11 research outputs found
Comorbidity Burden in Trial-Aligned Patients with Established Gout in Germany, UK, US, and France: a Retrospective Analysis
Identification and characterization of CYP79D16 and CYP71AN24 catalyzing the first and second steps in l-phenylalanine-derived cyanogenic glycoside biosynthesis in the Japanese apricot, Prunus mume Sieb. et Zucc.
CYP79 P450 monooxygenases in gymnosperms: CYP79A118 is associated with the formation of taxiphyllin in Taxus baccata
Urinary excretion of uric acid is negatively associated with albuminuria in patients with chronic kidney disease: a cross-sectional study
The ABCG2 Q141K hyperuricemia and gout associated variant illuminates the physiology of human urate excretion
Genome-wide association analysis identifies multiple loci associated with kidney disease-related traits in Korean populations
Identification of candidate genes related to calanolide biosynthesis by transcriptome sequencing of Calophyllum brasiliense (Calophyllaceae)
Does physical activity reduce risk for Alzheimer’s disease through interaction with the stress neuroendocrine system?
Lack of physical activity (PA) is a risk factor for Alzheimer's disease (AD) and PA interventions are believed to provide an effective non-pharmacological approach for attenuating the symptoms of this disease. However, the mechanism of action of these positive effects is currently unknown. It is possible that the benefits may be at least partially mediated by effects on the neuroendocrine stress system. Chronic stress can lead to dysfunction of the hypothalamic pituitary adrenal (HPA) axis, leading to aberrant basal and circadian patterns of cortisol secretion and a cascade of negative downstream events. These factors have been linked not only to reduced cognitive function in the non-demented but also increased levels of Amyloid β plaques and protein Tau "tangles" (the neuropathological hallmarks of AD) in mouse models of this disease. However, there is evidence that PA can have restorative effects on the stress neuroendocrine system and related risk factors relevant to AD. We explore the possibility that PA can positively impact upon AD by restoring normative HPA axis function, with consequent downstream effects upon underlying neuropathology and associated cognitive function. We conclude with suggestions for future research to test this hypothesis in patients with AD