2,109 research outputs found

    Approximative two-flavor framework for neutrino oscillations with nonstandard interactions

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    In this paper, we develop approximative two-flavor neutrino oscillation formulas including subleading nonstandard interaction effects. Especially, the limit when the small mass-squared difference approaches zero is investigated. The approximate formulas are also tested against numerical simulations in order to determine their accuracy and they will probably be most useful in the GeV energy region, which is the energy region where most upcoming neutrino oscillation experiments will be operating. Naturally, it is important to have analytical formulas in order to interpret the physics behind the degeneracies between standard and nonstandard parameters.Comment: 21 pages, 7 figures, REVTeX4. Final version published in Phys. Rev.

    Probing non-unitary mixing and CP-violation at a Neutrino Factory

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    A low energy non-unitary leptonic mixing matrix is a generic feature of many extensions of the Standard Model. In such a case, the task of future precision neutrino oscillation experiments is more ambitious than measuring the three mixing angles and the leptonic (Dirac) CP-phase, i.e., the accessible parameters of a unitary leptonic mixing matrix. A non-unitary mixing matrix has 13 parameters that affect neutrino oscillations, out of which four are CP-violating. In the scheme of Minimal Unitarity Violation (MUV) we analyse the potential of a Neutrino Factory for determining or constraining the parameters of the non-unitary leptonic mixing matrix, thereby testing the origin of CP-violation in the lepton sector.Comment: 21 pages, 8 eps figures, REVTeX

    Signatures from an extra-dimensional seesaw model

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    We study the generation of small neutrino masses in an extra-dimensional model, where right-handed neutrinos are allowed to propagate in the extra dimension, while the Standard Model particles are confined to a brane. Motivated by the fact that extra-dimensional models are non-renormalizable, we truncate the Kaluza-Klein towers at a maximal extra-dimensional momentum. The structure of the bulk Majorana mass term, motivated by the Sherk-Schwarz mechanism, implies that the right-handed Kaluza-Klein neutrinos pair to form Dirac neutrinos, except for a number of unpaired Majorana neutrinos at the top of each tower. These heavy Majorana neutrinos are the only sources of lepton number breaking in the model, and similarly to the type-I seesaw mechanism, they naturally generate small masses for the left-handed neutrinos. The lower Kaluza-Klein modes mix with the light neutrinos, and the mixing effects are not suppressed with respect to the light-neutrino masses. Compared to conventional fermionic seesaw models, such mixing can be more significant. We study the signals of this model at the Large Hadron Collider, and find that the current low-energy bounds on the non-unitarity of the leptonic mixing matrix are strong enough to exclude an observation.Comment: 17 pages, 3 figures, REVTeX4. Final version published in Phys. Rev.

    Salivary Biomarkers for Alzheimer's Disease and Related Disorders

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    The search for accessible and cost-effective biomarkers to complement current cerebrospinal fluid (CSF) and imaging biomarkers in the accurate detection of Alzheimer disease (AD) and other common neurodegenerative disorders remains a challenging task. The advances in ultra-sensitive detection methods has highlighted blood biomarkers (e.g. amyloid-β and neurofilament light) as a valuable and realistic tool in a diagnostic or screening process. Saliva, however, is also a rich source of potential biomarkers for disease detection and offers several practical advantages over biofluids that are currently examined for neurodegenerative disorders. However, while this may be true for the general population, challenges in collecting saliva from an elderly population should be seriously considered. In this review, we begin by discussing how saliva is produced and how age-related conditions can modify saliva production and composition. We then focus on the data available which support the concept of salivary amyloid-β, tau species and novel biomarkers in detecting AD and alpha-synuclein (α-syn) in Parkinson’s disease (PD)

    Cerebrospinal fluid Aβ42/40 corresponds better than Aβ42 to amyloid PET in Alzheimer’s disease

