The center cannot hold: A Bayesian chronology for the collapse of Tiwanaku.

The timing of Tiwanaku's collapse remains contested. Here we present a generational-scale chronology of Tiwanaku using Bayesian models of 102 radiocarbon dates, including 45 unpublished dates. This chronology tracks four community practices: residing short- vs. long-term, constructing monuments, discarding decorated ceramics, and leaving human burials. Tiwanaku was founded around AD 100 and around AD 600, it became the region's principal destination for migrants. It grew into one of the Andes' first cities and became famous for its decorated ceramics, carved monoliths, and large monuments. Our Bayesian models show that monument building ended ~AD 720 (the median of the ending boundary). Around ~AD 910, burials in tombs ceased as violent deaths began, which we document for the first time in this paper. Ritualized murders are limited to the century leading up to ~AD 1020. Our clearest proxy for social networks breaking down is a precise estimate for the end of permanent residence, ~AD 1010 (970-1050, 95%). This major inflection point was followed by visitors who used the same ceramics until ~AD 1040. Temporary camps lasted until roughly ~AD 1050. These four events suggest a rapid, city-wide collapse at ~AD 1010-1050, lasting just ~20 years (0-70 years, 95%). These results suggest a cascading breakdown of community practices and social networks that were physically anchored at Tiwanaku, though visitors continued to leave informal burials for centuries. This generation-scale chronology suggests that collapse 1) took place well before reduced precipitation, hence this was not a drought-induced societal change and 2) a few resilient communities sustained some traditions at other sites, hence the chronology for the site of Tiwanaku cannot be transposed to all sites with similar material culture.

Reduced expression of the Kinesin-Associated Protein 3 (KIFAP3) gene increases survival in sporadic amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis is a degenerative disorder of motor neurons that typically develops in the 6th decade and is uniformly fatal, usually within 5 years. To identify genetic variants associated with susceptibility and phenotypes in sporadic ALS, we performed a genome-wide SNP analysis in sporadic ALS cases and controls. A total of 288,357 SNPs were screened in a set of 1,821 sporadic ALS cases and 2,258 controls from the U.S. and Europe. Survival analysis was performed using 1,014 deceased sporadic cases. Top results for susceptibility were further screened in an independent sample set of 538 ALS cases and 556 controls. SNP rs1541160 within the KIFAP3 gene (encoding a kinesin-associated protein) yielded a genome-wide significant result (P = 1.84 x 10(-8)) that withstood Bonferroni correction for association with survival. Homozygosity for the favorable allele (CC) conferred a 14.0 months survival advantage. Sequence, genotypic and functional analyses revealed that there is linkage disequilibrium between rs1541160 and SNP rs522444 within the KIFAP3 promoter and that the favorable alleles of rs1541160 and rs522444 correlate with reduced KIFAP3 expression. No SNPs were associated with risk of sporadic ALS, site of onset, or age of onset. We have identified a variant within the KIFAP3 gene that is associated with decreased KIFAP3 expression and increased survival in sporadic ALS. These findings support the view that genetic factors modify phenotypes in this disease and that cellular motor proteins are determinants of motor neuron viability.