Background and objectives: Canine-assisted therapy has been receiving growing attention as a means of aiding children with autism spectrum disorder (ASD). Yet, only limited studies have been done and a great deal of literature related to this intervention is anecdotal. The present study aims at providing additional quantitative evidence on the potential of dogs to positively modulate the behavior of children with ASD. Settings/location, subjects, and interventions: A 12-year-old boy diagnosed with ASD was exposed, at his usual treatment location (the Portuguese Association for Developmental Disorders and Autism at Vila Nova de Gaia, Portugal), to the following treatment conditions: (1) one-to-one structured activities with a therapist assisted by a certified therapy dog, and (2) one-to-one structured activities with the same therapist alone (as a control). To accurately assess differences in the behavior of the participant between these treatment conditions, the therapist followed a strict research protocol. The behavior of the participant was continuously video-recorded during both treatment conditions for further analysis and comparison. Treatment outcomes: In the presence of the dog, the participant exhibited more frequent and longer durations of positive behaviors (such as smiling and positive physical contacting) as well as less frequent and shorter durations of negative behaviors (such as aggressive manifestations). Conclusions: These findings are in accordance with previous experimental work and provide additional support for the assertion that dogs can prime autistic children for therapy. Ultimately, this study may contribute toward a change for full acceptance of canine-assisted therapy programs within the medical milieu. Additional studies using a similar research protocol on more autistic children will certainly help professionals to work on the most effective methods to individually serve this population through canine-assisted interventions.

Nervous tissue homeostasis requires the regulation of microglia activity. Using conditional gene targeting in mice, we demonstrate that genetic ablation of the small GTPase Rhoa in adult microglia is sufficient to trigger spontaneous microglia activation, producing a neurological phenotype (including synapse and neuron loss, impairment of long-term potentiation [LTP], formation of β-amyloid plaques, and memory deficits). Mechanistically, loss of Rhoa in microglia triggers Src activation and Src-mediated tumor necrosis factor (TNF) production, leading to excitotoxic glutamate secretion. Inhibiting Src in microglia Rhoa-deficient mice attenuates microglia dysregulation and the ensuing neurological phenotype. We also find that the Rhoa/Src signaling pathway is disrupted in microglia of the APP/PS1 mouse model of Alzheimer disease and that low doses of Aβ oligomers trigger microglia neurotoxic polarization through the disruption of Rhoa-to-Src signaling. Overall, our results indicate that disturbing Rho GTPase signaling in microglia can directly cause neurodegeneration.

Binge drinking may cause anxiety by triggering microglia to destroy excitatory synapses.

Group B streptococcal (GBS) meningitis remains a devastating disease. The absence of an animal model reproducing the natural infectious process has limited our understanding of the disease and, consequently, delayed the development of effective treatments. We describe here a mouse model in which bacteria are transmitted to the offspring from vaginally colonised pregnant females, the natural route of infection. We show that GBS strain BM110, belonging to the CC17 clonal complex, is more virulent in this vertical transmission model than the isogenic mutant BM110∆cylE, which is deprived of hemolysin/cytolysin. Pups exposed to the more virulent strain exhibit higher mortality rates and lung inflammation than those exposed to the attenuated strain. Moreover, pups that survive to BM110 infection present neurological developmental disability, revealed by impaired learning performance and memory in adulthood. The use of this new mouse model, that reproduces key steps of GBS infection in newborns, will promote a better understanding of the physiopathology of GBS-induced meningitis.