Reconciling mantle attenuation-temperature relationships from seismology, petrology, and laboratory measurements

Seismic attenuation measurements provide a powerful tool for sampling mantle properties. Laboratory experiments provide calibrations at seismic frequencies and mantle temperatures for dry melt-free rocks, but require ∼10²−10³ extrapolations in grain size to mantle conditions; also, the effects of water and melt are not well understood. At the same time, body wave attenuation measured from dense broadband arrays provides reliable estimates of shear wave attenuation (Q_S⁻¹), affording an opportunity for calibration. We reanalyze seismic data sets that sample arc and back-arc mantle in Central America, the Marianas, and the Lau Basin, confirming very high attenuation (Q_S ∼ 25–80) at 1 Hz and depths of 50–100 km. At each of these sites, independent petrological studies constrain the temperature and water content where basaltic magmas last equilibrated with the mantle, 1300–1450°C. The Q_S measurements correlate inversely with the petrologically inferred temperatures, as expected. However, dry attenuation models predict Q_S too high by a factor of 1.5–5. Modifying models to include effects of H₂O and rheology-dependent grain size shows that the effects of water-enhanced dissipation and water-enhanced grain growth nearly cancel, so H₂O effects are modest. Therefore, high H₂O in the arc source region cannot explain the low Q_S, nor in the back arc where lavas show modest water content. Most likely, the high attenuation reflects the presence of melt, and some models of melt effects come close to reproducing observations. Overall, body wave Q_S can be reconciled with petrologic and laboratory inferences of mantle conditions if melt has a strong influence beneath arcs and back arcs

Alzheimer disease models and human neuropathology: similarities and differences

Animal models aim to replicate the symptoms, the lesions or the cause(s) of Alzheimer disease. Numerous mouse transgenic lines have now succeeded in partially reproducing its lesions: the extracellular deposits of Aβ peptide and the intracellular accumulation of tau protein. Mutated human APP transgenes result in the deposition of Aβ peptide, similar but not identical to the Aβ peptide of human senile plaque. Amyloid angiopathy is common. Besides the deposition of Aβ, axon dystrophy and alteration of dendrites have been observed. All of the mutations cause an increase in Aβ 42 levels, except for the Arctic mutation, which alters the Aβ sequence itself. Overexpressing wild-type APP alone (as in the murine models of human trisomy 21) causes no Aβ deposition in most mouse lines. Doubly (APP × mutated PS1) transgenic mice develop the lesions earlier. Transgenic mice in which BACE1 has been knocked out or overexpressed have been produced, as well as lines with altered expression of neprilysin, the main degrading enzyme of Aβ. The APP transgenic mice have raised new questions concerning the mechanisms of neuronal loss, the accumulation of Aβ in the cell body of the neurons, inflammation and gliosis, and the dendritic alterations. They have allowed some insight to be gained into the kinetics of the changes. The connection between the symptoms, the lesions and the increase in Aβ oligomers has been found to be difficult to unravel. Neurofibrillary tangles are only found in mouse lines that overexpress mutated tau or human tau on a murine tau −/− background. A triply transgenic model (mutated APP, PS1 and tau) recapitulates the alterations seen in AD but its physiological relevance may be discussed. A number of modulators of Aβ or of tau accumulation have been tested. A transgenic model may be analyzed at three levels at least (symptoms, lesions, cause of the disease), and a reading key is proposed to summarize this analysis

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder