The HIFI spectral survey of AFGL 2591 (CHESS). II. Summary of the survey

This paper presents the richness of submillimeter spectral features in the high-mass star forming region AFGL 2591. As part of the CHESS (Chemical Herschel Survey of Star Forming Regions) Key Programme, AFGL 2591 was observed by the Herschel/HIFI instrument. The spectral survey covered a frequency range from 480 up to 1240 GHz as well as single lines from 1267 to 1901 GHz (i.e. CO, HCl, NH3, OH and [CII]). Rotational and population diagram methods were used to calculate column densities, excitation temperatures and the emission extents of the observed molecules associated with AFGL 2591. The analysis was supplemented with several lines from ground-based JCMT spectra. From the HIFI spectral survey analysis a total of 32 species were identified (including isotopologues). In spite of the fact that lines are mostly quite week, 268 emission and 16 absorption lines were found (excluding blends). Molecular column densities range from 6e11 to 1e19 cm-2 and excitation temperatures range from 19 to 175 K. One can distinguish cold (e.g. HCN, H2S, NH3 with temperatures below 70 K) and warm species (e.g. CH3OH, SO2) in the protostellar envelope.Comment: Accepted to A&

Insights into mitochondrial dysfunction: aging, amyloid-β, and tau-A deleterious trio

Significance: Alzheimer's disease (AD) is an age-related progressive neurodegenerative disorder mainly affecting elderly individuals. The pathology of AD is characterized by amyloid plaques (aggregates of amyloid-β [Aβ]) and neurofibrillary tangles (aggregates of tau), but the mechanisms underlying this dysfunction are still partially unclear. Recent Advances: A growing body of evidence supports mitochondrial dysfunction as a prominent and early, chronic oxidative stress-associated event that contributes to synaptic abnormalities and, ultimately, selective neuronal degeneration in AD. Critical Issues: In this review, we discuss on the one hand whether mitochondrial decline observed in brain aging is a determinant event in the onset of AD and on the other hand the close interrelationship of this organelle with Aβ and tau in the pathogenic process underlying AD. Moreover, we summarize evidence from aging and Alzheimer models showing that the harmful trio "aging, Aβ, and tau protein" triggers mitochondrial dysfunction through a number of pathways, such as impairment of oxidative phosphorylation (OXPHOS), elevation of reactive oxygen species production, and interaction with mitochondrial proteins, contributing to the development and progression of the disease. Future Directions: The aging process may weaken the mitochondrial OXPHOS system in a more general way over many years providing a basis for the specific and destructive effects of Aβ and tau. Establishing strategies involving efforts to protect cells at the mitochondrial level by stabilizing or restoring mitochondrial function and energy homeostasis appears to be challenging, but very promising route on the horizon