About Bianchi I with VSL

In this paper we study how to attack, through different techniques, a perfect fluid Bianchi I model with variable G,c and Lambda, but taking into account the effects of a $c$-variable into the curvature tensor. We study the model under the assumption,div(T)=0. These tactics are: Lie groups method (LM), imposing a particular symmetry, self-similarity (SS), matter collineations (MC) and kinematical self-similarity (KSS). We compare both tactics since they are quite similar (symmetry principles). We arrive to the conclusion that the LM is too restrictive and brings us to get only the flat FRW solution. The SS, MC and KSS approaches bring us to obtain all the quantities depending on \int c(t)dt. Therefore, in order to study their behavior we impose some physical restrictions like for example the condition q<0 (accelerating universe). In this way we find that $c$ is a growing time function and Lambda is a decreasing time function whose sing depends on the equation of state, w, while the exponents of the scale factor must satisfy the conditions $\sum_{i=1}^{3}\alpha_{i}=1$ and $\sum_{i=1}^{3}\alpha_{i}^{2}<1,$ $\forall\omega$, i.e. for all equation of state$,$ relaxing in this way the Kasner conditions. The behavior of $G$ depends on two parameters, the equation of state $\omega$ and $\epsilon,$ a parameter that controls the behavior of $c(t),$ therefore $G$ may be growing or decreasing.We also show that through the Lie method, there is no difference between to study the field equations under the assumption of a $c-$var affecting to the curvature tensor which the other one where it is not considered such effects.Nevertheless, it is essential to consider such effects in the cases studied under the SS, MC, and KSS hypotheses.Comment: 29 pages, Revtex4, Accepted for publication in Astrophysics & Space Scienc

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

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