Peculiarities in the Amino Acid Composition of Sow Colostrum and Milk, and Their Potential Relevance to Piglet Development.

The composition of mother's milk is considered the ideal diet for neonates. This study investigated how conserved or variable the amino acid profile of sow colostrum and milk is throughout lactation, compared with other studies in sows and other species. Twenty-five sows (parity one to seven) from one farm with gestation lengths of 114 to 116 d were sampled on d 0, 3, and 10 after parturition. The total amino acid profile of the samples was analyzed through ion-exchange chromatography, and the results were displayed as the percentage of total amino acid and compared with literature data. Most of the amino acid concentrations in sow milk decreased significantly (p < 0.05) throughout the lactation period, while the amino acid profile generally showed a conserved pattern, especially from d 3 to d 10, and was rather similar across different studies. Glutamine + glutamate was the most abundant amino acid in milk at all sampling moments, accounting for 14-17% of total amino acids. The proportions of proline, valine, and glycine in sow milk nearly accounted for 11%, 7%, and 6% respectively, and were higher compared to human, cow, and goat milk, while the methionine proportion was less than the other three. Compared to the large variations often reported in macronutrient concentrations, the amino acid profile of sow milk in the present study, as well as in others, seems well conserved across the lactation period. Similarities with characteristic differences were also observed between sow milk and piglet body composition, which might reflect the nutrition requirements of preweaning piglets. This study warrants further research exploring the link between the whole amino acid profile and the particular amino acids for suckling piglets and could facilitate insight for optimizing creep feed.

Tryptophan Metabolism in Inflammaging: From Biomarker to Therapeutic Target.

Inflammation aims to restore tissue homeostasis after injury or infection. Age-related decline of tissue homeostasis causes a physiological low-grade chronic inflammatory phenotype known as inflammaging that is involved in many age-related diseases. Activation of tryptophan (Trp) metabolism along the kynurenine (Kyn) pathway prevents hyperinflammation and induces long-term immune tolerance. Systemic Trp and Kyn levels change upon aging and in age-related diseases. Moreover, modulation of Trp metabolism can either aggravate or prevent inflammaging-related diseases. In this review, we discuss how age-related Kyn/Trp activation is necessary to control inflammaging and alters the functioning of other metabolic faiths of Trp including Kyn metabolites, microbiota-derived indoles and nicotinamide adenine dinucleotide (NAD+). We explore the potential of the Kyn/Trp ratio as a biomarker of inflammaging and discuss how intervening in Trp metabolism might extend health- and lifespan.

Neuropsychiatric Disturbances in Alzheimer's Disease: What Have We Learned from Neuropathological Studies?

Neuropsychiatric symptoms (NPS) are an integral part of the dementia syndrome and were therefore recently included in the core diagnostic criteria of dementia. The near universal prevalence of NPS in Alzheimer's disease (AD), combined with their disabling effects on patients and caregivers, is contrasted by the fact that few effective and safe treatments exist, which is in part to be attributed to our incomplete understanding of the neurobiology of NPS. In this review, we describe the pathological alterations typical for AD, including spreading and evolution of burden, effect on the molecular and cellular integrity, functional consequences and atrophy of NPS-relevant brain regions and circuits in correlation with specific NPS assessments. It is thereby clearly established that NPS are fundamental expressions of the underlying neurodegenerative brain disease and not simply reflect the patients' secondary response to their illness. Neuropathological studies, moreover, include a majority of end-stage patient samples, which may not correctly represent the pathophysiological environment responsible for particular NPS that may already be present in an early stage, or even prior to AD diagnosis. The burdensome nature and high prevalence of NPS, in combination with the absence of effective and safe pharmacotherapies, provide a strong incentive to continue neuropathological and neurochemical, as well as imaging and other relevant approaches to further improve our apprehension of the neurobiology of NPS.