Comment on "Atlantic and Pacific multidecadal oscillations and Northern Hemisphere temperatures".

Steinman et al. (Reports, 27 February 2015, p. 988) argue that appropriately rescaled multimodel ensemble-mean time series provide an unbiased estimate of the forced climate response in individual model simulations. However, their procedure for demonstrating the validity of this assertion is flawed, and the residual intrinsic variability so defined is in fact dominated by the actual forced response of individual models.

Deconvolution of the factors contributing to the increase in global hurricane intensity.

To better understand the change in global hurricane intensity since 1970, we examined the joint distribution of hurricane intensity with variables identified in the literature as contributing to the intensification of hurricanes. We used a methodology based on information theory, isolating the trend from the shorter-term natural modes of variability. The results show that the trend of increasing numbers of category 4 and 5 hurricanes for the period 1970-2004 is directly linked to the trend in sea-surface temperature; other aspects of the tropical environment, although they influence shorter-term variations in hurricane intensity, do not contribute substantially to the observed global trend.

Changes in tropical cyclone number, duration, and intensity in a warming environment.

We examined the number of tropical cyclones and cyclone days as well as tropical cyclone intensity over the past 35 years, in an environment of increasing sea surface temperature. A large increase was seen in the number and proportion of hurricanes reaching categories 4 and 5. The largest increase occurred in the North Pacific, Indian, and Southwest Pacific Oceans, and the smallest percentage increase occurred in the North Atlantic Ocean. These increases have taken place while the number of cyclones and cyclone days has decreased in all basins except the North Atlantic during the past decade.

Intraneuronal Abeta, non-amyloid aggregates and neurodegeneration in a Drosophila model of Alzheimer's disease.

We have developed models of Alzheimer's disease in Drosophila melanogaster by expressing the Abeta peptides that accumulate in human disease. Expression of wild-type and Arctic mutant (Glu22Gly) Abeta(1-42) peptides in Drosophila neural tissue results in intracellular Abeta accumulation followed by non-amyloid aggregates that resemble diffuse plaques. These histological changes are associated with progressive locomotor deficits and vacuolation of the brain and premature death of the flies. The severity of the neurodegeneration is proportional to the propensity of the expressed Abeta peptide to form oligomers. The fly phenotype is rescued by treatment with Congo Red that reduces Abeta aggregation in vitro. Our model demonstrates that intracellular accumulation and non-amyloid aggregates of Abeta are sufficient to cause the neurodegeneration of Alzheimer's disease. Moreover it provides a platform to dissect the pathways of neurodegeneration in Alzheimer's disease and to develop novel therapeutic interventions.