Velocity-force characteristics of an interface driven through a periodic potential

We study the creep dynamics of a two-dimensional interface driven through a periodic potential using dynamical renormalization group methods. We find that the nature of weak-drive transport depends qualitatively on whether the temperature $T$ is above or below the equilibrium roughening transition temperature $T_c$. Above $T_c$, the velocity-force characteristics is Ohmic, with linear mobility exhibiting a jump discontinuity across the transition. For $T \le T_c$, the transport is highly nonlinear, exhibiting an interesting crossover in temperature and weak external force $F$. For intermediate drive, $F>F_*$, we find near $T_c^{-}$ a power-law velocity-force characteristics $v(F)\sim F^\sigma$, with $\sigma-1\propto \tilde{t}$, and well-below $T_c$, $v(F)\sim e^{-(F_*/F)^{2\tilde{t}}}$, with $\tilde{t}=(1-T/T_c)$. In the limit of vanishing drive ($F\ll F_*$) the velocity-force characteristics crosses over to $v(F)\sim e^{-(F_0/F)}$, and is controlled by soliton nucleation.Comment: 18 pages, submitted to Phys. Rev.

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele