Crystal structure of 1-meth-oxy-2,2,2-tris-(pyrazol-1-yl)ethane.

The title compound, C12H14N6O, consists of three pyrazole rings bound via nitro-gen to the distal ethane carbon of meth-oxy ethane. The dihedral angles between the three pyrazole rings are 67.62 (14), 73.74 (14), and 78.92 (12)°. In the crystal, mol-ecules are linked by bifurcated C-H,H⋯N hydrogen bonds, forming double-stranded chains along [001]. The chains are linked via C-H⋯O hydrogen bonds, forming a three-dimensional framework structure. The crystal was refined as a perfect (0.5:0.5) inversion twin.

Bis[1-meth-oxy-2,2,2-tris-(pyrazol-1-yl-κN (2))ethane]-nickel(II) bis-(tri-fluoro-methane-sulfonate) dihydrate.

In the title salt, [Ni(C12H14N6O)2](CF3SO3)2·2H2O, the Ni(II) cation is located on an inversion centre and is coordinated by six N atoms from two tridentate 1-meth-oxy-2,2,2-tris-(pyrazol-1-yl)ethane ligands in a distorted octa-hedral geometry. The Ni-N distances range from 2.0594 (12) to 2.0664 (12) Å, intra-ligand N-Ni-N angles range from 84.59 (5) to 86.06 (5)°, and adjacent inter-ligand N-Ni-N angles range between 93.94 (5) and 95.41 (5)°. In the crystal, inversion-related pyrazole rings are π-π stacked, with an inter-planar spacing of 3.4494 (18) Å, forming chains that propagate parallel to the a-axis direction. Inter-molecular O-H⋯O hydrogen bonds are present between water mol-ecules and tri-fluoro-methane-sulfonate anions.

Bis[1-meth-oxy-2,2,2-tris-(pyrazol-1-yl-κN (2))ethane]-nickel(II) bis-(tri-fluoro-methane-sulfonate) methanol disolvate.

In the title salt, [Ni(C12H14N6O)2](CF3SO3)2·2CH3OH, the Ni(II) ion is coordinated by six N atoms from two tridentate 1-meth-oxy-2,2,2-tris-(pyrazol-1-yl)ethane ligands in a distorted octa-hedral geometry. The Ni(II) ion is situated on an inversion centre. The Ni-N distances range from 2.0589 (19) to 2.0757 (19) Å, intra-ligand N-Ni-N angles range from 84.50 (8) to 85.15 (8)°, and adjacent inter-ligand N-Ni-N angles range between 94.85 (8) and 95.50 (8)°. In the crystal, O-H⋯O hydrogen bonds between methanol solvent mol-ecules and tri-fluoro-methane-sulfonate anions are observed.

Tetra-ethyl-ammonium tris-(thio-cyanato-κN)[tris-(1H-pyrazol-1-yl-κN(2))methane]-nickelate(II).

The title salt, (C8H20N)[Ni(NCS)3(C10H10N6)], consists of a tetra-ethyl-ammonium cation and an anion comprising an octa-hedral Ni(II) atom surrounded by three N atoms from a tripodal tris-(pyrazol-1-yl)methane ligand, and three thio-cyanate ligands, each bound at the N-atom end. The ligand Ni-N distances range from 2.097 (2) to 2.127 (2) Šfor the tripodal ligand and from 2.045 (2) to 2.075 (2) Šfor the thio-cyanate ligands. The dihedral angles between the three pyrazole rings are 59.03 (12), 53.09 (10) and 67.90 (10)°.

Bis[tris-(3,5-dimethyl-1H-pyrazol-1-yl-κN(2))meth-yl]sodium trifluoro-methane-sulfonate.