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    Background: Decreased concentrations of amyloid-β 1-42 (Aβ(42)) in cerebrospinal fluid (CSF) and increased retention of Aβ tracers in the brain on positron emission tomography (PET) are considered the earliest biomarkers of Alzheimer’s disease (AD). However, a proportion of cases show discrepancies between the results of the two biomarker modalities which may reflect inter-individual differences in Aβ metabolism. The CSF Aβ(42/40) ratio seems to be a more accurate biomarker of clinical AD than CSF Aβ(42) alone. Objective: We tested whether CSF Aβ(42) alone or the Aβ(42/40) ratio corresponds better with amyloid PET status and analyzed the distribution of cases with discordant CSF-PET results. Methods: CSF obtained from a mixed cohort (n = 200) of cognitively normal and abnormal research participants who had undergone amyloid PET within 12 months (n = 150 PET-negative, n = 50 PET-positive according to a previously published cut-off) was assayed for Aβ(42) and Aβ(40) using two recently developed immunoassays. Optimal CSF cut-offs for amyloid positivity were calculated, and concordance was tested by comparison of the areas under receiver operating characteristic (ROC) curves (AUC) and McNemar’s test for paired proportions. Results: CSF Aβ(42/40) corresponded better than Aβ(42) with PET results, with a larger proportion of concordant cases (89.4% versus 74.9%, respectively, p < 0.0001) and a larger AUC (0.936 versus 0.814, respectively, p < 0.0001) associated with the ratio. For both CSF biomarkers, the percentage of CSF-abnormal/PET-normal cases was larger than that of CSF-normal/PET-abnormal cases. Conclusion: The CSF Aβ(42/40) ratio is superior to Aβ(42) alone as a marker of amyloid-positivity by PET. We hypothesize that this increase in performance reflects the ratio compensating for general between-individual variations in CSF total Aβ

    Sulfatide in health and disease. The evaluation of sulfatide in cerebrospinal fluid as a possible biomarker for neurodegeneration

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    Sulfatide (3-O-sulfogalactosylceramide, SM4) is a glycosphingolipid, highly multifunctional and particularly enriched in the myelin sheath of neurons. The role of sulfatide has been implicated in various biological fields such as the nervous system, immune system, host-pathogen recognition and infection, beta cell function and haemostasis/thrombosis. Thus, alterations in sulfatide metabolism and production are associated with several human diseases such as neurological and immunological disorders and cancers. The unique lipid-rich composition of myelin reflects the importance of lipids in this specific membrane structure. Sulfatide has been shown to be involved in the regulation of oligodendrocyte differentiation and in the maintenance of the myelin sheath by influencing membrane dynamics involving sorting and lateral assembly of myelin proteins as well as ion channels. Sulfatide is furthermore essential for proper formation of the axo-glial junctions at the paranode together with axonal glycosphingolipids. Alterations in sulfatide metabolism are suggested to contribute to myelin deterioration as well as synaptic dysfunction, neurological decline and inflammation observed in different conditions associated with myelin pathology (mouse models and human disorders). Body fluid biomarkers are of importance for clinical diagnostics as well as for patient stratification in clinical trials and treatment monitoring. Cerebrospinal fluid (CSF) is commonly used as an indirect measure of brain metabolism and analysis of CSF sulfatide might provide information regarding whether the lipid disruption observed in neurodegenerative disorders is reflected in this body fluid. In this review, we evaluate the diagnostic utility of CSF sulfatide as a biomarker for neurodegenerative disorders associated with dysmyelination/demyelination by summarising the current literature on this topic. We can conclude that neither CSF sulfatide levels nor individual sulfatide species consistently reflect the lipid disruption observed in many of the demyelinating disorders. One exception is the lysosomal storage disorder metachromatic leukodystrophy, possibly due to the genetically determined accumulation of non-metabolised sulfatide. We also discuss possible explanations as to why myelin pathology in brain tissue is poorly reflected by the CSF sulfatide concentration. The previous suggestion that CSF sulfatide is a marker of myelin damage has thereby been challenged by more recent studies using more sophisticated laboratory techniques for sulfatide analysis as well as improved sample selection criteria due to increased knowledge on disease pathology

    Serum Neurofilament Light Protein as a Marker for Diffuse Axonal Injury: Results from a Case Series Study

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    Diffuse axonal injury (DAI) is an important cause of morbidity in patients with traumatic brain injury (TBI). There is currently no simple and reliable technique for early identification of patients with DAI, or to prognosticate long-term outcome in this patient group. In the present study, we examined acute serum concentrations of neurofilament light (NFL) in nine patients with severe TBI and DAI using a novel ultrasensitive single molecule array (Simoa) assay. The relationships between the NFL concentrations and MRI in the acute stage as well as clinical outcome and magnetic resonance diffusion tensor imaging (MR-DTI) parameters at 12 months were analyzed. We found that the mean NFL concentrations among the patients displayed a 30-fold increase compared with controls, and that NFL completely discriminated between the patients and controls. We also found a relationship between serum NFL and MR-DTI parameters, with higher NFL concentrations in patients with higher trace (R2 = 0.79) and lower fractional anisotropy (FA) (R 2 = 0.83). These results suggest that serum NFL may be a valuable blood biomarker for TBI, reflecting the severity of DAI
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