Trolling is a subject of apparent academic confusion; the few studies conducted thus far yielded a variety of conflicting definitions regarding what constitutes trolling behaviour and little information regarding trolling motivations. In order to shed further light on this phenomenon, the present study aimed to (1) determine which behaviours actual trolls consider as trolling, (2) explore the motivations behind trolling, and (3) examine the online community's response to trolling as perceived by the troll. After performing semi-structured interviews with 22 self-confessed trolls, we found that there is a variety of behaviours trolls consider trolling which can now be put in clear categories based on target and method. Three key motivations to troll emerged: personal enjoyment, revenge, and thrill-seeking. Trolling also appears to be a cyclical, self-perpetuating phenomenon enabled by the online community at large. Theoretical implications for future trolling research are also discussed. KeywordsInterviews, motivation, trolling, online community, online gamesIn the world of online gaming, undesirable behaviour is commonplace. Players will kill teammates, verbally abuse their peers, and misdirect new community members, spreading chaos and disorder (see Riot Games, 2015). These people are called 'trolls'

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Amyloid-β peptide (Aβ) plays an essential pathophysiological role in Alzheimer disease (AD) and elevation of luteinizing hormone (LH) levels during aging has been implicated in its pathogenesis. To assess the effect of LH receptor deficiency on Aβ accumulation, we generated a bigenic mouse model APPsw+/Lhr−/− that expresses human amyloid precursor protein (APPsw) in the background of LH receptor (Lhr) knockout. Genetic ablation of Lhr resulted in a significant decrease in the number of Aβ plaques and protein content in the hippocampus and cerebral cortex in both male and female mice. Accordingly, several Aβ deposition-related neuropathologic features and functionally relevant molecules were markedly improved, including decreased astrogliosis, reductions of elevated phosphorylated tau, c-fos, α7-nicotinic acetylcholine receptor, and restoration of the altered neuropeptide Y receptors Y1 and Y2. Diminution of Aβ accumulation in the absence of LHR supports the contention that dysregulation of LH may impact the pathogenesis of AD. The APPsw+/Lhr−/− mouse may be a useful tool for advancing understanding of the role of LH-mediated events in AD and a model in which to test therapeutic interventions.