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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 109 records · Page 6
All sourcesNASA NTRSDOE OSTI
DOE OSTI2011

Tau and muon lepton flavor violations in the littlest Higgs model with T parity

Lepton flavor violation in {tau} and {mu} processes is studied in the littlest Higgs model with T parity. We consider various asymmetries defined in polarized {tau} and {mu} decays. Correlations among branching ratios and asymmetries are shown in the following lepton flavor violation processes: {mu}{sup +}{yields}e{sup +}{gamma}, {mu}{sup +}{yields}e{sup +}e{sup +}e{sup -}, {mu}{sup -}A{yields}e{sup -}A (A=Al, Ti, Au, and Pb), {tau}{sup +}{yields}{mu}{sup +}{gamma}, {tau}{sup +}{yields}{mu}{sup +}{mu}{sup +}{mu}{sup -}, {tau}{sup +}{yields}{mu}{sup +}e{sup +}e{sup -}, {tau}{sup +}{yields}{mu}{sup +}P (P={pi}{sup 0}, {eta} and {eta}{sup '}), {tau}{sup +}{yields}{mu}{sup +}V (V={rho}{sup 0}, {omega} and {phi}), {tau}{sup +}{yields}e{sup +}{gamma}, {tau}{sup +}{yields}e{sup +}e{sup +}e{sup -}, {tau}{sup +}{yields}e{sup +}{mu}{sup +}{mu}{sup -}, {tau}{sup +}{yields}e{sup +}P, {tau}{sup +}{yields}e{sup +}V, {tau}{sup +}{yields}{mu}{sup +}{mu}{sup +}e{sup -} and {tau}{sup +}{yields}e{sup +}e{sup +}{mu}{sup -}. It is shown that large parity asymmetries and time-reversal asymmetries are allowed in {mu}{sup +}{yields}e{sup +}e{sup +}e{sup -}. For {tau} lepton flavor violation processes, sizable asymmetries are possible reflecting characteristic chirality structure of lepton flavor violating interactions in this model.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗
DOE OSTI2017

Comparison of multiple tau-PET measures as biomarkers in aging and Alzheimer's disease

The recent development of tau-specific positron emission tomography (PET) tracers enables in vivo quantification of regional tau pathology, one of the key lesions in Alzheimer's disease (AD). Tau PET imaging may become a useful biomarker for clinical diagnosis and tracking of disease progression but there is no consensus yet on how tau PET signal is best quantified. The goal of the current paper was to evaluate multiple whole-brain and region-specific approaches to detect clinically relevant tau PET signal. Two independent cohorts of cognitively normal adults and amyloid-positive (Aβ + ) patients with mild cognitive impairment (MCI) or AD-dementia underwent [ 18 F]AV-1451 PET. Methods for tau tracer quantification included: (i) in vivo Braak staging, (ii) regional uptake in Braak composite regions, (iii) several whole-brain measures of tracer uptake, (iv) regional uptake in AD-vulnerable voxels, and (v) uptake in a priori defined regions. Receiver operating curves characterized accuracy in distinguishing Aβ - controls from AD/MCI patients and yielded tau positivity cutoffs. Clinical relevance of tau PET measures was assessed by regressions against cognition and MR imaging measures. Key tracer uptake patterns were identified by a factor analysis and voxel-wise contrasts. Braak staging, global and region-specific tau measures yielded similar diagnostic accuracies, which differed between cohorts. While all tau measures were related to amyloid and global cognition, memory and hippocampal/entorhinal volume/thickness were associated with regional tracer retention in the medial temporal lobe. Key regions of tau accumulation included medial temporal and inferior/middle temporal regions, retrosplenial cortex, and banks of the superior temporal sulcus. Finally, our data indicate that whole-brain tau PET measures might be adequate biomarkers to detect AD-related tau pathology. However, regional measures covering AD-vulnerable regions may increase sensitivity to early tau PET signal, atrophy and memory decline.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2011

Measurements of Charged Current Lepton Universality and |Vus| using Tau Lepton Decays to e- v v, __- v v, pi- v and K- v

Using 467 fb{sup -1} of e{sup +}e{sup -} annihilation data collected with the BABAR detector, they measure {Beta}({tau}{sup -} {yields} {mu}{sup -}{bar {nu}}{sub {mu}}{nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} e{sup -} {bar {nu}}{sub e}{nu}{sub {tau}}) = (0.9796 {+-} 0.0016 {+-} 0.0036), {Beta}({tau}{sup -} {yields} {pi}{sup -} {nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} e{sup -}{bar {nu}}{sub e}{nu}{sub {tau}}) = (0.5945 {+-} 0.0014 {+-} 0.0061), and {Beta}({tau}{sup -} {yields} K{sup -}{nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} e{sup -}{bar {nu}}{sub e}{nu}{sub {tau}}) = (0.03882 {+-} 0.00032 {+-} 0.00057), where the uncertainties are statistical and systematic, respectively. From these precision {tau} measurements, they test the Standard Model assumption of {mu}-e and {tau}-{mu} charge current lepton universality and provide determinations of |V{sub us}| experimentally independent of the decay of a kaon.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗
DOE OSTI2016

Pioglitazone prevents tau oligomerization

Tau aggregation and amyloid β protein (Aβ) deposition are the main causes of Alzheimer's disease (AD). Peroxisome proliferator-activated receptor γ (PPARγ) activation modulates Aβ production. To test whether the PPARγ agonist pioglitazone (PIO) is also effective in preventing tau aggregation in AD, we used a cellular model in which wild-type tau protein (4R0N) is overexpressed (M1C cells) (Hamano et al., 2012) as well as primary neuronal cultures. PIO reduced both phosphorylated and total tau levels, and inactivated glycogen synthase kinase 3β, a major tau kinase, associated with activation of Akt. In addition, PIO decreased cleaved caspase3 and C-terminal truncated tau species by caspase, which is expected to decrease tau aggregation. A fractionation study showed that PIO reduced high molecular-weight (120 kDa), oligomeric tau species in Tris Insoluble, sarkosyl-soluble fractions. Tau decrease was reversed by adding GW9662, a PPARγ antagonist. Together, our current results support the idea that PPARγ agonists may be useful therapeutic agents for AD. - Highlights: • PPARγ agonist pioglitazone decreased tau oligomerization. • The mechanism lies on the reduction of phosphorylated tau and caspase cleaved tau. • Pioglitazone inactivated GSK3β and caspase3. • Tau decrease was reversed by the PPAR γ antagonist GW9662.

60 APPLIED LIFE SCIENCES↗