Background: Urban neighbourhood environments may impact older adults' cognitive health. However, longitudinal studies examining key environmental correlates of cognitive health are lacking. We estimated cross-sectional and longitudinal associations of neighbourhood built and natural environments and ambient air pollution with multiple cognitive health outcomes in Australian urban dwellers aged 60+ years.
View Article and Find Full Text PDFBackground: Most studies examining the effects of neighbourhood urban design on cardiometabolic health focused solely on the built or natural environment. Also, they did not consider the roles of neighbourhood socio-economic status (SES) and ambient air pollution in the observed associations, and the extent to which these associations were mediated by physical activity and sedentary behaviours.
Methods: We used data from the AusDiab3 study (N = 4141), a national cohort study of Australian adults to address the above-mentioned knowledge gaps.
In this cross-sectional study, we examined the extent to which features of the neighbourhood natural, built, and socio-economic environments were related to cognitive age in adults (N = 3418, M = 61 years) in Australia. Machine learning estimated an individual's cognitive age from assessments of processing speed, verbal memory, premorbid intelligence. A 'cognitive age gap' was calculated by subtracting chronological age from predicted cognitive age and was used as a marker of cognitive age.
View Article and Find Full Text PDFPremanifest Huntington's disease (pre-HD) individuals typically show increased task-related functional magnetic resonance imaging (fMRI), suggested to reflect compensatory strategies. Despite the evidence, no study has attempted to understand the compensatory process in light of 'formal' models of compensation. We used a quantitative model of compensation - the Compensation-Related Utilization of Neural Circuits Hypothesis (CRUNCH), to characterise compensation in pre-HD using fMRI.
View Article and Find Full Text PDFHuntington's disease (HD) is a progressive autosomal dominant disorder characterised by impairment of movement, cognitive decline and psychiatric impairment. During the premanifest stages of HD (pre-HD), there are notable structural and functional brain changes detectable many decades prior to clinical diagnosis. Although caudate atrophy is one of the earliest and most prominent sites of neuropathology, there is also evidence of cortical atrophy, compromised white and grey matter integrity, cortical hypometabolism, and aberrant task-related functional magnetic resonance imaging (fMRI) activity.
View Article and Find Full Text PDFThe 'reserve' hypothesis posits that the brain undergoes structural and functional reorganisation to actively cope with brain damage or disease. Consistent with passive and active components of 'reserve', the brain moderates its biological substrates (brain reserve) and differentially changes the level of neural activity in tasks-specific networks and/or by recruiting additional non-task related brain regions (cognitive reserve) to optimise behavioural performance. How the 'reserve' hypothesis applies in neurodegenerative disorders such as Huntington's disease (HD) remains unknown.
View Article and Find Full Text PDFA comparative analysis of intermale aggression in the resident-intruder test was conducted with gray rats from a wild unselected population bred at the laboratory for three generations and gray rats selected for elimination (tame) and enhancement (aggressive) of aggressiveness towards human for 71-72 generations. Males from the laboratory line Wistar were used as neutral opponents. Rats from the tame line were characterized by reduced aggression manifest as longer attack latency, decreased number of attacks, upright postures, chases, kicks, and shorter total time of aggressive behavior compared to unselected males.
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