Influence of off-stoichiometry on the properties of the heavy fermion superconductors UNi₂Al₃ and UPd₂Al₃

We have investigated the influence of deviations from stoichiometry on the metallurgical, superconducting and magnetic properties of UNi2Al3 and UPd2Al3. Deviations from stoichiometry in UNi2Al3 generally increase the width of the superconducting transition and can lead to a complete suppression of the anomalies related to the antiferromagnetic (AF) ordering. By contrast, in UPd2Al3 we have observed a reduction in the superconducting transition temperature T-c whereas the AF transition is not affected. We discuss the implication of these results on the metallurgical phase diagram and on the nature of both the superconducting and the AF state of these compounds

Doping effects on UPd₂Al₃

We present first results of a doping study on the U site on UPd2Al3. These results give further support for a tetravalent uranium configuration and an induced type of antiferromagnetic ordering. They confirm the importance of an unperturbed electronic configuration for both antiferromagnetic long-range ordering and heavy-fermion superconductivity. Implications for the interaction between both phenomena are discussed

U(Pd_1-xNi_x)₂Al₃ - An Alloy Between Two Heavy-Fermion Superconductors

We present and analyze measurements of the electrical resistivity, the dc-and ac-susceptibility and the specific-heat of the quasi-binary alloy U(Pd1-xNix)2Al3 in the temperature range from 0.3K to 300K. All investigated properties indicate a continuous change from UPd2AI3 to UNi2Al3, with the exception of superconductivity, which dissappears for 0.12 less-than-or-equal-to x less-than-or-equal-to 0.95. The results stress the importance of crystal field effects

4f-conduction electron hybridization in ternary CeTMAl compounds

We present an investigation of Ce-TM-Al phase diagrams with TM = Ru, Pd, Pt and Au. Several new compounds have been characterized by measurements of the electrical resistivity rho(T), the dc susceptibility chi(T) and, in some cases, the specific heat C(T). We find that in the compounds with TM=Ru, the hybridization strength between 4f and conduction electrons is strong, leading in most compounds to an intermediate valent (IV) state. By contrast, most of the investigated compounds with TM = Pd, Pt and Au order magnetically indicating a much weaker hybridization strength. However, some of the Pt and especially Pd compounds are very near to the crossover from the magnetic to the non-magnetic regime as deduced from a Kondo-type maximum in the resistivity and a large electronic specific heat at low temperatures

Early Aβ reduction prevents progression of cerebral amyloid angiopathy

OBJECTIVE: Clinical trials targeting Aβ for Alzheimer's disease (AD) failed for arguable reasons that include selecting the wrong stages of AD pathophysiology or Aβ being the wrong target at all. Targeting Aβ to prevent cerebral amyloid angiopathy (CAA) has not been rigorously followed although the causal role of Aβ for CAA and related hemorrhages is undisputed. CAA occurs with normal aging and to various degree in AD where its impact and treatment is confounded by the presence of parenchymal Aβ deposition. METHODS: APPDutch mice develop CAA in the absence of parenchymal amyloid, mimicking hereditary cerebral hemorrhage with amyloidosis - Dutch (HCHWA-D). Mice were treated with a BACE1 inhibitor. 3D-ultramicroscopy and immunoassays were used for visualizing CAA and assessing Aβ in CSF and brain. RESULTS: CAA onset in mice was at 22-24 mo of age, first in frontal leptomeningeal and superficial cortical vessels followed by vessels penetrating the cortical layers. CSF Aβ increased with aging followed by a decrease of both, Aβ40 and Aβ42 upon CAA onset supporting that combined reduction of CSF Aβ40 and 42 is a specific biomarker for vascular amyloid. BACE1 inhibitor treatment starting at CAA onset and continued for 4 mo revealed a 90% Aβ reduction in CSF and largely prevented CAA progression and associated pathologies. INTERPRETATION: This is the first study showing that Aβ reduction at early disease time points largely prevents CAA in the absence of parenchymal amyloid. Our observation provides a preclinical basis for Aβ-reducing treatments in patients at risk of CAA and in presymptomatic HCHWA-D. This article is protected by copyright. All rights reserved