Recent results on B -> mu(+)mu(-) decays with the CMS experiment
MODERN PHYSICS LETTERS A
Authors: Langenegger, Urs
Abstract
Results on B -> mu(+)mu(-) decays with the CMS experiment are reported, using 61 fb(-1) of data recorded during LHC Run 1 and 2016. With an improved muon identification algorithm and refined unbinned maximum likelihood fitting methods, the decay B-s(0) -> mu(+)mu(-) is observed with a significance of 5.6 standard deviations. Its branching fraction is measured to be (B) over bar (B-s(0) -> mu(+)mu(-) ) = [2.9 +/- 0.7 (exp)+/- 0.2 (frag)]x 10(-9), where the first error is the combined statistical and systematic uncertainty and the second error quantifies the uncertainty of the B-s(0) and B+ fragmentation probability ratio. The B-s(0) -> mu(+)mu(-) effective lifetime is tau(mu+mu)- = 1.70+(+0.61)(-0.44) ps. No evidence for the decay B-0 -> mu(+)mu(-) is found and an upper limit of B(B-0 -> mu(+)mu(-)) < 3.6 x 10(-10) (at 95% confidence level) is determined. All results are consistent with the standard model of particle physics.
Tau accumulation in astrocytes of the dentate gyrus induces neuronal dysfunction and memory deficits in Alzheimer's disease
NATURE NEUROSCIENCE
Authors: Richetin, Kevin; Steullet, Pascal; Pachoud, Mathieu; Perbet, Romain; Parietti, Enea; Maheswaran, Mathischan; Eddarkaoui, Sabiha; Begard, Severine; Pythoud, Catherine; Rey, Maria; Caillierez, Raphaelle; Do, Kim Q.; Halliez, Sophie; Bezzi, Paola; Buee, Luc; Leuba, Genevieve; Colin, Morvane; Toni, Nicolas; Deglon, Nicole
Abstract
Alzheimer's disease is often considered a disease of neurons. This study reveals that astrocytes are also impaired by the disease and that these cells contribute more to memory deterioration than previously thought. Alzheimer's disease (AD) is characterized by the accumulation of the tau protein in neurons, neurodegeneration and memory loss. However, the role of non-neuronal cells in this chain of events remains unclear. In the present study, we found accumulation of tau in hilar astrocytes of the dentate gyrus of individuals with AD. In mice, the overexpression of 3R tau specifically in hilar astrocytes of the dentate gyrus altered mitochondrial dynamics and function. In turn, these changes led to a reduction of adult neurogenesis, parvalbumin-expressing neurons, inhibitory synapses and hilar gamma oscillations, which were accompanied by impaired spatial memory performances. Together, these results indicate that the loss of tau homeostasis in hilar astrocytes of the dentate gyrus is sufficient to induce AD-like symptoms, through the impairment of the neuronal network. These results are important for our understanding of disease mechanisms and underline the crucial role of astrocytes in hippocampal function.
COA
Publication 
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