In the title salt, [Na(C(16)H(22)N(6))(2)]CF(3)SO(3), the Na(+) cation is coordinated by six N atoms from two tridentate tris-(3,5-dimethyl-pyrazol-1-yl)methane ligands in a distorted octa-hedral geometry. The Na-N distances range from 2.427 (3) to 2.507 (3) Å, intra-ligand N-Na-N angles range from 74.71 (8) to 79.31 (9)°, and adjacent inter-ligand N-Na-N angles range between 100.42 (9) and 104.97 (9)°. The structure is twinned by inversion [occupancy factors = 0.50 (9)] and the trifluoro-methane-sulfonate anion is disordered, with two end-over-end orientations of unequal occupancy [0.781 (3) and 0.219 (3)].

A potential role for zinc alterations in the pathogenesis of Alzheimer's disease.

Alzheimer's disease (AD), one of the major causes of disability and mortality in Western societies, is a progressive age-related neurodegenerative disorder. Increasing evidence suggests that the etiology of AD may involve disruptions of zinc (Zn) homeostasis. This review discusses current evidence supporting a potential role of Zn and zinc transporters (ZnTs) in processing of the amyloid beta protein precursor (APP) and amyloid beta (Aß) peptide generation and aggregation.

Bis[tris-(1H-pyrazol-1-yl-κN)methane]-nickel(II) bis-{[tris-(1H-pyrazol-1-yl-κN)methane]-tris-(thio-cyanato-κN)nickelate(II)} methanol disolvate.

Attempts to prepare the mononuclear [(tpm)Ni(II)L(3)](-1) [tpm = tris-(1H-pyrazol-1-yl)methane and L = thio-cyanate] anion yielded the methanol-solvated salt, [(tpm)(2)Ni(II)][(tpm)Ni(II)(NCS)(3)](2)·2CH(3)OH or [Ni(C(10)H(10)N(6))(2)][Ni(NCS)(3)(C(10)H(10)N(6))](2)·2CH(3)OH. The asymmetric unit consists of half a centrosymmetric bis-[tris-(1H-pyrazol-1-yl)methane]-nickel(II) cation and an octa-hedral nickelate(II) anion bound to one tpm and three L ligands, and a methanol solvent mol-ecule. One of the L ligands is disordered over two positions with occupancy factors of 0.650 (3) and 0.350 (3). There are O-H⋯S inter-actions between the methanol and the disordered thio-cyanate anion, and a weak C-H⋯O hydrogen bond between the cation and the methanol O atom.

Tetra-ethyl-ammonium (2,2'-bipyridine)tetra-cyanidocobaltate(III) sesquihydrate acetonitrile solvate.

The title complex, (C(8)H(20)N)[Co(CN)(4)(C(10)H(8)N(2))]·CH(3)CN·1.5H(2)O, consists of tetra-ethyl ammonium cations, mononuclear [Co(III)bpy(CN)(4)](-) anions and uncoordinated water and acetonitrile mol-ecules. The Co(III) atom is six-coordinated by two 2,2'-bipyridine (bpy) N atoms and four cyanide C atoms in a distorted octa-hedral geometry. The acute bite angle of the chelating bpy [82.28 (8)°] is the main factor accounting for this distortion. In addition, the tetra-ethyl-ammonium cation is significantly disordered [occupancy ratio 0.611 (3):0.389 (3)]. The presence of water mol-ecules, one of which is disordered over two positions about an inversion center, results in the formation of a network of O-H⋯N hydrogen bonds involving the cyanide N atoms.

Dichloridobis(3,4,5-trimethyl-1H-pyrazole-κN)cobalt(II).

In the title compound, [Co(II)Cl(2)(C(6)H(10)N(2))(2)], a pair of 3,4,5-trimethyl-pyrazoles act as monodentate ligands. Two Cl(-) anions are also bonded directly to the Co(II) atom, which has a CoN(2)Cl(2) chromophore in a slightly distorted tetra-hedral geometry. The two mol-ecules in the asymmetric unit are related by an approximate twofold rotation roughly parallel to the a axis. The amino H atom in the pyrazole ring participates in weak N-H⋯Cl hydrogen bonds to form chains that propagate roughly parallel to the c axis.

