Agility and search and rescue training differently affects pet dogs' behaviour in socio-cognitive tasks

Both genetic factors and life experiences appear to be important in shaping dogs' responses in a test situation. One potentially highly relevant life experience may be the dog's training history, however few studies have investigated this aspect so far. This paper briefly reviews studies focusing on the effects of training on dogs' performance in cognitive tasks, and presents new, preliminary evidence on trained and untrained pet dogs' performance in an 'unsolvable task'. Thirty-nine adult dogs: 13 trained for search and rescue activities (S&R group), 13 for agility competition (Agility group) and 13 untrained pets (Pet group) were tested. Three 'solvable' trials in which dogs could obtain the food by manipulating a plastic container were followed by an 'unsolvable' trial in which obtaining the food became impossible. The dogs' behaviours towards the apparatus and the people present (owner and researcher) were analysed. Both in the first 'solvable' and in the 'unsolvable' trial the groups were comparable on actions towards the apparatus, however differences emerged in their human-directed gazing behaviour. In fact, results in the 'solvable' trial, showed fewer S&R dogs looking back at a person compared to agility dogs, and the latter alternating their gaze between person and apparatus more frequently than pet dogs. In the unsolvable trial no difference between groups emerged in the latency to look at the person however agility dogs looked longer at the owner than both pet and S&R dogs; whereas S&R dogs exhibited significantly more barking (always occurring concurrently to looking at the person or the apparatus) than both other groups. Furthermore, S&R dogs alternated their gaze between person and apparatus more than untrained pet dogs, with agility dogs falling in between these two groups. Thus overall, it seems that the dogs' human-directed communicative behaviours are significantly influenced by their individual training experiences. © 2009 Elsevier B.V. All rights reserved.

MRZ-99030 – a novel modulator of Aβ aggregation: II – reversal of Aβ oligomer-induced deficits in long-term potentiation (LTP) and cognitive performance in rats and mice.

β-amyloid1-42 (Aβ1-42) is a major endogenous pathogen underlying the aetiology of Alzheimer's disease (AD). Recent evidence indicates that soluble Aβ oligomers, rather than plaques, are the major cause of synaptic dysfunction and neurodegeneration. Small molecules that suppress Aβ aggregation, reduce oligomer stability or promote off-pathway non-toxic oligomerization represent a promising alternative strategy for neuroprotection in AD. MRZ-99030 was recently identified as a dipeptide that modulates Aβ1-42 aggregation by triggering a non-amyloidogenic aggregation pathway, thereby reducing the amount of intermediate toxic soluble oligomeric Aβ species. The present study evaluated the relevance of these promising results with MRZ-99030 under pathophysiological conditions i.e. against the synaptotoxic effects of Aβ oligomers on hippocampal long term potentiation (LTP) and two different memory tasks. Aβ1-42 interferes with the glutamatergic system and with neuronal Ca2+ signalling and abolishes the induction of LTP. Here we demonstrate that MRZ-99030 (100–500 nM) at a 10:1 stoichiometric excess to Aβ clearly reversed the synaptotoxic effects of Aβ1-42 oligomers on CA1-LTP in murine hippocampal slices. Co-application of MRZ-99030 also prevented the two-fold increase in resting Ca2+ levels in pyramidal neuron dendrites and spines triggered by Aβ1-42 oligomers. In anaesthetized rats, pre-administration of MRZ-99030 (50 mg/kg s.c.) protected against deficits in hippocampal LTP following i.c.v. injection of oligomeric Aβ1-42. Furthermore, similar treatment significantly ameliorated cognitive deficits in an object recognition task and under an alternating lever cyclic ratio schedule after the i.c.v. application of Aβ1-42 and 7PA2 conditioned medium, respectively. Altogether, these results demonstrate the potential therapeutic benefit of MRZ-99030 in AD.

Public perceptions of personalised nutrition through the lens of Social Cognitive Theory

Social Cognitive Theory has been used to explain findings derived from focus group discussions (N = 4) held in the United Kingdom with the aim of informing best practice in personalised nutrition. Positive expectancies included weight loss and negative expectancies surrounded on-line security. Monitoring and feedback were crucial to goal setting and progress. Coaching by the service provider, family and friends was deemed important for self-efficacy. Paying for personalised nutrition symbolised commitment to behaviour change. The social context of eating, however, was perceived a problem and should be considered when designing personalised diets. Social Cognitive Theory could provide an effective framework through which to deliver personalised nutrition.

Fractionated Radiation Exposure of Rat Spinal Cords Leads to Latent Neuro- Inflammation in Brain, Cognitive Deficits,and Alterations in Apurinic Endonuclease 1

Ionizing radiation causes degeneration of myelin, the insulating sheaths of neuronal axons, leading to neurological impairment. As radiation research on the central nervous system has predominantly focused on neurons, with few studies addressing the role of glial cells, we have focused our present research on identifying the latent effects of single/ fractionated -low dose of low/ high energy radiation on the role of base excision repair protein Apurinic Endonuclease-1, in the rat spinal cords oligodendrocyte progenitor cells’ differentiation. Apurinic endonuclease-1 is predominantly upregulated in response to oxidative stress by low- energy radiation, and previous studies show significant induction of Apurinic Endonuclease-1 in neurons and astrocytes. Our studies show for the first time, that fractionation of protons cause latent damage to spinal cord architecture while fractionation of HZE (28Si) induce increase in APE1 with single dose, which then decreased with fractionation. The oligodendrocyte progenitor cells differentiation was skewed with increase in immature oligodendrocytes and astrocytes, which likely cause the observed decrease in white matter, increased neuro-inflammation, together leading to the observed significant cognitive defects.