Medication adherence and persistence according to different antihypertensive drug classes: A retrospective cohort study of 255,500 patients.

Background: Suboptimal adherence to antihypertensives leads to adverse clinical outcomes. This study aims to determine and compare medication adherence and persistence to different first-line antihypertensive drug classes in a large cohort.

Methods: A cohort study was performed using claims data for prescriptions in the German statutory health insurance scheme that insures approximately 90% of the population.

Generic switch after ramipril patent expiry is not associated with decreased pharmacy refill compliance: a retrospective study using the DAPI database.

Objective: For treatment success in chronic diseases such as hypertension, adequate adherence to long-term pharmacotherapy is a prerequisite. The purpose of this study was to evaluate whether switching from brand name ramipril to a generic product after patent expiry may negatively affect patients' refill compliance.

Methods: Claims data for ambulatory prescriptions within the statutory health insurance system were evaluated.

Aging sensitizes toward ROS formation and lipid peroxidation in PS1M146L transgenic mice.

Mutations in the presenilins (PS) account for the majority of familial Alzheimer disease (FAD) cases. To test the hypothesis that oxidative stress can underlie the deleterious effects of presenilin mutations, we analyzed lipid peroxidation products (4-hydroxynonenal (HNE) and malondialdehyde) and antioxidant defenses in brain tissue and levels of reactive oxygen species (ROS) in splenic lymphocytes from transgenic mice bearing human PS1 with the M146L mutation (PS1M146L) compared to those from mice transgenic for wild-type human PS1 (PS1wt) and nontransgenic littermate control mice. In brain tissue, HNE levels were increased only in aged (19-22 months) PS1M146L transgenic animals compared to PS1wt mice and not in young (3-4 months) or middle-aged mice (13-15 months).

Proteomic and functional analyses reveal a mitochondrial dysfunction in P301L tau transgenic mice.

Transgenic mice overexpressing the P301L mutant human tau protein exhibit an accumulation of hyperphosphorylated tau and develop neurofibrillary tangles. The consequences of tau pathology were investigated here by proteomics followed by functional analysis. Mainly metabolism-related proteins including mitochondrial respiratory chain complex components, antioxidant enzymes, and synaptic proteins were identified as modified in the proteome pattern of P301L tau mice.

Impaired Cu/Zn-SOD activity contributes to increased oxidative damage in APP transgenic mice.

Oxidative stress plays an important role in the pathogenesis of Alzheimer's disease. To determine which mechanisms cause the origin of oxidative damage, we analyzed enzymatic antioxidant defense (Cu/Zn-superoxide dismutase Cu/Zn-SOD, glutathione peroxidase GPx and glutathione reductase GR) and lipid peroxidation products malondialdehyde MDA and 4-hydroxynonenal HNE in two different APP transgenic mouse models at 3-4 and 12-15 months of age. No changes in any parameter were observed in brains from PDGF-APP695(SDL) mice, which have low levels of Abeta and no plaque load.