Objective With an elderly population that is set to more than double by 2050 worldwide, there will be an increased demand for elderly care. This poses several impediments in the delivery of high-quality health and social care. Socially assistive robot (SAR) technology could assume new roles in health and social care to meet this higher demand. This review qualitatively examines the literature on the use of SAR in elderly care and aims to establish the roles this technology may play in the future. Design Scoping review. Data sources Search of CINAHL, Cochrane Library, Embase, MEDLINE, PsychINFO and Scopus databases was conducted, complemented with a free search using Google Scholar and reference harvesting. All publications went through a selection process, which involved sequentially reviewing the title, abstract and full text of the publication. No limitations regarding date of publication were imposed, and only English publications were taken into account. The main search was conducted in March 2016, and the latest search was conducted in September 2017. Eligibility criteria The inclusion criteria consist of elderly participants, any elderly healthcare facility, humanoid and pet robots and all social interaction types with the robot. Exclusions were acceptability studies, technical reports of robots and publications surrounding physically or surgically assistive robots. Results In total, 61 final publications were included in the review, describing 33 studies and including 1574 participants and 11 robots. 28 of the 33 papers report positive findings. Five roles of SAR were identified: affective therapy, cognitive training, social facilitator, companionship and physiological therapy. Conclusions Although many positive outcomes were reported, a large proportion of the studies have methodological issues, which limit the utility of the results. Nonetheless, the reported value of SAR in elderly care does warrant further investigation. Future studies should endeavour to validate the roles demonstrated in this review. Systematic review registration NIHR 58672.

Introduction: The impact of pro-inflammatory cytokines on neuroinflammation and cognitive function after lipopolysaccharide (LPS) challenge remains elusive. Herein we provide evidence that there is a temporal correlation between high-mobility group box 1 (HMGB-1), microglial activation, and cognitive dysfunction. Disabling the interleukin (IL)-1 signaling pathway is sufficient to reduce inflammation and ameliorate the disability. Methods: Endotoxemia was induced in wild-type and IL-1R^-/- mice by intra peritoneal injection of E. Coli LPS (1 mg/kg). Markers of inflammation were assessed both peripherally and centrally, and correlated to behavioral outcome using trace fear conditioning. Results: Increase in plasma tumor necrosis factor-α (TNFα) peaked at 30 minutes after LPS challenge. Up-regulation of IL-1β, IL-6 and HMGB-1 was more persistent, with detectable levels up to day three. A 15-fold increase in IL-6 and a 6.5-fold increase in IL-1β mRNA at 6 hours post intervention (P < 0.001 respectively) was found in the hippocampus. Reactive microgliosis was observed both at days one and three, and was associated with elevated HMGB-1 and impaired memory retention (P < 0.005). Preemptive administration of IL-1 receptor antagonist (IL-1Ra) significantly reduced plasma cytokines and hippocampal microgliosis and ameliorated cognitive dysfunction without affecting HMGB-1 levels. Similar results were observed in LPS-challenged mice lacking the IL-1 receptor to those seen in LPS-challenged wild type mice treated with IL-1Ra. Conclusions: These data suggest that by blocking IL-1 signaling, the inflammatory cascade to LPS is attenuated, thereby reducing microglial activation and preventing the behavioral abnormality.

Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. The modern management of severe TBI has fallen into the domain of a multidisciplinary team led by neurointensivists, neuroanaesthetists, and neurosurgeons and is based on the avoidance of secondary injury, maintenance of cerebral perfusion pressure (CPP), and optimization of cerebral oxygenation. In this review, we will discuss the intensive care management of severe TBI with emphasis on the specific measures directed at the control of intracranial pressure and CPP.

Elderly patients undergoing major surgery often develop cognitive dysfunction and the mechanism of this postoperative complication remains elusive. We sought to determine whether postoperative cognitive dysfunction in old mice is associated with the pathogenesis of Alzheimer's disease. Prospective, randomized study. University teaching hospital-based research laboratory. One-hundred and twenty C57BL/6 14-mo-old male mice (weighing 30-40 g). Mice received intraperitoneal injections of either vehicle or Celastrol (a potent anti-inflammatory compound) for 3 days before undergoing sham surgery or partial hepatectomy, on the surgery day, and for a further 4 days after surgery. Cognitive function, hippocampal neuroinflammation, and pathologic markers of Alzheimer's disease were assessed 1 day after surgery day 1, 3, or 7. Cognitive impairment following surgery was associated with the appearance of certain pathologic hallmarks of Alzheimer's disease: microgliosis, astrogliosis, enhanced transcriptional and translational activity of β-amyloid precursor protein, β-amyloid production, and τ protein hyperphosphorylation in the hippocampus. Surgery-induced changes in cognitive dysfunction were prevented by the administration of Celastrol as were changes in β-amyloid and τ processing. These data suggest that surgery can provoke astrogliosis, β-amyloid accumulation, and τ phosphorylation in old subjects, which is likely to be associated with the cognitive decline seen in postoperative cognitive dysfunction.