain impairment, however there is limited understanding as to the important predictors of adaptive behavior. In a study of 39 children with FASD and 29 comparison children, we found that social cognition (specifically recognizing emotions) was the only significant independent predictor of teacher-rated adaptive functioning even after including IQ, executive functioning, and adverse childhood experiences into the model. In this current study, Māori (Indigenous people of Aotearoa New Zealand) were overrepresented; therefore, the research was supported by a strong partnership with Te Wāhanga Hauora Māori (Māori Health Service). Aotearoa New Zealand's colonized history is recognized and findings are discussed with regard to both the psychological literature and a Te Ao Māori worldview.

Objective. A systematic review with a meta-analysis explored effects of cognitively loaded physical activity interventions on global cognition in community-dwelling older adults (≥65 years of age) experiencing mild cognitive impairment (MCI), compared to any control. Methods. A literature search was conducted in 4 databases (MEDLINE [OvidSP], PubMed, CINAHL, and the Cochrane Central Register of Controlled Trials [Wiley]) from inception until January 30, 2018. The meta-analysis was conducted with Review Manager 5.3. Results. Six randomized controlled trials (RCTs) with 547 participants were identified. The interventions ranged from 4 to 52 weeks. Baseline and initial follow-up assessments were used. The primary pooled analysis of all RCTs demonstrated a nonsignificant trivial effect (standardized mean difference [SMD] 0.07, 95% confidence interval [CI] −0.44 to 0.58) favoring the intervention. In pooled subanalysis of 4 RCTs (n = 405) using the same global cognition measure (Mini-Mental State Examination) and duration of intervention >12 weeks, the intervention group achieved a small but significant improvement for global cognition (SMD 0.45, 95% CI 0.14 to 0.75). Conclusion. When all the RCTs were pooled, the effect of cognitively loaded physical activity intervention on global cognitive function in older adults with MCI remained unclear. The subgroup analysis provides translation evidence for future RCT study designs.

Huntington's disease (HD) is an autosomal dominant inherited neurodegenerative disease caused by a CAG repeat expansion in exon 1 of the Huntington gene (HD) also known as IT15. Despite the disease being caused by dysfunction ofa single gene, expressed as an expanded polyglutamine in the huntingtin protein, there is a major variability in the symptom profile of patients with Huntington's disease as well as great variability in the neuropathology. The symptoms vary throughout the course of the disease and vary greatly between cases. These symptoms present as varying degrees of involuntary movements, mood, personality changes, cognitive changes and dementia. To determine whether there is a morphological basis for this symptom variability, recent studies have investigated the cellular and neurochemical changes in the striatum and cerebral cortex in the human brain to determine whether there is a link between the pathology in these regions and the symptomatology shown by individual cases. These studies together revealed that cases showing mainly mood symptom profiles correlated with marked degeneration in the striosomal compartment of the striatum, or in the anterior cingulate gyrus of the cerebral cortex. In contrast, in cases with mainly motor symptoms neurodegeneration was especially marked in the primary motor cortex with variable degeneration in both the striosomes and matrix compartments of the striatum. These studies suggest that the variable degeneration of the striatum and cerebral cortex correlates with the variable profiles of Huntington's disease.

In transgenic mouse models of Huntington disease (HD) environmental enrichment significantly delays disease onset. A questionnaire-based survey of 154 adults with diagnosed HD (mean 4.2 years postdiagnosis) and a known IT15 CAG repeat length, explored whether premorbid lifestyle may relate to age-at-onset (AO). Participants were drawn from HD outpatient clinics in Australia and New Zealand. Premorbid physical, intellectual, and passive activity levels were used to generate scores in the categories of leisure, nonleisure (education, occupation and domestic duties) and total lifestyle. AO was associated with increased CAG repeat length as expected (r = -0.72, P0.001), but also with a lifestyle that included higher levels of passive activity (r = -0.38, P0.001). Multiple linear regression modeling showed lifestyle passivity to be a variable independent of CAG repeat length in predicting AO (R(2) = 0.54, b = -0.22, P = 0.005). Comparison of the mean AO across tertiles of lifestyle passivity scores showed onset 4.6 years (95% CI = 1.3-7.9) later in the least compared with the most passive tertile. CAG repeat length was also shown to predict lifestyle passivity (R(2) = 0.12, b = 1.08, P0.0005). Neither intellectual nor physical activity showed significant relationships to AO or CAG repeat length in this cohort. Our study leads to two conclusions: that a passive lifestyle may be a preclinical expression of HD, and that it actually contributes to the earlier onset of symptoms. Overcoming the tendency to be passive may substantially delay onset of HD. (c) 2010 Movement Disorder Society.