Jeopardies of Aversive Leadership: A Conservation of Resources Theory Approach.

The research on the dark side of leadership is still in its infancy. We have contributed to this line of research by proposing that work alienation acts as an underlying mechanism through which aversive leadership results in reduced job performance. We further propose that psychological capital (PsyCap) acts as an important personal resource that reduces the negative effects of aversive leadership in the form of work alienation. The proposed model gets its support from the conversation of resources theory given by Hobfoll (1989) which suggests that stressful situation like an aversive leadership results in the loss of employee resources as a result of that he/she indulges in work alienation and shows poor job performance to retain back the lost resources. People with better personal resources in the form of PsyCap are better able to cope-up with the aversive leader behavior and make them able to avoid work alienation. It is a time-lagged study. The data for the current study was collected from 321 employees working in the service sector organizations, particularly universities, banks and telecom organizations, through personally administered questionnaires. The results supported the mediation and moderation hypothesis. Limitations and future research along with theoretical and practical implications are given at the end.

Downregulation of the Repressor Element 1-Silencing Transcription Factor (REST) Is Associated with Akt-mTOR and Wnt-ß-Catenin Signaling in Prion Diseases Models.

Prion diseases are a group of infectious diseases characterized by multiple neuropathological changes, yet the mechanisms that preserve function and protect against prion-associated neurodegeneration are still unclear. We previously reported that the repressor element 1-silencing transcription factor (REST) alleviates neurotoxic prion peptide (PrP106-126)-induced toxicity in primary neurons. Here we confirmed the findings of the in vitro model in 263K infected hamsters, an in vivo model of prion diseases and further showed the relationships between REST and related signaling pathways. REST was depleted from the nucleus in prion infected brains and taken up by autophagosomes in the cytoplasm, co-localizing with LC3-II. Importantly, downregulation of the Akt-mTOR and at least partially inactivation of LRP6-Wnt-ß-catenin signaling pathways correlated with the decreased levels of REST in vivo in the brain of 263K-infected hamsters and in vitro in PrP106-126-treated primary neurons. Overexpression of REST in primary cortical neurons alleviated PrP106-126 peptide-induced neuronal oxidative stress, mitochondrial damage and partly inhibition of the LRP6-Wnt-ß-catenin and Akt-mTOR signaling. Based on our findings, a model of REST-mediated neuroprotection in prion infected animals is proposed, with Akt-mTOR and Wnt-ß-catenin signaling as the key pathways. REST-mediated neuronal survival signaling could be explored as a viable therapeutic target for prion diseases and related neurodegenerative diseases.