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http://dx.doi.org/10.1056/NEJMc1912185 | DOI Listing |
J Neurochem
January 2025
The Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA.
Alzheimer disease is a neurodegenerative pathology-modifying mitochondrial metabolism with energy impairments where the effects of biological sex and DNA repair deficiencies are unclear. We investigated the therapeutic potential of dietary ketosis alone or with supplemental nicotinamide riboside (NR) on hippocampal intermediary metabolism and mitochondrial bioenergetics in older male and female wild-type (Wt) and 3xTgAD-DNA polymerase-β-deficient (3xTg/POLβ) (AD) mice. DNA polymerase-β is a key enzyme in DNA base excision repair (BER) of oxidative damage that may also contribute to mitochondrial DNA repair.
View Article and Find Full Text PDFAnimal
October 2024
Department of Animal Science, Federal University of Paraná, Curitiba, PR 80035-050, Brazil.
The use of exogenous phytase and vitamin D metabolites such as 25-hydroxycholecalciferol (25-OH-D) for poultry is well consolidated, but the potential for additive effects when supplementing both requires further investigation. This study investigated possible interactions between supplementation of 25-OH-D and high doses of phytase for broilers fed Ca- and P-deficient diets. A total of 1 200 one-d-old male broiler chicks were randomly allocated from one of four dietary treatments in a 2 × 2 factorial arrangement: 600 or 2 000 phytase units (FYT)/kg and with or without the inclusion of 25-OH-D at 69 µg/kg, with 12 replicates of 25 broilers each.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
January 2025
Department of Pharmacology and Toxicology. School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Severe vitamin D (vitD) deficiency is a very common condition in patients with pulmonary arterial hypertension (PAH) and it is predictor of poor prognosis. There is emerging evidence suggesting a connection between the insufficient response to phosphodiesterase-5 inhibitors (PDE5i) and vitD deficiency in patients with PAH. In the present translational study, vitD deficiency was induced in Wistar rats by exposure to vitD free diet for 5 weeks and followed by Su5416 administration and hypoxia (10%) for 3 weeks, a standard experimental model of PAH.
View Article and Find Full Text PDFJ Pediatr Gastroenterol Nutr
January 2025
Department of Paediatrics, University Medical Centre Maribor, Maribor, Slovenia.
Anaemia is a frequent consequence of many gastrointestinal (GI) diseases in children and it can even be the initial presenting symptom of underlying chronic GI disease. The definition of anaemia is age and gender-dependent and it can be classified based on pathophysiology, red cell morphology, and clinical presentation. Although nutritional deficiencies, including GI malabsorption of nutrients and GI bleeding, play a major role, other pathophysiologic mechanisms seen in chronic GI diseases, whether inflammatory (e.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Georgia, College of Pharmacy, Athens, GA, USA.
Background: Lipids are key modulators in the pathogenesis of Alzheimer's disease (AD). Dysregulation of lipid homeostasis may disrupt the blood brain barrier, alter myelination, disturb cellular signaling and cause abnormal processing of the amyloid precursor protein. The purpose of this scoping review was to evaluate fatty acid supplementation in patients with AD.
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