Alterations of zinc transporter proteins ZnT-1, ZnT-4 and ZnT-6 in preclinical Alzheimer's disease brain.

Our previous studies demonstrate alterations of zinc (Zn) transporter proteins ZnT-1, ZnT-4 and ZnT-6 in vulnerable brain regions of subjects with mild cognitive impairment (MCI), and early and late stage Alzheimer's disease (AD), suggesting disruptions of Zn homeostasis may play a role in the pathogenesis of AD. A preclinical stage of AD (PCAD) has been described in which subjects show no overt clinical manifestations of AD, but demonstrate significant AD pathology at autopsy. To determine if alterations of ZnT proteins occur in PCAD, we measured ZnT-1, ZnT-4 and ZnT-6 in the hippocampus/parahippocampal gyrus (HPG) and cerebellum (CER) of seven PCAD subjects and seven age-matched normal control (NC) subjects using Western blot analysis and immunohistochemistry. Our results show a significant decrease (P < 0.05) of ZnT-1 in HPG of PCAD subjects, along with an increase of ZnT-4 in PCAD CER and ZnT-6 in PCAD HPG, but a significant decrease in PCAD CER compared to NC subjects. Confocal microscopy of representative sections of HPG shows altered ZnTs are associated with neurons immunopositive for MC-1, a monoclonal antibody that identifies neurons early in formation of neurofibrillary tangles. Overall, our results suggest that alterations in Zn transport proteins may contribute to the pathology observed in PCAD subjects before onset of clinical symptoms.

Organoselenium (Sel-Plex diet) decreases amyloid burden and RNA and DNA oxidative damage in APP/PS1 mice.

To evaluate potential antioxidant characteristics of organic selenium (Se), double knock-in transgenic mice expressing human mutations in the amyloid precursor protein (APP) and human presenilin-1 (PS1) were provided a Se-deficient diet, a Se-enriched diet (Sel-Plex), or a control diet from 4 to 9 months of age followed by a control diet until 12 months of age. Levels of DNA, RNA, and protein oxidation as well as lipid peroxidation markers were determined in all mice and amyloid beta-peptide (Abeta) plaques were quantified. APP/PS1 mice provided Sel-Plex showed significantly (P<0.05) lower levels of Abeta plaque deposition and significantly decreased levels of DNA and RNA oxidation. Sel-Plex-treated mice showed no significant differences in levels of lipid peroxidation or protein oxidation compared to APP/PS1 mice on a control diet. To determine if diminished oxidative damage was associated with increased antioxidant enzyme activities, brain glutathione peroxidase (GSH-Px), glutathione reductase, and glutathione transferase activities were measured. Sel-Plex-treated mice showed a modest but significant increase in GSH-Px activity compared to mice on a normal diet (P<0.5). Overall, these data suggest that organic Se can reduce Abeta burden and minimize DNA and RNA oxidation and support a role for it as a potential therapeutic agent in neurologic disorders with increased oxidative stress.

Bis(tripyrazol-1-ylmethane)nickel(II) tetra-cyanidonickelate(II) dihydrate.

The title complex, [Ni(C(10)H(10)N(6))(2)][Ni(CN)(4)]·2H(2)O, contains an octa-hedral nickel(II) cation and a square-planar nickel(II) anion. Both the cation and the anion reside on a crystallographic center of inversion. The Ni(II) center in the cation is coordinated by six pyrazol-1-yl rings of two chelating tripyrazol-1-ylmethane [HC(pz)(3)] ligands, with Ni-N distances that range between 2.0647 (19) and 2.0828 (19) Å. The Ni(II) center in the anion is coordinated by four cyanide ligands, with Ni-C distances in the range 1.869 (2)-1.869 (3) Å. The [Ni(CN)(4)](2-) anions are linked by inversion-related water mol-ecules into extended chains that run parallel to the a axis.