With the continued success of the open RISC-V architecture, practical deployment of RISC-V processors necessitates an in-depth consideration of their testability, safety and security aspects. This... Show moreWith the continued success of the open RISC-V architecture, practical deployment of RISC-V processors necessitates an in-depth consideration of their testability, safety and security aspects. This survey provides an overview of recent developments in this quickly-evolving field. We start with discussing the application of state-of-the-art functional and system-level test solutions to RISC-V processors. Then, we discuss the use of RISC-V processors for safety-related applications; to this end, we outline the essential techniques necessary to obtain safety both in the functional and in the timing domain and review recent processor designs with safety features. Finally, we survey the different aspects of security with respect to RISC-V implementations and discuss the relationship between cryptographic protocols and primitives on the one hand and the RISC-V processor architecture and hardware implementation on the other. We also comment on the role of a RISC-V processor for system security and its resilience against side-channel attacks. Show less
Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis occurs early in Alzheimer's disease (AD), associated with elevated circulating glucocorticoids (GC) and glucocorticoid receptors (GR)... Show moreDysregulation of the hypothalamic-pituitary-adrenal (HPA) axis occurs early in Alzheimer's disease (AD), associated with elevated circulating glucocorticoids (GC) and glucocorticoid receptors (GR) signaling impairment. However, the precise role of GR in the pathophysiology of AD remains unclear. Using an acute model of AD induced by the intracerebroventricular injection of amyloid-beta oligomers (oA beta), we analyzed cellular and behavioral hallmarks of AD, GR signaling pathways, processing of amyloid precursor protein, and enzymes involved in Tau phosphorylation. We focused on the prefrontal cortex (PFC), particularly rich in GR, early altered in AD and involved in HPA axis control and cognitive functions. We found that oA beta impaired cognitive and emotional behaviors, increased plasma GC levels, synaptic deficits, apoptosis and neuroinflammatory processes. Moreover, oA beta potentiated the amyloidogenic pathway and enzymes involved both in Tau hyperphosphorylation and GR activation. Treatment with a selective GR modulator (sGRm) normalized plasma GC levels and all behavioral and biochemical parameters analyzed. GR seems to occupy a central position in the pathophysiology of AD. Deregulation of the HPA axis and a feed-forward effect on PFC GR sensitivity could participate in the etiology of AD, in perturbing A beta and Tau homeostasis. These results also reinforce the therapeutic potential of sGRm in AD. Show less
