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Clinical and biochemical diversity of Parkinson's disease (PD) and numerous demographic, clinical, and pathological measures influencing cognitive function and its decline in PD create problems with the determination of effects of individual measures on cognition in PD. This is particularly the case where these measures significantly interrelate with each other producing intricate networks of direct and indirect effects on cognition. Here, we use generalized structural equation modelling (GSEM) to identify and characterize significant paths for direct and indirect effects of 14 baseline measures on global cognition in PD at baseline and at 4 years later. We consider 269 drug-naïve participants from the Parkinson's Progression Marker Initiative database, diagnosed with idiopathic PD and observed for at least 4 years after baseline. Two GSEM networks are derived, highlighting the possibility of at least two different molecular pathways or two different PD sub-types, with either CSF p-tau181 or amyloid beta (1–42) being the primary protein variables potentially driving progression of cognitive decline. The models provide insights into the interrelations between the 14 baseline variables, and determined their total effects on cognition in early PD. High CSF amyloid concentrations (> 500 pg/ml) are associated with nearly full protection against cognitive decline in early PD in the whole range of baseline age between 40 and 80 years, and irrespectively of whether p-tau181 or amyloid beta (1–42) are considered as the primary protein variables. The total effect of depression on cognition is shown to be strongly amplified by PD, but not at the time of diagnosis or at prodromal stages. CSF p-tau181 protein could not be a reliable indicator of cognitive decline because of its significantly heterogeneous effects on cognition. The outcomes will enable better understanding of the roles of the clinical and pathological measures and their mutual effects on cognition in early PD. [ABSTRACT FROM AUTHOR]

Recent research has shown that the ecology of stress has hitherto been neglected, but it is in fact an important influence on the distribution and numbers of wild vertebrates. Environmental changes have the potential to cause physiological stress that can affect population dynamics. Detailed information on the influence of environmental variables on glucocorticoid levels (a measure of stress) at the trailing edge of a species’ distribution can highlight stressors that potentially threaten species and thereby help explain how environmental challenges, such as climate change, will affect the survival of these populations. Rainfall determines leaf moisture and/or nutritional content, which in turn impacts on cortisol concentrations. We show that higher faecal cortisol metabolite (FCM) levels in koala populations at the trailing arid edge of their range in southwestern Queensland are associated with lower rainfall levels (especially rainfall from the previous two months), indicating an increase in physiological stress when moisture levels are low. These results show that koalas at the semi-arid, inland edge of their geographic range, will fail to cope with increasing aridity from climate change. The results demonstrate the importance of integrating physiological assessments into ecological studies to identify stressors that have the potential to compromise the long-term survival of threatened species. This finding points to the need for research to link these stressors to demographic decline to ensure a more comprehensive understanding of species’ responses to climate change. [ABSTRACT FROM AUTHOR]