Constructions of Generalized Sidon Sets

We give explicit constructions of sets S with the property that for each integer k, there are at most g solutions to k=s_1+s_2, s_i\in S; such sets are called Sidon sets if g=2 and generalized Sidon sets if g\ge 3. We extend to generalized Sidon sets the Sidon-set constructions of Singer, Bose, and Ruzsa. We also further optimize Koulantzakis' idea of interleaving several copies of a Sidon set, extending the improvements of Cilleruelo & Ruzsa & Trujillo, Jia, and Habsieger & Plagne. The resulting constructions yield the largest known generalized Sidon sets in virtually all cases.Comment: 15 pages, 1 figure (revision fixes typos, adds a few details, and adjusts notation

Author Correction: Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing (Nature Genetics, (2019), 51, 3, (414-430), 10.1038/s41588-019-0358-2)

An amendment to this paper has been published and can be accessed via a link at the top of the paper

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